WEEK 1 | MODULE 1 DR. CONSUELO C.

REYES
PERIODONTICS 1 Ð LECTURE DENT 4C Ð 2nd SEM

DEFINITION OF TERMS ¥ Romans

1. Periodontium Ð cementum, periodontl ligament (PDL), ¥ Aulus Cornelius Celsus
alveolar bone; and gingiva ¥ Paul of Aegina
III. Middle Ages
MODULE 1: TOPIC ¥ Ottoman Empire
CANVAS - BASED ¥ Albucasis
LESSON 1: ¥ Avicenna
PERIODONTICS/PERIODONTOLOGY
- is a branch of Dentistry that deals with diagnosis and IV. Renaissance
treatment of diseases and supporting structures of the ¥ Serefeddin Sabuncuoglu
teeth which includes the gingiva cementum, periodontal ¥ Ambroise ParŽ
ligament and alveolar bone (periodontium) ¥ Girolamo Cardano

Ø Study of normal and diseased periodontium includes V. 18th Century

structural, functional and environmental factors. ¥ Pierre Fauchard
Ø Include topics on assessment, etiology, pathology, ¥ John Hunter
histopathology, and role of inflammation in periodontal
disease, as well as classification of periodontal diseases VI. 19th Century
Ø application of treatment modalities , therapeutic and ¥ Leonard Koecker
preventive periodontics to the clinical setting. ¥ Levi Spear Parmly
¥ John Riggs
Diagnostics Aids : ¥ Salomon Robicsek
¥ Probes
¥ Radiographs VII. 20th Century
¥ Imaging techniques ¥ Bernhard Gottlieb
¥ Microbial analysis ¥ Oskar Weski
¥ Robert Neumann
Periodontal Therapy: ¥ Per-Ingvar BrŠnemark
¥ Non-surgical ¥ Jens Waerhaug
¥ Surgical

Scope: WEEK 1: 02/08/2022 DISCUSSION:

¥ Periodontics - Orthodontics
¥ Periodontics - Prosthodontics PERIODONTOLOGY/ PERIODONTICS
¥ Periodontics - Oral Surgery - Special branch of dentistry that deals with prevetion,
¥ Periodontics - Restorative Dentistry diagnosis, treatment of diseases of supporting
¥ Periodontics - Endodontics structures of the teeth and their substitues and the
¥ Periodontics - Forensics implantation or transplantation of teeth and their
¥ Periodontology - Geriatrics substitues
¥ Periodontology - Internal Medicine Peri Ð around, or surrounding
o Pulmonology Odont Ð tooth
o Cardiology Logos/logy- a study
o OB - Gyn
LESSON 2: HISTORY OF PERIODONTOLOGY TISSUES OF THE PERIODONTIUM
Periodontics was recognized as a dental specialty by the American 1. Gingiva
Dental Association in 1947. However, periodontal disease was 2. Periodontal ligamentss
common among bones unearthed from ancient civilizations. Through 3. Cementum
the centuries, pioneering individuals contributed to the advancement 4. Alveolar bone
of periodontics from developing new concepts to inventing new
equipment that would eventually lead to modern and better methods. GINGIVA
Watch this brief summary of the History of Periodontology and meet - Part of the oral mucoa that covers the alveolar processes
some of them. of the jaws and surrounds the necks of the teeth
Required Reading: Chapter 1: Newmann & CarranzaÕs Clinical - They stabilize the tooth
PERIODONTOLOGY: Newman, Takei, Klokkevold and Carranza,
13th edition/12thed
Clinical Periodontology and Implant Dentistry: Nicklaus Lang and Jan
Lindhe, 6th ed; History of Periodontics/Periodontology
I. Early Civilizations
¥ India
¥ China
¥ Hebrews

II. Classical World Parts:

¥ Greeks 1. Marginal gingiva/free gingiva Ð along the margins.
¥ Hippocrates
Synonymous with free gingiva

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WEEK 1 | MODULE 1 DR. CONSUELO C. REYES
PERIODONTICS 1 Ð LECTURE DENT 4C Ð 2nd SEM

2. Free gingival groove

3. Interdental gingiva Ð occupies the gingival embrasure
from facial to lingual
4. Interdental groove Ð searates the free and attched
gingiva
5. Attached gingiva - attached
6. Alveolar mucosa Ð covers the alvolar bone, more 6. INTERDENTAL GINGIVA Ð occupies the gingival
reddish (bc not keratinized) embrasure
7. Mucogingival junction/line Ð demarcation of the Consists of 2 papillae:
alveolar mucosa and attached gingiva 1 facial and 1 lingual; and the COL
8. Interdental papilla Ð triangular in shape gingiva. COL Ð is a valley-like depression which connects the 2 papillae and
9. Gingival sulcus Ð V shaped groove/space inside the free conforms to the shape of the interproximal contact areas.
gingiva. Space bounded by hard surface (crown) and NO CONTACT AREA, NO COL, NO PAPILLAE
other lining of sulcular epithelium. COL or Interpapillary Saddle

7. GINGIVAL SULCUS Ð depth is from 0-3mm. It is V-

shaped space around the tooth bounded by the gingiva
on 1 side and the tooth surface on the other side.
If depth goes beyond 3mm Ñ> periodontal pocket

8. BLEEDING Ð no observable bleeding upon probing or

slight provocation.

Characteristics of Inflamed or Diseased Gingiva

Characteristics of a healthy gingiva

1. COLOR Ð the gingiva is reddish. (Inflammed bc blood

1. COLOR Ð coral pink due to vascular supply, thickness vessels are dilated, engorged with blood, loose/less
and degree of keratinization (produced by keratinocytes, keratinization)
makes gingiva and hard palate strnger and firmer) of the 2. CONTOUR Ð the marginal gingiva is less scalloping or
gingiva somewhat straighter. Attached gingiva is less
Melanin pigmentation Ð is prominent in black individuals deviating accentuated due to shallowing of interdental grooves
from the coral pink. 3. CONSISTENCY Ð the gingiva feels spongy, soft or
2. CONTOUR Ð the marginal gingiva is scalloping following fluctuant (compressible/movable)
the shape and alignment of the teeth in the arch 4. TEXTURE Ð smooth and slimy
3. CONSISTENCY Ð the attached gingiva is firm and 5. INTERDENTAL PAPILLAE Ð blunt, rounded, cup-
resilient and well anchored to the bone shaped.
4. TEXTURE Ð has textured surface similar to an orange 6. GINGIVAL SULCUS Ð greater than 3mm = periodontal
peel called ÒstipplingsÓ pocket
5. INTERDENTAL PAPILLA Ð is triangular in shape and tips 7. BLEEDS Ð upon slight provocation
are pointed and knife-edged 8. DEMARCATION Ð between the free gingiva and attached
Presence of diastema = abence of interdental papilla gingiva is lost.

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WEEK 2 | MODULE 2 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C 2ND SEM

WEEK 2: 02/15/2022 Discussion Ø It has the same function as OE, which gives resistance to
GINGIVAL EPITHELIUM mechanical forces and impermeability to fluid and cells.
- The lining of the gingiva that you can see clinically
- Encompasses the external surface of the gingiva including 3. Junctional epithelium (JE) Ð forms the dentoepithelial
the movable and attached areas as well as the gingival junction apical to the sulcus.
sulcus and the junctional epithelium. Dento Ð tooth
- From lining of the outer surface from attached mucosa Epithelium Ð soft tissue
to junctional epithelium Ø Important when doing periodontal therapy/ resto
procedures.
Ø Its coronal end forms the bottom of the gingival sulcus and
is overlapped by the sulcular epithelium.
Ø It is attached by one broad surface to the tooth and by the
other to the gingival connective tissue.
Ø It is the stratified non-keratinizing epithelium that surrounds
the tooth like a collar.
Gold standard in measuring periodontal pocket: Periodontal probe = >
3mm, diseased. <3mm normal

Non-keratinized layer:
1. Superficial layer
2. Intermediate layer
3. Basal layer
4. Lamina propria
3 sections:
1. Oral epithelium (OE)Ð Extends from the mucogingival ¥ The junctional epithelium is more permeable than the oral
junction to the marginal gingiva/gingival margin/free or sulcular epithelium
gingiva. ¥ It serves as the route for the passage of bacterial products
Ø Keratinized Ð dead cells which makes it stronger and from the sulcus into the connective tissue and for fluid and
serves as a protective barrier cells from the connective tissue into the sulcus.
Ø It is the stratified squamous keratinizing epithelium that
lines the vestibular and oral surfaces of the gingiva. THE GINGIVAL FIBERS
Ø Function of OE: designed for protection against - Connective tissue fibers which are found in the gingival
mechanical injury during mastication. Because its tissue adjacent to the teeth.
keratinized - Aid in holding the gingival tissue firmly against the teeth
Ø It is connected to the underlying connective tissue of the
lamina propria (light pink) by an irregular interface Ð rete
ridges
Ø OE connected to lamia propria via the rete ridges
(interlocked)

The oral epithelium consists of:

1. Basal layer Ð stratum basale
2. Spinous layer Ð stratum spinosum
3. Granular layer Ð stratum granulosum
4. Cornified layer Ð stratum corneum

Functions:
1. To brace firmly the marginal gingiva against the tooth
2. Provide rigidity necessary to withstand forces of
mastication without being deflected away from the tooth
2. Sulcular epithelium (SE) Ð from marginal gingiva up to surface
overlaps the coronal potion part of the junctional 3. To unite marginal gingiva with root cementum and the
epithelium. adjacent attached gingiva
Ø it is the stratified, squamous epithelium, non-keratinized or
parakeratined, that is continuous with the oral epithelium
and lines the lateral surface of the sulcus
Ø Gingival sulcus
Ø Apically, it overlaps the coronal border of the junctional
epithelium.

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WEEK 2 | MODULE 2 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C 2ND SEM

GINGIVAL FIBERS ARE SUBDIVIDED INTO 8 PRINCIPAL FIBERS

8. Transseptal fibers
- Course from one approximal tooth surface to the
approximal surface of the adjacent tooth

MODULE 2: ANATOMY OF THE PERIODONTIUM

CANVAS Ð BASED

LESSON 1: NORMAL ANATOMY OF THE PERIODONTIUM

GINGIVA
The gingiva is the soft tissue structure that surrounds the teeth and
alveolar bone. In a healthy state, the gingiva is coral pink, which may
sometimes be pigmented depending on the person's ethnicity. It is
firm in consistency, and is attached to the underlying alveolar
bone. The surface of gingiva is keratinized and may exhibit an
orange peel appearance, called stipplings.

1. Dentogingival fibers
- Insert into the cementum apical to the junctional epithelium
and fan out into the adjacent connective tissue.

2. Dentoperiosteal fibers
- Insert into the cementum apical to the junctional epithelium
and blend with the periosteal covering of the adjacent
alveolar process.
- Periosteal (periosteum, outer covering of the bone)
1. The free gingiva (or marginal gingiva, not to be
3. Alveologingival fibers confused with gingival margin)
- Insert into the alveolar crest and fan out into the adjacent is unattached at the terminal edge, usually 1mm wide, that surrounds
gingival connective tissues. the teeth like a collar. The margin of the free gingiva is rounded in
such a way that a small invagination or gingival sulcus is formed
4. Circumferential fibers between the tooth and the gingiva.
- Follow a circular course around individual dental units
2. The attached gingiva
5. Semicircular fibers is the keratinized tissue that is firmly attached to the underlying
- Insert on the approximal surfaces of a tooth and follow a periosteum of the alveolar bone. It extends from the free gingiva
semicircular course to insert on the opposite side of the (delineated by the free gingival groove) to the loose,
same tooth. unkeratinized alveolar mucosa facially (delineated by
the mucogingival junction). It is generally wider in the anterior region
6. Transgingival fibers and gets narrower towards the posterior region.
- Insert into the approximal surface of a tooth and fan out
toward the oral or vestibular surface

7. Intergingival fibers
- Course along the oral or vestibular surfaces of the dental
arch

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WEEK 2 | MODULE 2 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C 2ND SEM

3. The interdental gingiva

is formed by the gingival tissues in the interproximal spaces beneath
the tooth contact. It can have a pyramidal shape where the tip of the
papilla is immediately below the contact point, or a col shape where it
has a valley-like depression that connects the facial and lingual 1. Gingival group is located around the necks of the teeth
papilla. 2. Dentoalveolar group surrounds the roots of the teeth.

Gingival Fiber Group

Transseptal Cervical tooth to Resist tooth
tooth mesial to separation mesial
distal to it distal
Microscopic examination reveals that gingiva is composed of the Attached gingiva Cervical tooth to Resist gingival
overlying stratified squamous epithelium (oral epithelium) and the attached gingiva displacement
underlying central core of connective tissue (lamina propria). Although Free gingival Cervical tooth to Resist gingival
the epithelium is predominantly cellular in nature, the connective free gingival displacement
tissue is less cellular and composed primarily of collagen fibers and Circumferential Continuous around Resist gingival
ground substance. These two tissues are considered separately. The neck of tooth displacement
stratum corneum is found on only keratinized tissues like the attached
gingiva. Dentoalveolar Fiber Group
Apical Apex of root of Resist vertical
fundic forces
Oblique Apical 1/3 of root to Resist vertical and
adjacent alveolar intrusive forces
bone proper
Horizontal Midroot to adjacent Resist horizontal
alveolar bone and tipping forces
proper
Alveolar crest Cervical root to Resist vertical and
alveolar crest of intrusive forces
alveolar bone
proper
Interradicular Between roots to Resist vertical and
alveolar bone lateral movement
PERIODONTAL LIGAMENT proper
The periodontal ligament is a specialized tissue that connects the
cementum to the gingiva and alveolar socket. It is composed mostly
of collagen bands and fibroblasts. Interstitial spaces contain the blood
vessels and nerve trunks, which communicate freely with vessels and
nerves at the apex of the roots and the alveolar bone. This tissue is
highly cellular, containing fibroblasts and vascular, neural, bone, and
cemental cells. The primary function of the periodontal ligament is
support for the teeth. The ligament also transmits neural input to the
masticatory apparatus and has a nutritive function essential to
maintaining the ligamentÕs health, which has important clinical
implications.
The periodontal ligament (PDL) is a connective tissue consisting
The collagen fibers are strategically arranged as variously orientated primarily of collagen fiber bundles (collagen types I and III) and cells
dense fiber bundles that connect alveolar bone and cementum, which found between the roots of teeth and the inner walls of the alveolar
may help to resist movement in specific directions. socket. The cells of the PDL are heterogeneous including fibroblasts,
Two groups of principal fibers are named according to their location osteoblasts, cementoblasts, and stem cells.
with respect to the teeth.
¥ The PDL firmly anchors the tooth to the bone via SharpeyÕs
fibres and distributes applied force to contiguous alveolar
bone.
¥ The PDL thus represents an essential tissue that maintains
the periodontal environment and function and is therefore

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WEEK 2 | MODULE 2 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C 2ND SEM

important in dentistry including in both periodontics and and partly cementoblasts and that the intrinsic fibers are secreted by
orthodontics. only cementoblasts. Acellular extrinsic fiber cementum (AEFC)
contains densely packed extrinsic fibers and no cementocytes. AEFC
CEMENTUM corresponds to classical acellular cementum. Cellular intrinsic fiber
The cementum is the mineralized tissue covering the dentin surfaces cementum (CIFC) contains intrinsic fibers and cementocytes. Cellular
of the tooth root and is known to be the attachment site for the mixed stratified cementum (CMSC) corresponds to classical cellular
periodontal ligaments. It is light yellow in appearance, and is thinner cementum. Typical CMSC is partitioned by intensely hematoxylin-
at the cervical area and thickens towards the root apex. stainable lines or incremental lines. The individual partitioned
cementum is CIFC, and occasionally AEFC. Namely, CMSC
Cementum is slightly softer than dentin and consists of about represents the whole of cellular cementum composed of stratified
45Ð50% inorganic mineral (mainly the apatite crystals) CIFC and AEFC. Cellular cementum with both intrinsic and extrinsic
50Ð55% organic matter (mainly collagen and glycoproteins) fibers is often found within CMSC. This type of cementum is not
water. distinctively classified and is regarded as a sub-variety of CIFC in the
current classification.
SharpeyÕs fibers (perforating fibers) are portions of the principal
collagenous fibers of the periodontal ligament embedded in the
cementum and alveolar bone. Cementum is formed continuously
throughout life because a new layer of cementum is deposited to keep
the attachment intact as the superficial layer of cementum ages, but
unlike bone tissue that can be constantly rebuilt and remodeled,
cementum has a stronger anti-absorption capacity compared to the
alveolar bone and is only capable of repairing itself to a limited degree.

The structure of cementum is similar to the compact bone. Both are ALVEOLAR BONE
composed of cells and mineralized extracellular matrix. But unlike The alveolar process is the part of the maxilla and mandible that
bone, it is avascular. Two kinds of cementum are formed, acellular and supports the roots of teeth and is composed of alveolar bone
cellular, and fibers can be intrinsic or extrinsic, which results in four proper and supporting bone. Alveolar bone proper is the bone lining
possible permutations. The cementum attached to the root dentin and the tooth socket. In clinical radiographic terms, it is defined as
covering the upper (cervical) portion of the root is acellular and thus is the lamina dura.
called acellular, or primary, cementum. The lower (apical) portion of Dense bone serves as the attachment bone that surrounds the roots
the root is covered by cellular, or secondary, cementum. In this case, of the teeth.
cementoblasts become trapped in lacunae within their own matrix, Supporting bone is the bone that serves as a dense cortical plate to
very much like osteocytes occupy lacunae in bone; these entrapped sustain the alveolar bone proper.
cells are now called cementocytes. Acellular cementum anchors PDL This cortical plate covers the surface of the maxilla and mandible and
fiber bundles to the tooth; cellular cementum has an adaptive role. supports the alveolar bone proper.
Bone, the PDL, and cementum together form a functional unit of The supporting cancellous bone underlies and supports the dense
special importance when orthodontic tooth movement is undertaken. cortical bone.
The existence of alveolar bone is entirely dependent on the presence
of teeth. Alveolar bone develops initially as a protection for the soft
developing primary teeth and later, as the roots develop, as a support
for the teeth. Finally, as the teeth are lost, the alveolar bone resorbs.
Teeth are responsible not only for the development but also for the
maintenance of the alveolar process of the mandible.

The coronal border of the alveolar process is known as the alveolar

crest. This crest is normally located approximately 1-2 mm below the
cementoenamel junction. It is pointed on the anterior region (1) and
nearly flat in the molar area (2). When teeth are viewed from the
buccolingual aspect, the alveolar crest may be thin or missing.

Cementum is a mineralized tissue covering the entire root

surface. Cementum exists fundamentally in mammalian teeth, which
fit into alveolar sockets of alveolar bone, and functions as a tooth-
supporting device in concert with the periodontal principal fibers and
alveolar bone. Cementum is often referred to as a bone-like tissue.
Cementum, however, is avascular, does not undergo dynamic
remodeling, and increases in thickness throughout life. On these
points, cementum is markedly different from bone.

Cementum has been classified into cellular and acellular cementum

by inclusion or non-inclusion of cementocytes. Generally, acellular
cementum is thin and covers the cervical root, whereas thick cellular Characteristic of all bones are a dense outer sheet of compact bone
cementum covers the apical root. Cementum contains two types of and a central, medullary cavity. This cavity is filled with red or yellow
fibers, i.e. extrinsic (Sharpey's) fibers which are embedded ends of the bone marrow that is interrupted, particularly at the extremities of long
principal fibers and intrinsic fibers which are fibers of cementum bones, by a network of bone trabeculae (trabecular,
proper. It is believed that the extrinsic fibers are secreted by fibroblasts

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WEEK 2 | MODULE 2 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C 2ND SEM

cancellous, or spongy bone are the terms used to describe this

network.

AGING AND THE PERIODONTIUM

The alveolar bone is the thickened ridge of bone that contains the Aging alone does not lead to critical loss of periodontal attachment in
tooth sockets (dental alveoli) on the maxilla and mandible that hold healthy elderly persons. The effects of aging on periodontal tissues
teeth. The alveolar process contains a region of compact bone are based on molecular changes in the periodontal cells, which
adjacent to the periodontal ligament (PDL), called the lamina dura intensify bone loss in elderly patients with periodontitis. These effects
when viewed on radiographs. It is this part which is attached to the may be associated with
cementum of the roots by the periodontal ligament. It is uniformly (1) alteration in differentiation and proliferation of osteoblasts and
radiopaque (or lighter). osteoclasts
(2) an increase in periodontal cell response to the oral microbiota and
The compact or dense bone that lines the tooth socket is of two types mechanical stress leading to the secretion of cytokines involved in
when viewed microscopically. This bone either contains perforating osseous restoration
fibers from the periodontal ligament or is similar to compact bone (3) systemic endocrine alterations in the elderly people.
found elsewhere in the body. Perforating fibers or Sharpey
fibers are bundles of collagen fibers embedded in the alveolar bone Epithelium
proper. These fibers are at right angles or oblique to the surface of the Changes in the gingival epithelium are directed for the most part by
alveolar bone proper and along the root of the tooth. The fiber bundles the subepithelial connective tissue. For the proliferation, and therewith
inserting in the bone are regularly spaced and appear similar to those the turnover of the epithelium, there are varying explanations: While
that insert into the root surface cementum. Perforating fibers are not some authors have described an increase in proliferative activity with
limited to periodontal bone. They also appear anywhere in the body age, others report stationary proliferation or even a decrease.
where ligaments or tendons attach to cartilage or bone. Because bone Regardless of these reports, there is consensus that the oral mucosa
of the alveolar process is regularly penetrated by collagen fiber and also the gingiva becomes thinner, Òsofter,Ó and drier (reduced
bundles, it can be appropriately termed bundle bone. Bundle bone, saliva production) and there is a loss of gingival stippling. In elderly
being synonymous with alveolar bone proper or lamina dura, appears individuals, all mucosal surfaces are more susceptible to mechanical
more dense radiographically than the adjacent supportive bone. This irritation in comparison to younger persons. Histologically, there is a
density is probably the result of the mineral content or orientation of reduction of keratinization of the gingiva, as well as atrophy in the
the mineral crystals surrounding the fiber bundles. Blood vessels and region of the Stratum spinosum. All of these alterations are more
nerves penetrate the lamina dura through small foramina. Because common in females during menopause than in males of equal age,
the mineral density is sufficient, this bone appears opaque in and may be explained by the reduction in ovarian function.
radiographs. Tension on the perforating fibers during mastication is
believed to stimulate this bone and is considered important in its Gingival Epithelium
maintenance. Thinning and decreased keratinization of the gingival epithelium have
been reported with age. The significance of these findings could mean
an increase in epithelial permeability to bacterial antigens, a
decreased resistance to functional trauma, or both. If so, such
changes may influence long-term periodontal outcomes. However,
other studies have found no age-related differences in the gingival
epithelium of humans or dogs. Other reported changes with aging
include the flattening of rete pegs and altered cell density. Conflicting
data regarding the surgical regeneration times for gingival epithelium
have been ascribed to problems with research methodology.

Junctional Epithelium
Research studies have not demonstrated any deviation from normal
structural relationships in the junctional epithelium with age.

Connective Tissue
Age-related connective tissue changes can be observed in the gingiva
The morphological and functional unit of the bone is the Haversian as well as in the periodontal ligament. The number of fibroblasts (and
system, the Haversian or central (longitudinal) canals connected by their mitotic activity) is reduced, as is collagen synthesis. The collagen
Volkmann's or perforating (transverse) canals. Officially, Haversian within the periodontal ligament exhibits normal distribution, but the
and Volkmann's canals are "nutrient and perforating canal" in fiber bundles are thicker and more dense. (Simultaneously, the
Terminologia Histologica. The canals have a concentric lamellar organic matrix is reduced. Hyaline zones may form, and these
organization and are of equal size. The bone is vascularized by (seldom) lead to cartilage-like or calcified regeneration. The number
vessels that penetrate the matrix from the periosteum. of Malassez epithelial rest cells becomes diminished.)

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WEEK 2 | MODULE 2 DR. CONSUELO C. REYES
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Gingival Connective Tissue

Increasing age results in coarser and denser gingival connective Bacterial Plaque
tissues. Qualitative and quantitative changes to collagen have been Dentogingival plaque accumulation has been suggested to increase
reported. These include an increased rate of conversion of soluble to with age. This might be explained by the increase in hard-tissue
insoluble collagen, increased mechanical strength, and increased surface area as a result of gingival recession and the surface
denaturing temperature. These results indicate increased collagen characteristics of the exposed root surface as a substrate for plaque
stabilization caused by changes in the macromolecular conformation. formation as compared with enamel. Other studies have shown no
Not surprisingly, an increased collagen content has been found in the difference in plaque quantity with age. This contradiction might reflect
gingivae of older animals, despite a lower rate of collagen synthesis the different age ranges of experimental groups as variable degrees
decreasing with age. of gingival recession and root surface exposure. For supragingival
plaque, no real qualitative differences have been shown for plaque
Periodontal Ligament composition. With regard to subgingival plaque, one study has shown
Changes in the periodontal ligament that have been reported with subgingival flora to be similar to normal flora, whereas another study
aging include decreased numbers of fibroblasts and a more irregular reported increased numbers of enteric rods and pseudomonas in older
structure, thus paralleling the changes seen in the gingival connective adults. Mombelli suggests caution when interpreting this finding
tissues. Other findings include decreased organic matrix production, because of the increased oral carriage of these species among older
epithelial cell rests, and increased amounts of elastic fiber. Conflicting adults. It has been speculated that a shift occurs in the importance of
results have been reported for changes in the width of the periodontal certain periodontal pathogens with age, specifically including an
ligament in human and animal models. Although true variation may increased role for Porphyromonas gingivalis and a decreased role
exist, this finding probably reflects the functional status of the teeth in for Aggregatibacter actinomycetemcomitans. However, differentiating
the studies: the width of the space will decrease if the tooth is true age effects from the changes in ecologic determinants for
unopposed (i.e., hypofunction) or increase with excessive occlusal periodontal bacteria will be difficult. This topic was considered in more
loading. Both scenarios can be anticipated as a result of tooth loss in detail in a recent review.
this population. These effects may also explain the variability in
studies that have reported qualitative changes within the periodontal Immune and Inflammatory Responses
ligament. Recent advances in the study of the effects of aging on the immune
response (i.e., immunosenescence) have altered the understanding
Cementum of this phenomenon. In particular, more recent studies have set tighter
Some consensus regarding the effect of aging on cementum exists. controls on excluding individuals with systemic conditions known to
An increase in cemental width is a common finding; this increase may affect the immune response. As a result, age has been recognized as
be 5 to 10 times with increasing age. This finding is not surprising, having much less effect on the alteration of the host response than
because deposition continues after tooth eruption. The increase in previously thought. Differences between younger and older individuals
width is greater apically and lingually. Although cementum has limited can be demonstrated for T and B cells, cytokines, and natural killer
capacity for remodeling, an accumulation of resorption bays explains cells but not for polymorphonuclear cells and macrophage activity.
the finding of increasing surface irregularity. The thickness of the McArthur concluded the following: ÒMeasurement of indicators of
cellular mixed-fiber cementum increases, especially in the apical third immune and inflammatory competency suggested that, within the
of the root surface and in furcation areas. parameters tested, there was no evidence for age-related changes in
host defenses correlating with periodontitis in an elderly (65 to 75
Bone years) group of individuals, with and without disease.Ó Recent
In elderly persons, osteoporotic changes in boneÑresorption of laboratory studies have shown age-related changes in the expression
compact bone and expansion of the marrow spacesÑ can also affect of pro-inflammatory mediators and innate immunity with the potential
the jaw bones, but in this intra-oral localization, these lytic processes to alter the pathology of periodontal diseases or antimicrobial function.
play a less significant role than was previously assumed. However, the relevance of these findings to the clinical situation has
Osteoporosis is much more often observed in the long bones and not been demonstrated.
vertebral column. Females, because of the reduction in estrogen
production, are more often affected than males; women should be
regularly tested following menopause (bone thickness/density
measurements).

Alveolar Bone
Reports of morphologic changes in alveolar bone mirror age-related
changes in other bony sites. Specific to the periodontium are findings This 61 y/o male depicts the clinical appearance of an old yet
of a more irregular periodontal surface of bone and the less-regular periodontally "healthy" man. Throughout his life he had performed
insertion of collagen fibers. Although age is a risk factor for the bone toothbrushing with a horizontal scrubbing technique. Gingival
mass reductions in individuals with osteoporosis, it is not causative recession (retraction) and wedge-shaped defects resulted. On tooth
and therefore should be distinguished from physiologic aging 31, the gingiva was complete lost. On the other hand, there were
processes. Overriding the diverse observations of bony changes with virtually no clinical symptoms of ÒpocketingÓ, or periodontitis. The
age is the important finding that the healing rate of bone in extraction gingival recession/shrinkageÑalso interdentallyÑ can be explained
sockets appears to be unaffected by increasing age. Indeed, the by external influences over many decades: Mild but chronic
success of osseointegrated dental implants, which relies on intact inflammation results in ÒshrinkageÓ of the gingiva and this is enhanced
bone healing responses, does not appear to be age related. However, by improper oral hygiene and possible iatrogenic irritation.
balancing this view is the recent observation that bone graft
preparations (i.e., decalcified freeze-dried bone) from donors who Elderly individuals endure somatic and psychic changes, which may
were more than 50 years old possessed significantly less osteogenic force the physician and the dentist to deviate from normal and usual
potential than graft material from younger donors. The possible treatment concepts. But this fact must never signify that our elderly
significance of this phenomenon for normal healing responses needs and possibly also medically compromised patients should be ÒpoorlyÓ
to be investigated.

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WEEK 2 | MODULE 2 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C 2ND SEM

treated; rather, the significance is that these patients must simply be

treated differently than young and medically healthy individuals.

LESSON 2: PATHOLOGIC FEATURES

Understanding the structure and histology of the periodontium is
clinically significant to the discussion of wound healing, drugs and
environmental factors affecting it, periodontal diseases, and overall
health risk factors. Lamina propria of gingiva regenerates more
readily due to fiber differentiation after wounding, compared to the
alveolar bone, which relies on osteocyte, bone marrow cells,
endosteum cells, and osteogenic cells of periosteum, which occupy
different compartments.
Histopathology of periodontal diseases is described in 4 stages:
1. Initially, the gingival crevicular fluid (GCF) amount is
increased due to vascular changes in response to the
initial insult. At this benign stage, polymorphonuclear
neutrophils are attracted to the lesion site, and T
lymphocytes are responsible for fibroblasts in the area.
2. The early lesion is characterized by redness of the lesion.
At this stage, PMNs clear and breakdown the collagen
fibers, which leads to an increase in the previously made
space for infiltrates.
3. At this stage, the established lesion is dominated by B
cells and leukocyte aggregation. This will initiate the
lesion side transformation by changing both junctional
and sulcular epithelium into an extremely vulnerable
epithelium called the pocket epithelium. This is apparent
as bleeding upon gentle gingival manipulation.
4. An advanced lesion characterized as loss of gingival
fibers and alveolar bone is caused by migration of biofilm
into the pocket and creating an environment for anaerobic
bacterial proliferation.

GINGIVITIS
Gingivitis is an initial response to combat the first insult to the
periodontium. As the name suggests is the inflammation of the
gingiva, which is a component of the periodontium resulting from the
accumulation of microbial plaque near the gingival sulcus. The most
common cause of inflamed gums is plaque. The likelihood of
developing gingivitis and periodontitis is also increased by various
factors, including smoking, metabolic diseases such as diabetes, and
hormonal changes during pregnancy.
Initial Lesion
This stage is characterized by an acute exudative inflammatory
response, a raised gingival fluid flow, and the migration of
neutrophils from the blood vessel of the subgingival plexus located in
the gingival connective tissue to the gingival sulcus. An alteration of
the matrix of the connective tissue located next to vessels results in
the accumulation of fibrin in the area. The initial lesion is seen within
Certain medications might cause the gingiva to enlarge, making it four days of the initiation of plaque accumulation. There is a
harder to clean the teeth properly and increasing the risk of gum destruction of collagen caused by collagenase and other
disease. Examples include medications that suppress the immune enzymes secreted by the neutrophils. About 5% to 10% of the
system and medications for cardiovascular disease. connective tissue is occupied by the inflammatory infiltrate in this
stage.

Early Lesion
The early lesion is consistent with delayed hypersensitivity. It usually
appears after one week from the beginning of plaque deposition. In
this stage, the clinical signs of gingivitis, such as redness and bleeding
from the gingiva start appearing. The inflammatory cells that
predominate in this lesion are lymphocytes accounting for 75% of the
total, and macrophages. A small number of plasma cells are also
seen. Along with the inflammatory infiltration that occupies 5% to 15%
of the connective tissue of the gingival margin, there is loss of collagen
in the affected area that reaches 60% to 70%.

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WEEK 2 | MODULE 2 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C 2ND SEM

Furthermore, the local fibroblasts undergo a series of pathological inhibited without reducing the rate of osteoclasts. It is observed on a
changes, and the gingival fluid flow and the number of leukocytes radiograph as reduced opacity of the alveolar crest.
migrating to the region continue to increase. Neutrophils and
mononuclear cells are also increased in the junctional epithelium. The
duration of the early lesion has not yet been determined, it can remain
for more time than previously expected.

Established Lesion
There is increased collagenolytic activity in this stage along with a rise
in the number of macrophages, plasma cells, T and B lymphocytes.
However, the predominant cells are plasma cells and B lymphocytes.
In this stage, a small gingival pocket lined with a pocket epithelium is
created. The lesion exhibits a high degree of organization. It has been
suggested that the severity of gingivitis correlates with a growth in the
B cells and plasma cells population, and a decrease in the number of
T cells.

An established lesion may follow two paths, it can either remain stable
for months or years; or progress to a more destructive lesion, which
appears to be related to a change in the microbial flora or infection of
the gingiva. This stage has shown to be reversible after an effective
periodontal therapy that results in an increase in the number of
microorganisms associated with periodontal health that directly
correlates with a reduction in the plasma cells and lymphocytes.

Advanced Lesion
This stage is a transition to periodontitis. It is characterized by
attachment loss that is irreversible. The inflammatory changes and the
bacterial infection starts affecting the supporting tissues of the teeth
and the surrounding structures such as gingival, periodontal ligament,
and alveolar bone resulting in their destruction and may eventually
result in tooth loss

If plaque is not removed, the gums can become inflamed within just a
few days. And plaque can harden and develop into tartar. Although
plaque forms very quickly, it can easily be removed by regular and
thorough cleaning. Treatment for gingivitis includes removing plaque
or any overhanging restorations that can cause plaque retentive
areas. Good oral hygiene can help to prevent gingivitis.

Gingivitis generally doesnÕt cause any pain or other symptoms, so it

remains undetected for quite some time. But it may spread to other
parts of the periodontium and progress into periodontitis.

PERIODONTITIS
The advanced lesion of periodontal disease is clinically recognized as
CEMENTUM
periodontitis, with the classical features of pocket formation, ulceration
of the pocketÕs epithelium, destruction of the collagenous periodontal Hyper-cementosis is thought to be due to growth factors
ligament, and bone resorption. These changes lead to mobility and disturbances in conditions such as acromegaly, gigantism, or PagetÕs
eventually to tooth loss. disease. Cementoblasts are located within the PDL and can undergo
remodeling and repair. Excessive cementoblast deposition can cause
hyper-cementosis. This can further cause concrescence which is the
adherence of two teeth together by the roots (hence a radiograph is
needed before tooth extraction).

Periodontitis is the inflammation of the periodontium as a whole

which extends to the alveolar bone and is irreversible.
Pathophysiology of the periodontitis is explained by replacement and
remodeling of previously normal alveolar bone, especially the spongy
bone, that can happen in healthy individuals due to chronic
inflammation. White blood cells are active during inflammation, and
Cementicle is a condition in which masses of acellular cementum
osteoclasts lineage is related to WBC. As a result, osteoblast is
appear in abnormal location due to disruption of oppositional growth

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WEEK 2 | MODULE 2 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C 2ND SEM

of cementum. This condition happens mostly in the elderly and

appears as psammoma body-like calcifications. The process is
thought to develop due to the encounter of cementoblasts with
thrombus lodged in a nearby capillary.

WIDENING OF PDL
Widening of PDL space: with occlusal/orthodontic trauma, the
fibroblast in PDL responds by increasing its activity and lead to the
widening of PDL (meaning the neighboring tissue is lost). This can
be seen on a radiograph and can be accompanied by bone loss or
hyper-cementosis. Certain medications such as bisphosphonate are
used to manage rheumatoid arthritis osteoporosis, osteogenesis
imperfecta, multiple myeloma. can cause PDL widening. In contrast,
conditions in which bone health such as radiation-induced bone
defect are affected and reduce the force and also cause widening of
the PDL space. Infection and inflammation, and malignancy also can
cause PDL widening.

DRIFTING

Mesial drift: Also known as physiological drift, is referred to as the

migration of teeth in a mesial direction caused by asymmetrical
remodeling of alveolar bone tissue. Two major concepts are believed
to cause this drift: First, unbalanced bone remodeling of 2 adjacent
teeth. And second, remodeling due to occlusal forces leads to an
imbalance of acellular cementum. This asymmetrical remodeling
causes tooth movement.

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WEEK 3 DR. CONSUELO C. REYES
PERIODONTICS 1 Ð LECTURE DENT 4C Ð 2ND SEM

WEEK 3: DISCUSSION Ð 2/22/22 Ø In the presence of inflammation they can be found in large
numbers, often as dense cellular aggregates that have
THE GINGIVAL CONNECTIVE TISSUE (LAMINA PROPRIA) replaced the fibrous elements in the connective tissue.

The major components of the gingiva connective tissue:

1. Collagen fibers Ð 60%
2. Fibroblast Ð 5%
3. Vessels, nerves, matrix Ð 25%

Consists of 2 layers:
1. Papillary layer Ð subadjacent to the epithelium which
consists of papillary projections between the epithelial rete
pegs/ rete ridges. (the ones that are interlocked with the The connective tissue also contains undifferentiated
rete ridges) ectomesenchymal cells that serve as a replacement source for more
2. Reticular layer Ð contiguous with the periosteum of the differentiated cells, primarily fibroblasts.
alveolar bone.
Fibroblasts are irregularly shaped cells, responsible for the synthesis
of various connective tissue fibers and the ground substance in which
they are embedded.

They are also responsible for the removal of these structural elements.

These cells play a key role in the maintenance and remodeling of

the connective tissue.

GINGIVAL VESSELS AND NERVES

Lymphatics:
The gingival tissues are supplied with lymphatic vessels that drain
Functions of the gingival Connective Tissue:
principally to submaxillary lymph nodes.
1. Provides firmness and solidity to the gingiva Ð because of
the gingiva fibers/CT
Blood supply:
2. Attaches the gingiva to the cementum of the root and the
The gingival blood supply originates from
alveolar bone
1. blood vessels in the periodontal ligament,
2. marrow spaces of the alveolar process
Major cellular elements in the gingival CT include:
3. supraperioste al blood vessels.
® Fibroblasts Ð produces collagen fibers
® Macrophages Ð immune defense cells These vessels in turn supply major capillary plexuses that are
® Mast cells located in the connective tissue adjacent to the oral epithelium and
® Osteoblasts and osteoblast precursor cells Ð these are the junctional epithelium,
specialized cells (mature cells), they give rise to specific
cells.
® Cementoblasts and cementoblast precursor cells
® Osteoclast and odontoblasts
® Assorted inflammatory cells
® Cells that make up vascular channels and nerves

Nerves:
Ø Maxillary and mandibular branches of the trigeminal nerve
provide sensory (cold, hot, pain) and proprioceptive
functions. (you feel it/ pressure etc.)
Ø In addition, autonomic nerve endings (sensory and motor
Inflammatory cells include: nerve endings) are associated with the vasculature.
WBCÕs Ð immune cells
¥ Polymorphonuclear leukocytes (granulocytes) TOOTH-SUPPORTING STRUCTURES
¥ Lymphocytes Ð cells in the lymphatic system/ vessels. (to - AKA Attachment structures/ apparatus
cleanse located along the course of the blood vessels)
¥ Plasma cells Ð if we have allergies, inflammation 1. Periodontal ligaments
2. Cementum
Ø Under normal circumstances (no infection/ inflammation) 3. Alveolar bone
they may be found in small numbers, as isolated cells
PERIODONTAL LIGAMENTS

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WEEK 3 DR. CONSUELO C. REYES
PERIODONTICS 1 Ð LECTURE DENT 4C Ð 2ND SEM

connective tissues that surround the tooth and connect it to the bone.
Cells of the periodontal ligaments
Principal Fibers of the Periodontal Ligament:
1. Alveolar crest group 1. Connective tissue cells. ( for maintenance e and
2. Horizontal group remodeling)
3. Oblique group - fibroblasts, cementoblasts,, osteoblast, cementoclasts
4. Apical group and osteoclasts
5. Interradicular group
2. Epithelial Rests of Malassez-
- isolated or interlacing strands; remnants of Hertwig's
epithelial root (formation of roots) sheath which
disintegrates during root development.

3. Defense cells
- neutrophils, lymphocytes, macrophages, mast cells

FUNCTIONS OF PERIODONTAL LIGAMENTS:

1) Physical
1. Alveolar crest group fibers 2) Formative and Remodelling
- extend obliquely from cementum beneath the 3) Nutritional
junctional epithelium to the alveolar crest 4) Sensory
- These prevent extrusion of tooth and resist lateral tooth
movements. 1. Physical:
2. Horizontal group a) Shock absorption - also called resistance to the impact of
- fibers are at right angles to the long axis of the tooth from occlusal forces. (serves as a cushion)
cementum to alveolar bone. b) Transmission of occlusal forces to the bone
c) Provision of soft tissue "casing" to protect blood vessels
3. Oblique group and nerves from injury by mechanical forces
- the largest group, extend from cementum in a coronal d) Maintenance of gingival tissues in their proper
direction obliquely to the bone. relationship
- They bear most of the vertical masticatory forces and e) Attachment of teeth to the bone
transform them into tension on the alveolar
2. Formative and Remodelling:
- cells of P.L. participate in the formation and resorption of
4. Apical group bone and cementum during physiologic tooth movement,
- fibers radiate from cementum to bone at apical portion of application of occlusal forces and repair of injuries.
the socket.
- They are absent in incompletely formed roots. P.L. has a very high turnover rate of collagen synthesis, twice
as fast in the gingiva and four times faster than that in the skin.
5. Interradicular group
- fibers fan out from cementum to the bone in furcation 3. Nutritional and Sensory :
areas of multirooted teeth. - The P.L. provides nutrients to the cementum, bone and
gingiva via its rich vascular network and provides
TERMINAL ENDS of principal fibers insert into cementum and lymphatic drainage.
bone and are called SHARPEY'S FIBERS.
The P.L, is abundantly supplied with nerve fibers for tactile,
pressure and pain sensations by trigeminal pathways. Free nerve
endings for pain, Ruffini-like mechanoreceptors located mainly
at apical areas;

Meissner's corpuscles, also a mechanoreceptor, at the

midroot area; and spindle like pressure and vibration endings at
the apex.
These nerve fibers follow the course of blood vessels.

SharpeyÕs fibers

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WEEK 3 DR. CONSUELO C. REYES
PERIODONTICS 1 Ð LECTURE DENT 4C Ð 2ND SEM

CEMENTUM 1. Serves to adjust bone architecture to meet changing

- calcified avascular mesenchymal tissue that covers the mechanical needs
anatomical root. 2. Helps to repair microdamages in bone matrix preventing
the accumulation of old bone.
2 types: 3. Plays an important role in maintaining plasma calcium
1. acellular cementum homeostasis (maintaining calcium level of the human
2. cellular cementum body)

[Link] Cementum MODULE 3: ETIOLOGY AND PATHOGENESIS OF

- 1st to form and covers the cervical third or half of the root. PERIODONTAL DISEASE
- This forms before the tooth reaches the occlusal plane.
- Sharpey's fibers comprise most of the structures of the acellular CANVAS OR LECTURE/PPT -BASED
cementum. Periodontal diseases are a series of complex, distinct, pathological
- Calcified collagen fibrils are also found. entities caused by interaction of bacterial plaque and the host. This
interaction results in destruction of the supporting alveolar bone and
2. Cellular Cementum connective tissue.
- forms after the tooth reaches the occlusal plane.
- more irregular and contain cells, cementocytes in lacunae (spaces) Although bacterial plaque has been implicated as the initiating or
which communicate through a system of canaliculi. primary etiologic agent in most forms of periodontal disease, there are
locally and systemic factors which may modify both microbial and host
components.

Local factors may favor plaque accumulation and maturation, while

systemic factors may modulate an decrease the host protective
response.

OBJECTIVES;
1. Explain the relationship of dental plaque to periodontal
disease
2. Discuss the role of calculus and bacterial products to
ALVEOLAR BONE formation of periodontitis
Alveolar Bone 3. Identify the oral microflora for pathogens
Alveolar process Ð
- portion of the maxilla and mandible that forms and LESSON 1: DENTAL PLAQUE BIOFILM
supports the tooth sockets (alveoli). Dental plaque is a diverse microbial community found on tooth
surface embedded in a matrix of polymers of bacterial and salivary
- It provides attachment to the periodontal ligaments and origin. Once tooth surface is cleaned, a conditioning film of protein
disappears after tooth loss. and glycoprotein is adsorbed rapidly to the tooth surface.

It consists of Dental plaque develops naturally, but it is also associated with two
1) Alveolar bone proper (lamina dura) - has series of most prevalent diseases affecting industrialized societies (caries and
openings, cribriform plates, for the neurovascular periodontal disease).
innervations.
- Lamina Dura Ð white thin line along the bone Required Reading: Carranza/Lindhe: CLINICAL
(radiopaque). Can be continuous, or discontinuous lamina PERIODONTOLOGY
dura. See the following ppt for the lecture
2) External plate of cortical bone
3) Cancellous trabeculae - lie between the lamina dura and MICROORGANISMS ASSOCIATED WITH SPECIFIC
compact bone. PERIODONTAL DISEASES
Periodontal disease is a mixed bacterial infection that produces
inflammatory destruction of periodontal tissues that surrounds and
supports the teeth
® periodontal microbiota form a complex ecosystem called
dental plaque biofilm, within which pathogens produce
virulence factors that allow them to evade the host
defenses, as well a provoke an immune response that is
damaging to the host tissue
® periodontal disease actually results from disruption of
homeostasis or balance that normally exists between
plaque bacteria, host immune system,and environmental
conditions during health

BONE REMODELING WHILE-TASK:

- Bone deposition by osteoblasts is balanced by resorption Refer to the powerpoint lecture in Module 4 Lesson 1.
by the osteoclasts during tissue remodelling and renewal. Required Reading: Carranza/Lindhe ; CLINICAL
PERIODONTOLOGY & Implantology

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WEEK 3 DR. CONSUELO C. REYES
PERIODONTICS 1 Ð LECTURE DENT 4C Ð 2ND SEM

Isolation and identification of periodontal pathogens characterize an

important tool for increasing knowledge on periodontal microbiota as
well as on etiology and progression of periodontal infection.

The prime step in the treatment of periodontal disease is the

identification of key pathogens, hence , the role of the novel
pathogenesis needs attention.

WHILE -TASK:
Refer to the powerpoint lecture in Module 4 Lesson 1
Required reading: Carranza/Lindhe Clinical Periodontology And
Implant Dentistry

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WEEK 4 | MODULE 3,4,6 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C Ð 2ND SEM

DISCUSSION: MARCH 01, 2022 Periodontal Micobial complex

Etiology of Periodontal Diseases
Modifiable and Nonmodifiable Periodontal Risk Factors The 'red complex' is an aggregate of three oral bacteria
Host Response 1. Porphyromonas gingivalis
Pathogenesis of Periodontitis 2. Tannerella forsythensis
3. Treponema denticola
They are responsible for severe clinical manifestations of periodontal
THE ETIOLOGY OF PERIODONTITIS (bacteria in dental plaque)
disease.
The primary cause of periodontitis is bacteria in dental plaque,
The bacterial numbers associated with disease are up to 10(5) times
larger than those associated with health.
The immune system attempts to eradicate the bacteria, which can
lead to inflammation in the area. and can potentially cause damage
to the gingiva, periodontal ligament, alveolar bone, and cementum.

The inflammation is the defense mechanism

INITIAL COLONIZER
Blue complex Actinomyces species
DENTAL BIOFILM/ DENTAL PLAQUE Purple complex Veillonella Parvula
- primary cause of PERIODONTITIS Actinomyces Odontolyticus
It is a colorless film of bacteria, and sugars (biofilm) that Green complex Eikenella Corrodens
constantly forms on the tooth surfaces and restorations; Capnocytiphaga Gingivalis
Capnocytiphaga Sputigena
Cannot be seen with the naked eye but can be felt with the tongue Capnocytiphaga Ochracea
due to its sticky properties. Capnocytiphaga Concisus
A. Actino. A
Yellow complex Streptococcus Mitis
Streptococcus Oralis
Streptococcus Sanguis
Streptococcus sp.
Streptococcus Gordonii
Plaque Composition Streptococcus Intermedius
1. Microorganism (MO's) which exist within an intercellular
matrix: Orange complex Caecilla Gracilis
a. Gram positive bacteria (initial colonizers) - 85% - Camplobacter Rectus
penetrable. We can take antibiotics. Camplobacter Showae
Eubacterium Nodatum
b. Gram negative bacteria ( secondary colonizers) - 15% -
Fusobacterium Nucleatum
harder to treat/ eradicate because of the outer harder
Fusobacterium Nucleatum Polymorphum
shell
Prevotella Intermedia
Peptostreptococcus Micros
(Gram staining test establish a mesh like membrane called
Prevotella Nigrescens
peptidoglycan; if bacteria with thick/with mesh peptidoglycan gram
Streptococcus Constellatus
positive, if thin/no peptidoglycan gram negative)
PUTATIVE PATHOGENS
Photo: Supragingival plaque, Sub gingival plaque Red complex Porphyromonas Gingivalis
Bacteroides Forsythus/ Tannerella
1) Intercellular matrix Forsythesis
a) organic components. Treponema Denticola
- polysaccharides, proteins, glycoproteins, lipid
b) inorganic components. RISK FACTORS FOR PERIODONTAL DISEASES
- mainly calcium & phosphorus & other minerals such as
sodium, potassium & fluoride Risk factor
- occurrence or characteristic that has been associated
with the increased rate of a subsequently occurring
disease

1
WEEK 4 | MODULE 3,4,6 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C Ð 2ND SEM

- associated with a disease but do not necessarily

cause the disease
- may be modifiable or non-modifiable

**contributing factor/ contributing to aggravating of the disease**

Modifiable risk factors

- usually environmental or behavioral in nature.
- it can be changed. (you can change your habit)

Non-modifiable risk factors/determinants

- usually intrinsic to the individual and therefore not easily
changed; are
- also known as determinants.

MODIFIABLE AND NONMODIFIABLEE PERIODONTAL RISK Smoking CANNOT cause periodontitis. It is only a modifiable
risk factors
FACTORS
2) the blood vessels are vasoconstricted thus nutrients are
having a hard time to go to the periodontal tissues
MODIFIABLE PERIODONTAL NON-MODIFIABLE RISK
RISK FACTORS FACTORS 2. Diabetes mellitus (type 2) - increase risk of developing
§ Microorganisms § Osteoporosis periodontal diseases
(specific pathogens) § Some hematological
¥ it causes blood vessel changes
§ Smoking disorders
§ Poorly controlled (eg,thrombocytopenia) ¥ The thickened blood vessels (vasoconsriction) can reduce
diabetes mellitus § Some host responses the flow of nutrients and removal of wastes from body
§ Stress § History of periodontitis tissues.
§ Poor self-care § Age ¥ This reduced blood flow can weaken the gingiva and
§ Untreated human § Gender alveolar bone.
immunodeficiency § Race ¥ There is impaired cell function & altered wound healing
virus or acquired § Genetic disorders
immunodeficiency § Bone levels
syndrome § Drug-induced
§ Oral effects of some disorders
medications § Normal hormonal
§ Local factors variations (eg,
§ Obesity pregnancy)
§ Improper diet
§ Chronic inflammation
§ Some host responses

SYSTEMIC FACTORS:
1. Nutritional influences
2. Endocrine disorders
3. Hematologic disorders
4. Immunodeficiency disorders
5. Psychosomatic disorders
LOCAL FACTORS FOR PERIODONTITIS
LOCAL FACTORS: - you can see clinically on mouth.
1. Dental plaque - these cannot be a direct cause periodontal disease. But
2. Tobacco use associated and can contribute/ aggravate the periodontal
3. Orthodontic therapy disease.
4. Malocclusion 1. Calculus Ð amorphous and rough surface. Dental plaque can
5. Restorative dentistry procedures easily adhere to calculus.
6. Design of RPD 2. Dental stains Ð eg. coffee stain, nicotine stains, orahex stain. If
7. Iatrogenic factors (illness cause by medical stain accumulate it elevates/ roughens à dental plaque adhere à
treatment/examination) periodontal disease
8. Calculus 3. latrogenic factors- (usually a result from a mistake made in
treatment/ diagnosis) overhanging margins of restorations, over
2 WELL ESTABLISHED RISK FACTORS FOR PERIODONTITIS contoured crowns, open contacts Ill-fitting dentures, vigorous scaling
5. Malocclusion - bc tooth surfaces are hard to reach/ brush
1. Tobacco smoking - exerts a substantial destructive effect [Link] therapy - excessive forces/load (trauma à resurface
on the periodontal tissues and increases the ratee of resorption on root surface = concavity on root surface)
periodontal disease progression. 7. Toothbrush trauma

2
WEEK 4 | MODULE 3,4,6 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C Ð 2ND SEM

HOST RESPONSE - A big - There is bone loss,

How an individual responds to bacterial attack greatly determines category periodontal pockets and
the disease progression. clinical loss

1. Host Innate Defense MODULE 3: ETIOLOGY AND PATHOGENESIS OF

2. Adaptive Defense
PERIODONTAL DISEASE
Innate Immune Response CANVAS Ð BASED
- Represents the first response of the body when an Periodontal diseases are a series of complex, distinct, pathological
intruder is detected. entities caused by interaction of bacterial plaque and the host. This
interaction results in destruction of the supporting alveolar bone and
- It is often referred to as "non- specific immunity'" connective tissue.
because it does not discriminate different pathogens, but
rather recognizes specific patterns of the foreign Although bacterial plaque has been implicated as the initiating or
organisms. primary etiologic agent in most forms of periodontal disease, there
are locally and systemic factors which may modify both microbial and
Adaptive immunity host components.
- Intervenes when the innate system is not sufficient
against an established infection. Local factors may favor plaque accumulation and maturation, while
systemic factors may modulate an decrease the host protective
- The cells of the adaptive system generate a pathogen- response.
specific immunologic response to eliminate the target
micro-organism and/or the infected cells. LESSON 1: DENTAL PLAQUE BIOFILM
Dental plaque is a diverse microbial community found on tooth surface
Summary of pathogenesis of periodontitis embedded in a matrix of polymers of bacterial and salivary
How the disease happened origin. Once tooth surface is cleaned, a conditioning film of protein
and glycoprotein is adsorbed rapidly to the tooth surface.

Dental plaque develops naturally, but it is also associated with two

most prevalent diseases affecting industrialized societies (caries and
periodontal disease).

Required Reading: Carranza/Lindhe: CLINICAL

PERIODONTOLOGY
See the following ppt for the lecture

LESSON 2: MICROORGANISMS ASSOCIATED WITH SPECIFIC

PERIODONTAL DISEASES
Periodontal disease is a mixed bacterial infection that produces
inflammatory destruction of periodontal tissues that surrounds and
Bacteria attacking the body: supports the teeth
¥ Antigens periodontal microbiota form a complex ecosystem called dental
¥ Lipopolysaccharides plaque biofilm, within which pathogens produce virulence factors that
¥ Other virulence factors allow them to evade the host defenses, as well a provoke an immune
response that is damaging to the host tissue periodontal disease
The body defense: actually results from disruption of homeostasis or balance that
¥ Antibodies normally exists between plaque bacteria, host immune system,and
environmental conditions during health
¥ Neutrophils
WHILE-TASK:
Inflammatory response releases:
Refer to the powerpoint lecture in Module 4 Lesson 1.
¥ Cytokines Required Reading: Carranza/Lindhe ; CLINICAL
¥ Prostanoids PERIODONTOLOGY & Implantology
¥ Matrix Metalloproteinases
MODULE 4: HOST IMMUNE RESPONSE AND INFLAMMATION
In patient A, who is NOT susceptible to periodontitis: tissue and bone
CANVAS Ð BASED
repair/healing. No clinical signs
The only reason that the human body survives is that it has a
In patient B, who is susceptible to periodontitis: tissue destruction protective defense system that is very effective at recognizing and
and bone loss. Deepening of periodontal pockets, furcation fighting disease-causing microorganisms.
involvement (there is resorption of interradicular bone) ,
contaminated cementum The Immune System is a complex body defense system that protects
the body against bacteria, viruses, fungi, toxins, and parasites.
The prime purpose of the Immune system is to defend the life of
PERIODONTAL PERIODONTITIS
individuals by identifying foreign substances in the body and
DISEASES - 1 type of periodontal
developing a defense against them.
diseases

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WEEK 4 | MODULE 3,4,6 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C Ð 2ND SEM

LESSON 1: CELLS OF IMMUNITY AND LEUKOCYTE FUNCTION Cytotoxic T cells are the primary effector cells of
Immune cells are the white blood cells or leukocytes. These cells work adaptive immunity.
together a part of the innate (non-specific) and adaptive (specific) Cytotoxic T cell Activated cytotoxic T cells can migrate through
immune system. blood vessel walls and non-lymphoid tissues. They
can also travel across the blood brain barrier.
Granulocytes are a type of leukocyte that contain granules in their
cytoplasm containing enzymes. Neutrophils, basophils and Helper T cells secrete cytokines that help B cells
eosinophils are types of granulocytes. Neutrophils are considered the Helper T cell differentiate into plasma cells. These cells also help
first responders of the innate immune system. Neutrophils and to activate cytotoxic T cells and macrophages.
macrophages circulate though the blood and reside in tissues
watching for potential problems. Both cells can ÒeatÓ bacteria, as well
as communicate with other immune cells if an issue arises. Regulatory T Regulatory T cells (or Tregs) help to suppress the
Cells of the adaptive immune system (also called immune effector cell immune system.
cells) carry out an immune function in response to a stimulus. Natural
killer T lymphocytes and B lymphocytes are examples of effector cells. Lymphocytes are immune cells found in the blood
For example, activated T lymphocytes destroy pathogens via cell- Lymphocyte and lymph tissue. T and B lymphocytes are the two
mediated response. Activated B cells secrete antibodies that aid in main types.
mounting an immune response. Effector cells are involved in the
destruction of cancer. Macrophages are large white blood cells that reside
in tissues that specialize in engulfing and digesting
Non-effector cells are antigen-presenting cells (APCs), such as Macrophage
cellular debris, pathogens and other foreign
dendritic cells, regulatory T cells, tumor-associated macrophages and substances in the body.
myeloid-derived suppressor cells. Non-effector cells cannot cause
tumor death on their own. Non-effector cells prevent the immune
Mast cells release histamine and help to get rid of
action of the effector cells. In cancer, non-effector cells allow tumor to Mast cell
allergens.
grow.

Glossary of Immune System Components Large white blood cells that reside in the blood
stream that specialize in engulfing and digesting
Component Description
Monocyte cellular debris, pathogens and other foreign
Antigen Any substance that is able to cause an immune substances in the body. Monocytes become
response in the body. macrophages.
Special proteins created by white blood cells that
can kill or weaken infection-causing organisms. A type of white blood cell, granulocyte, and
Antibody (Ab) Neutrophil
Antibodies travel through the blood stream looking phagocyte that aids in fighting infection. Neutrophils
for specific pathogens. kill pathogens by ingesting them.
PPT Ð CANVAS
A basophil is a type of phagocytic immune cell that LESSON 2: MICROBE-HOST INTERACTION
Basophil
has granules. Inflammation causes basophils to Microbial Virulence Factors
release histamine during allergic reactions. The subgingival bacteria contribute directly to tissue damage
A B lymphocyte is a type of white blood cell that by the release of noxious substances, but their primary importance in
B lymphocyte develops in the bone marrow and makes periodontal pathogenesis is that of activating immune-inflammatory
antibodies. responses that in turn result in tissue damage, which may well be
beneficial to the bacteria located within the periodontal pocket by
B cells that are long lived and remember past providing nutrient sources.
Memory B cell
antigen exposure.
Lipopolysaccharides (LPS) are large molecules composed of
a lipid component (lipid A) and a polysaccharide component found in
Activated B cells that produce antibodies. Only one the outer membrane of gram-negative bacteria acting as endotoxins
Plasma B cell
type of antibody is produced per plasma B cell. and elicit strong immune responses in animals. Lipoteichoic acid is a
component of gram-positive cell walls which also stimulate immune
An eosinophil is a type of immune cell (leukocyte, responses less potently than LPS. Both LPS and lipoteichoic acid are
Eosinophil or white blood cell). They help fight infection or released from the bacteria present in the biofilm and stimulate
cause inflammation. inflammatory responses in the tissues thereby resulting in increased
vasodilation and vascular permeability.
Granulocytes (including eosinophils, neutrophils
and basophils) are a type of white blood cell that Plaque bacteria produce metabolic waste products such as
Granulocyte releases toxic materials, such as antimicrobial ammonia (NH3) and hydrogen sulfide (H2S) as well as short-chain
agents, enzymes, nitrogen oxides and other carboxylic acids such as butyric acid and propionic acid. These are
proteins, during an attack from a pathogen. detectable in the GCF and found in increasing concentrations as the
severity of periodontal diseases increases.
Type of white blood cell that is involved with the
T lymphocyte Host-derived Inflammatory Mediators
immune system. T lymphocytes mature in the
(also called T The inflammatory and immune processes that develop in the
thymus and differentiate into cytotoxic, memory,
cell) periodontal tissues in response to the long-term presence of the
helper and regulatory T cells.
subgingival biofilm are protective by intent but result in considerable

4
WEEK 4 | MODULE 3,4,6 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C Ð 2ND SEM

tissue damage. This is referred to as bystander damage which The initiation phase of acute inflammation is characterized by the rapid
denotes that the host response is mainly responsible for the tissue infiltration of polymorphonuclear neutrophils (PMNs) followed by the
damage that occurs, thereby leading to the clinical signs and infiltration of monocytes that mature into macrophages, and edema
symptoms of periodontal disease. formation in response to injury. PMNs provide the first line of immune
defense by migrating to sites of injury and neutralizing invading
Cytokines play a fundamental role in inflammation and they microorganisms or noxious materials by phagocytosis. In the
are key inflammatory mediators in periodontal disease. These are resolution phase, PMNs undergo apoptosis and are ingested by
soluble proteins acting as messengers to transmit signals from once macrophages that emigrate rapidly from the inflamed site to the
cell to another. draining lymph nodes.

Prostaglandins (PGs) are a group of lipid compounds derived from The three phases of inflammation are the ff:
arachidonic acid, a polyunsaturated fatty acid found in the plasma Phase 1: Acute (Inflammatory response)
membrane of most cells. PGs are important mediators of Tissue damage due to trauma, microbial invasion or noxious
inflammation, particularly Prostaglandin E2 (PGE2) which results in compounds can induce acute inflammation. The purpose of vascular
vasodilation and induces cytokine production by a variety of cell types. change is to increase blood flow to the local area, mobilize and
transport cells to the are to initiate healing. The damaged cells are
Matrix mettaloproteinases (MMPs) are a family of proteolytic enzymes removed and the body begins to put new collagen in the area of injury
that degrade extracellular matrix molecules such as collagen, gelatin, It starts rapidly, initiated immediately after the injury, becomes severe
and elastin. They are produced by a variety of cell types, including in a short time and symptoms may last for 3-5 days. There is evident
neutrophils, macrophages, fibroblasts, epithelial cells, osteoblasts and redness. (erythema)and swelling due to vascular changes. Exudation
osteoclasts. of cells and chemicals cause swelling and pain and tenderness. A
hematoma may form if there is bleeding within the tissues. The five
Below is the model of pathogenesis of periodontitis (adapted cardinal signs of inflammation are manifested.
from Kornman, et al, Journal of Periodontology, 2008). Although the
bacteria are the main etiological agents, most of the tissue destruction Phase 2: Sub-acute or Proliferation (Repair and regeneration)
occurs as a consequence of the host immune-inflammatory response The sub-acute phase is the commencement of healing and
against the microbial challenge. This response is modulated by both repair characterized by new collagen formation. New collagen fibers
genetic and environmental risk factors. are laid down in a disorganized manner in the form of a scar and there
are weak links between each fiber. Thus, the new tissue is weak and
susceptible to disruption by overly aggressive activity. Noxious
chemicals are further neutralized and new capillary beds growing into
the damaged areas are supported by connective tissue growth
(collagen fibers).
Visible signs of inflammation start to subside, less warmth and
swelling, palpable tenderness decreases.

Phase 3: Chronic (Remodelling and Maturation)

Chronic inflammation is referreed to as slow, long-term
inflammation lasting for prolonged period of months to years. The
extent and effects of chronic inflammation vary with the cause of the
injury and the ability of the body to repair and overcome the damage.
This is the period when tissue remodeling takes place. As healing
LESSON 3: INFLAMMATORY RESPONSES
progresses, the tissue continues to remodel, strengthen and improve
Inflammatory response plays a critical role in immunity. When tissues its cellular organization. There is less new collagen formation, but
are damaged, the inflammatory response is initiated, and the increased organization of the collagen fibers, and stronger bonds
immune system becomes mobilized. The immune cells of the innate between them.
immune system are first recruited to the site of tissue injury or Signs of inflammation are absent and scar tissue is maturing.
damage via blood vessels and lymphatic system, followed by Maturation refers to the growth of the fibroblasts to fibrocytes and
macrophages. remodeling refers to the organization and shrinking of collagen fibers
along the line of stress
The goals of the inflammatory response are to:
MODULE 6: PREDISPOSING, MODIFYING AND RISK FACTORS
1. Prevent initial establishment of infection or remove damaged
tissue OF PERIODNTAL DISEASE
2. Prevent the spread of infection or repair damaged tissue CANVAS
3. Recruit effector cells if the immune cells of the innate immune A risk factor can be defined as an occurrence or characteristic that has
system cannot control infection or repair damaged tissue been associated with the increased rate of subsequently occurring
4. Mobilize effector cells (T and B lymphocytes) disease . Risk factors can modifiable or non-modifiable.

Risk factors play an important role in an individual's response to

periodontal infection. Identification of these risk factors help target
patients for prevention and treatment, with modification of risk factors
critical to the control of periodontal disease.

Periodontal disease is the most common dental problem worldwide.

This causes destruction of the supporting structures such as the
alveolar bone, periodontal ligament, and its supporting structures.

5
WEEK 4 | MODULE 3,4,6 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C Ð 2ND SEM

Patients can suffer from gingivitis, and if left untreated may lead to 3. Tobacco Smoking
chronic periodontitis, and/ or periodontitis as a manifestation of Tobacco smoking has several effects in the oral cavity, from simple
systemic diseases. tooth staining to oral cancer. Studies have shown that tobacco
smoking has strong evidence in the progression of the periodontal
There are several risk factors in periodontal disease, it can be disease due to the destructive effect to periodontal tissues.
systemic, local, genetic and even environmental factors.
Effects of tobacco smoking on the periodontium:
This module will discuss the risk factors that are associated with § Increased bone, attachment, and tooth loss
periodontal disease. § Deeper pockets
§ More attachment loss is seen in the mandibular anterior
LESSON 1: MODIFIABLE RISK FACTORS and maxillary palatal area.
1. Microorganisms and Periodontal Disease § Fibrotic gingiva
The oral microbiome consists of 700 microorganisms. In a patient with § Limited gingival erythema and edema
a periodontal disease, the subgingival microflora involves 400 of these § Bleeding on probing is reduced
species but only a small number of bacteria are associated with the
progression of this condition. Subgingival plaque found in deep
pockets are mostly gram-negative anaerobic rods and spirochetes.

The microorganisms that are responsible for the pathogenesis of

periodontitis in adults are Porhyromonas gingivalis and Aggrebacter
actinomycetemcomitans. In addition, Bacteroides forsythus,
Prevotela intermedia, Pepstreptococcus micros, and Fusobacerium
nucleatum have shown a strong link with the progression of adult
periodontitis.

2. Diabetes
Diabetes is an endocrine condition that has a strong link to
periodontal disease. Clinically, patients with diabetes, whether
insulin-dependent or non-insulin dependent, have a significantly
higher gingival inflammation compared to those who do not have
diabetes with similar plaque level.

Patients with diabetes often shows presence of:

§ Gingival inflammation
§ Increased pocket depth
§ Increased attachment, bone, and tooth loss 4. Cardiovascular Disease
§ Patients who have an uncontrolled or undiagnosed There are several biological mechanisms that have been proposed
diabetes may also experience multiple recurring between periodontal disease and cardiovascular disease, especially
periodontal abscesses. periodontitis that can elicit a systemic inflammatory response. C-
reactive protein is a systemic marker of inflammation that is found in
With periodontal therapy outcomes, a patient with a well-controlled periodontitis. An increase in the level of C-reactive protein has
diabetes can respond well to non-surgical treatment and can achieve shown to be associated with cardiovascular disease.
a reduced probing depth and gain some attachment. However, for a
patient with a poorly controlled diabetes, the response to periodontal Microorganisms found in periodontitis and dental disease are known
therapy is unpredictable as tissue repair and wound healing is to be the primary cause of infective endocarditis. Particularly on
compromised. patients that have undergone heart valve surgery have a high risk of
life-threatening infective endocarditis.

5. Drug-induced disorder
Some medications cause a significant decrease in the salivary flow,
such as antihypertensive drugs, narcotic analgesics, some
tranquilizers and sedatives, antihistamines, and antimetabolites.
Liquid form drugs and chewable form that contain added sugar can
alter the pH composition of plaque, making it more able to adhere to
tooth surfaces.

There are also drugs that may induce gingival overgrowth such as
the anticonvulsant drugs, calcium channel blockers and
cyclosporine.

6. Stress
Stress can affect the periodontium negatively. The effect of stress on
the periodontium can be described as an indirect or direct effect.

Indirect effects: It is mediated by lifestyle changes that can be

Lindhe's Clinical Periodontology and Implant Dentistry exacerbated with periodontal destruction, such as compromised oral
hygiene, inattention to dental visits for prevention/care. Deterioration

6
WEEK 4 | MODULE 3,4,6 DR. CONSUELO C. REYES
PERIODONTICS 1 - LECTURE DENT 4C Ð 2ND SEM

of metabolic control in diabetes, increase in smoking or alcohol and

illicit drug use, and inability to maintain healthy eating habits. 2. Sex
Disease susceptibility may increase due to hormone related
Direct effect: may be mediated both via modification of the alterations in women that affects the gingival blood flow and
composition of the subgingival biofilm and/or exaggeration of the composition of saliva. Men are found with worse periodontal health.
host inflammatory response.
3. Socioeconomic
7. Obesity Studies have shown that lower socioeconomic status is usually
Studies have shown that obesity has been linked as a risk factor for attributed to decreased dental awareness and decreased dental visits
periodontal disease. Patients who consume less than the when compared to individuals with higher socioeconomic status.
recommended dietary allowance (RDA) of calcium and vitamin C have
slightly higher rates of periodontal disease. 4. Education and Race
Periodontal disease has an indirect relationship with educational level,
LESSON 2: NON MODIFIABLE RISK FACTOR it means that, the lower the educational level, the higher the
1. Osteoporosis periodontal disease.
Osteoporosis is a disease characterized by loss of bone mineral
density that can lead to bone fragility and increase susceptibility to Race is not a modifiable risk factor, but some studies have shown that
bone fractures. different racial populations have found some difference in the
expression of periodontal disease.
Studies have shown that low bone mineral density in the maxilla and
mandible due to osteoporosis may contribute to periodontal disease 5. Genetic Consideration
by accelerating alveolar bone resorption initiated by periodontal Bacterial infection is the etiologic agent in periodontal disease, but
infection. studies showing the identical twins suggest 50% of susceptibility to
periodontal disease is due to host factors. Indigenous populations
2. Hematogolical Disorder have shown to develop periodontal disease that differs from group to
Hemorrhagic gingival overgrowth is the common early manifestation group.
of acute leukemia. Chemotherapy or any therapy associated with
bone marrow transplantation has an effect in gingival health. 6. C-Reactive Protein
C-reactive protein is part of the bodyÕs normal response to infection
3. Host Response and inflammation. elevated C reactive protein is observed with
Chronic periodontitis involves microbial factors and susceptible patients with periodontitis. Periodontitis is an inflammatory reaction of
factors. The components of bacteria such as lipopolysaccharide and the supporting tissues of the teeth.
cytokines activate macrophages to produce interleukin 1 and tumor
necrosis factor, which also activate the fibroblasts that reside in the
periodontium.

4. Female Hormonal Alteration

Changes during puberty, menstrual cycle, pregnancy, menopause
may alter the status of periodontal health due to hormonal fluctuation.

Also females using oral contraceptives/pills, women who are in

hormonal replacement therapy, may experience gingival
inflammation, this is mainly because prolonged use may detrimentally
affect the periodontium.

5. Pregnancy
Studies have shown that there is more attachment loss among
mothers with preterm low birth weight, compared with mothers of
normal term babies.

Therefore, Periodontal disease may increase the risk of having a

preterm low birth weight infant. This is thought to be the effect of
biologic mediators of inflammatory process, such as prostaglandin E2
and TNF

LESSON 3: RISK CHARACTERISTICS

1. Age
Both the prevalence and severity of periodontal disease increases
with age. The increased severity of periodontal disease and bone loss
with age is probably related to the length of time where the periodontal
tissues have been exposed to bacterial plaque.

Evidence of loss of attachment may be more in younger patients,

because the younger the patient the longer they have exposure to
causative factors, therefore with higher risk for continued disease as
they age.

7
WEEK 5 | MODULE DR. CONNIE C. REYES
PERIODONTICS 1 Ð LECTURE DENT 4C Ð 2ND SEM

CLASSIFICATION OF PERIODONTAL AND PERI-IMLPANT Periodontitis - >4mm periodontal pockets, bone loss, clinical
DISEASES 2017 attachment loss, gingival recession, tooth mobility, bleeding on
LECTURE Ð 03/08/2022 probing
Classification systems are designed to guide clinicians in the proper
and simple diagnosis of a condition. PERIODONTAL HEALTH, GINGIVAL DISEASES/CONDITIONS
1. Periodontal health and gingival health
The New Classification is the product of the World Workshop on the a. Clinical gingival health on an intact periodontium
Classification of Periodontal and Peri-implant Diseases and b. Clinical gingival health on a reduced periodontium
Conditions, held in Chicago in November 2017. i. Stable periodontitis patient
ii. Non-periodontitis patient
The World Workshop was organised jointly by the American Academy
2. Gingivitis - dental biofilm-induced
of Periodontology (AAP) and the European Federation of
a. Associated with dental biofilm alone
Periodontology (EFP) to create a consensus knowledge base for a
b. Mediated by systemic or local risk factors
new classification to be promoted globally.
c. Drug-influenced gingival enlargement Ð
WHAT'S NEW? 2017 Classification 3. Gingival diseases - non-dental biofilm induced. Not
¥ A definition of periodontal health for patients with an intact caused by bacteria
(no existing disease) or a reduced but healthy a. Genetic/developmental disorders
periodontium (periodontium that has undergone b. Specific infections
periodontal treatment) has been developed. c. Inflammatory and immune conditions
d. Reactive processes
An intact periodontiumÑa periodontium with no loss of e. Neoplasms
periodontal tissue (no loss of connective tissue or alveolar bone). f. Endocrine, nutritional & metabolic diseases
g. Traumatic lesions
A reduced periodontiumÑa periodontium with pre-existing loss h. Gingival pigmentation
of periodontal. tissue but, is not currently undergoing loss of
connective tissue/alveolar bone.
GINGIVITIS: DENTAL BIOFILM INDUCED;
GINGIVAL DISEASES: NON DENTAL BIOFILM INDUCED
¥ In defining a state of health, gingivitis, or periodontal
disease, it was agreed that bleeding on probing (BOP) BIOFILM-INDUCED GINGIVITIS
should be among the primary parameters to set thresholds is a site-specific inflammatory condition initiated by dental biofilm
for diagnosis and treatment planning. accumulation and characterized by gingival redness, edema and the
absence of periodontal attachment loss.
¥ Updated from the 1999 classification of chronic,
aggressive (localized or generalized), necrotizing or as a NON-DENTAL BIOFILM-INDUCED GINGIVAL DISEASES
manifestation of systemic disease, the newly revised arŽ less common but are often of major significance for patients.
classification system is based on a staging and grading These are often manifestations of systemic conditions. They may
system. represent pathologic changes limited to the gingiva and the
classification is based on the etiology of the lesions
¥ The previous four subsets of periodontitis have been
simplified into three: necrotizing periodontitis, periodontitis
as a manifestation of systemic disease, and periodontitis The diagnosis of dental biofilm-induced gingivitis
(previously considered as either chronic or aggressive). - is graded and identified based on the extent and the severity of a
patient's BOP score (%).
Formula: bleeding sites / sites evaluated x 100
BOP sites (facial, lingual, mesial, distal)
§ When only a few sites (<10%) are affected by gingival
inflammation, this is defined as incipient gingivitis.

§ Incipient gingivitis may rapidly progress to localized

gingivitis (10-30% BOP) if left untreated.
Ex: 18/72 x100 = 24%
§ Generalized gingivitis involves BOP scores of greater
than 30%.

§ Similarly, the severity of gingival inflammation can be

categorized as MILD/ MODERATE/ SEVERE.

The extent and severity of gingival enlargements are included in

the diagnosis of gingivitis.
CLINICAL PARAMETERS:
Gingivitis Ð no attachment loss, no bone loss, no pocket depth. Only Most often due to medication, gingival enlargements may either be
Ø localized or
inflammation of gingiva.
Ø generalized

1
WEEK 5 | MODULE DR. CONNIE C. REYES
PERIODONTICS 1 Ð LECTURE DENT 4C Ð 2ND SEM

It can be MILD /MODERATE/ SEVERE GINGIVAL ENLARGEMENT b) Extent and distribution: localized, generalized;
molar-incisor distribution
Oral contraceptives and menstrual cycle have been removed as a c) Grades: evidence of risk of rapid progression,
modifying risk factor in the new 2017 classification system
anticipated treatment response
Several systemic risk factors impact dental biofilm- induced gingivitis Grade A: Slow rate of progression
including uncontrolled hyperglycemia ,leukemia, smoking, and Grade B: Moderate rate of progression
malnutrition (i.e., Vitamin C deficiency) Grade C: Rapid rate of progression
PERIODONTITIS
OUTCOMES FOR PERIODONTAL HEALTH FOR PLAQUE- Based on the pathophysiology, three categories of periodontitis
ASSOCIATED PERIODONTAL DISEASE have been defined:
1. Necrotizing periodontitis
2. Periodontitis as a direct manifestation of systemic disease
3. Periodontitis

Regardless of the category, in the clinical context a patient is

considered a periodontitis case if
(1) interproximal CAL is detectable at two or more non-
adjacent teeth
(2) buccal or oral CAL is g3mm with pocketing g3mm is
detectable at two or more teeth, but the observed CAL
cannot be due to non-periodontitis related causes such
as:
a. Gingival recession of traumatic origin,
b. Dental caries extending in the cervical area of the tooth,
c. Presence of CAL on the distal aspect of a second molar and
associated with malposition or extraction of a third molar,
d. Endodontic lesion draining through the marginal periodontium,
and
e. Occurrence of a vertical root fracture.

Periodontal disease stability Ð diseases responded

FORMS OF PERIODONTITIS
1. NECROTIZING PERIODONTAL DISEASES
a) Necrotizing Gingivitis
b) Necrotizing Periodontitis
c) Necrotizing Stomatitis

2. PERIODONTITIS AS MANIFESTATION OF SYSTEMIC

DISEASES PERIODONTAL MANIFESTATIONS OF SYSTEMIC DISEASES
Classification of these conditions should be based on the primary AND DEVELOPMENTAL AND ACQUIRED CONDITIONS
systemic disease according to the International Statistics 1. Systemic diseases or conditions affecting the
periodontal supporting tissues
Classification of Diseases and Related Health Problems (ICD) codes
2. Other Periodontal Conditions
3. PERIODONTITIS a) Periodontal Abscesses
a) Stages: based on Severity and Complexity of b) Endodontic-Periodontal Lesions
Management
Stages I: initial periodontitis 3. Mucogingival deformities and conditions around
teeth
Stage II: moderate periodontitis
a) Gingival phenotype - thickness of gingiva
Stages III: severe periodontitis with potential for b) Gingival/soft tissue recession
additional tooth loss c) Lack of gingiva
Stages IV: severe periodontitis with potential for loss d) Decreased vestibular depth
of the dentition e) Aberrant frenum/muscle position
f) Gingival excess
g) Abnormal color

2
WEEK 5 | MODULE DR. CONNIE C. REYES
PERIODONTICS 1 Ð LECTURE DENT 4C Ð 2ND SEM

h) Condition of the exposed root surface GRADING OF PERIODONTITIS

4. Traumatic occlusal forces

a) Primary occlusal trauma - the excessive forces
whether, if the periodontal tissues condition of the
tooth
b) Secondary occlusal trauma
c) Orthodontic forces

5. Prostheses and tooth-related factors that modify or

predispose to plaque-induced gingival
diseases/periodontitis
a) Localized tooth-related factors
b) Localized dental prostheses-related factors

STAGES OF PERIODONTITIS

STAGES TO STAGING AND GRADING A PERIODONTAL CASE

STAGING
Ø Degree of the periodontal breakdown (attachment loss,
h/v bone loss, p. pockets) at the time of diagnosis
GRADING
Ø Rate of progression

STAGE I (INITIAL) STAGE II (MODERATE)

STAGE III (SEVERE WITH POTENTIAL STAGE IV (SEVERE WITH POTENTIAL

FOR ADDITIONAL TOOTH LOSS) FOR LOSS OF DENTITION)

3
PERIODONTAL INSTRUMENTS
 INTRODUCTION

Periodontal instruments are designed for

calculus removal, biofilm removal, and
root planing.
PARTS OF INSTRUMENTS
 PARTS OF PERIODONTAL INSTRUMENTS
1. Handle/shaft Ð held during activation of the working end
- cone-socket handles or fixed; may be smooth, ribbed or knurled
 PARTS OF PERIODONTAL INSTRUMENTS
2. Shank Ð connects working end with the handle
 PARTS OF PERIODONTAL INSTRUMENTS
3. Working-end Ð blade of the instrument
 CLASSIFICATIONS OF PERIODONTAL INSTRUMENTS
A. Periodontal instruments are classified according to their purposes.
1. Periodontal probes
2. Explorers
3. Scaling, root planing, and curettage instruments
4. Periodontal endoscopes
5. Cleansing and polishing instruments
B. 1. Assessment instruments
2. Calculus removal instruments
C. Based on design:
1. Single-ended
2. Double-ended
PERIODONTAL PROBES

* UNC15 Probe / WHO probe

* Naber's Probe
Periodontal Probe Technique
PERIODONTAL PROBES
PERIODONTAL EXPLORER

* ODU 11/12 Perio Explorer (optional)

* No. 23/17 Dental Explorer
SICKLE SCALERS

* Hygienist/Universal Scaler
* Jacquette Scaler

Sickle Scaler, Hygienist H6/H7

SICKLE SCALERS

* Hygienist/Universal Scaler
* Jacquette Scaler

Sickle Scaler, Hygienist H6/H7

PERIODONTAL CURETTES
* Reduced Standard Set Gracey Curette:
5/6 Gracey Curette
7/8 Gracey Curette
11/12 or 15/16 Gracey Curette
13/14 or 17/18 Gracey Curette
Columbia 13/14 Universal Curette

Gracey 11/12 Curette

Reduced Standard Set Gracey Curette:
5/6 Gracey Curette
7/8 Gracey Curette
11/12 or 15/16 Gracey Curette
13/14 or 17/18 Gracey Curette
WEEK 1 | MODULE 1 PROFERSSOR
PERIODONTICS 1Ð LABORATORY DENT 4I Ð 1ST SEM

MODULE 1: PERIODONTAL INSTRUMENTATION AND

ERGONOMICS
CANVAS OR LECTURE/PPT -BASED

LESSON 1: PERIODONTAL INSTRUMENTS

A. Parts of a Periodontal Instrument

b. Kinds:
1. Single Ð ended eg. Periodontal probe
2. Double ended
¥ Unpaired working ends Ð eg. Curet/sickle scaler
1. Handle Ð for holding the instrument ¥ Paired working ends e. Gracey curettes
2. Shank Ð connects the handle to the working-end
a. Types: B. Classification of Periodontal Instruments
- Simple 1. Assessment Instruments
(a) Periodontal probes
- complex
(b) Explorers

2. Calculus Removal Instruments

(a) Sickle scaler
(b) Curettes
(1) Universal curet
(2) Area-specific curet
(c) Periodontal Files

C. Techniques in Instrument Sharpening

1. Moving instrument technique
b. lower shank lengths: 2. Moving stone technique
- standard shank
- extended shank LESSON 2: PERIODONTAL INSTRUMENTATION
Read: Gehrig, J. Sroda, R and D. Saccuzzo, Fundamentals of
Periodontal Instrumentation & Advanced Root Instrumentation, 8th
edition.
Module 9 Movement and Orientation to Tooth Surface
Module 10 Adaptation
Module 11 Instrumentation Strokes

Periodontal instrumentation is a skill comprised of small

movements carried out when the brain, nervous system and muscles
3. working end Ð does the work of the instrument work together. Basically this is about brain-body coordination. To
parts: perform these complex movements, it requires a lot of repeated
practice.
A. The Wrist-rocking Motion

B. Digital Motion Activation

- moving the instrument by flexing the thumb, index and middle
fingers

2018-00070 1
WEEK 1 | MODULE 1 PROFERSSOR
PERIODONTICS 1Ð LABORATORY DENT 4I Ð 1ST SEM

C. Instrumentation Strokes
Types:
1. Assessment or Exploratory stroke Phase II (Surgical Phase )
2. Calculus Removal Stroke ¥ Periodontal therapy, including placements of implants
3. Root Debridement Stroke ¥ Endodontic therapy

D. Adaption of the Working-End

1. Leading third is the anterior portion of the working-end is always Phase III ( Restorative Phase )
in contact with the tooth surface ¥ Final restorations
2. Adapt the tip-third to the midline of the tooth ¥ Fixed and removable prosthodontic appliances
3. Adapt the tip-third to the line of the angle of the tooth ¥ Evaluation of response to restorative procedures
¥ Periodontal examination
E. Stroke Direction
1. Vertical and oblique strokes Phase IV ( Maintenance )
2. Horizontal stroke Periodic Re-checking :
3. Multidirectional stroke
¥ Plaque and calculus
¥ Gingival condition (pockets, inflammation)
¥ Occlusion, tooth mobility
¥ Other pathologic changes

The master plan or the treatment plan includes all aspects of the oral
cavity. Short-term goals and long-term goals of the treatment are all
incorporated in the treatment plan. Overall, the total establishment,
restoration and maintenance of periodontal health are the desired
outcomes of the entire treatment.

MODULE 5: TREATMENT PLAN AND TREATMENT

LESSON 1: PHASES OF TREATMENT

Periodontal therapy procedures are divided into 4 phases :
Phase 1, Non-Surgical Phase; Fig. 10.1 Sequence of periodontal therapy
Phase 2 Surgical Phase;
Phase 3 Restorative Phase and The diagram above shows the proper periodontal therapy
Phase 4 Maintenance Phase. sequence in which the first step is the preliminary phase and not start
with Phase I. Preliminary Phase attends to emergency treatments
These are 4 major aspects in periodontal treatment. But that need to be prioritized like acute pain, abscesses, swellings, etc.
a Preliminary Phase comes before these major procedures. and only after such emergencies are attended to, will the clinician now
The Preliminary phasetreats emergencies in the oral cavity Ð dental proceed to Phase I or Non-surgical therapy. Upon completion of
or periodontal. Phase I, the next step must be Phase IV or Maintenance Phase which
includes re-evaluation of the periodontal tissuesÕ response to the non-
Preliminary Phase surgical treatment ideally 8 weeks after Phase I. Only then, the
Emergency treatment (pain, acute infections) decision to proceed to Phase II and Phase III can be made. So the
Teeth requiring extraction (may be postponed to a more convenient periodontal treatment process has to be re-evaluated as maintenance
time) every 3 months before going to the next phase.

Phase 1 (Non-Surgical Phase) LESSON 2: SCALING, ROOT PLANNING, POLISHING AND

Plaque control and patient education FLOSSING
¥ Diet control (patients with rampant caries) NON-SURGICAL THERAPY (PHASE I)
¥ Removal of calculus and root planning Before starting this lesson, you must be ready with the different
¥ Correction of restorative and prosthetic irritational factors instruments that you need to prepare before starting with your actual
¥ Excavation of caries and restoration (temporary or final, patient in the clinics. Your professor will provide you a list of the
depending on whether a definitive prognosis for the tooth materials and instruments that you need to bring as you enter the
has been determined and the location of caries) clinics. You need to be informed of the following:
¥ Antimicrobial therapy (local or systemic)
¥ Occlusal therapy ¥ Rules in the Clinic and Rules for the Periodontics Section
¥ Minor orthodontic movement ¥ Filling up of the OD Forms
¥ Provisional splinting and prosthesis
Preparing the Dental Module Before, During and After the Procedure
*** Evaluation of Response to Non-Surgical Phase
¥ Pocket depth and gingival inflammation
¥ Plaque and calculus, caries

2018-00070 2
WEEK 1 | MODULE 1 PROFERSSOR
PERIODONTICS 1Ð LABORATORY DENT 4I Ð 1ST SEM

In most cases, Phase I therapy is the only set of procedures that will LESSON 3: PERIODONTAL MEDICINE (ANTI-INFECTIVE
restore periodontal health, or as the preparatory procedure for THERAPHY)
surgical phase. An anti-infective agent is a chemotherapeutic agent that acts by
reducing the number of bacteria present.
Procedures:
1. Plaque Control Instruction ( to be discussed seaparately) 1. Antibiotic - naturally occuring, semi-synthetic or synthetic
2. Removal of Supragingival and Subgingival calculus type of ant-infective agent that destroys or inhibits the
3. Recontouring Defective restorations and Crowns growth of select micro-organisms
4. Elimination of Carious Lesions 2. Antiseptic - a chemical antimicrobial agent that can be
5. Tissue Reevaluation applied topically or subgingivally to mucous , wounds or
intact dermal surfaces to destroy microorganisms and
CLINICAL PROCEDURES: inhibit their reproduction or metabolism.
I. Disclosing a. Disinfectant (subcategory of antiseptic) -
Disclosing determines the presence or absence of plaque with antimicrobial agents applied to inanimate
the use of disclosing agents such as tablets or solutions. The first step objects to destroy microorganisms
in the Scaling and Polishing Procedure is to disclose the teeth by
wiping the disclosing solution on all surfaces using a cotton ball and Systemic administration of antibiotics is done to reduce the number of
allowing the patient to rinse to remove the excess solution. After which bacteria present in the diseased periodontal pocket. This is a
you will see that the disclosed areas (colored) are those with the necessary adjunct for controlling bacterial infection because bacteria
presence of plaque. can invade periodontal tissues, thereby making mechanical therapy
alone sometime ineffective.
Instruments needed:
1. Disclosing solution or tablet Common Antibiotic Regimens used to Treat Periodontal
2. Cotton plier Diseases
3. Cotton pellet or applicator
4. Dappen dish
Single Agent Regimen Dosage/Duration
II. Scaling and Root Planing (SRP) Three times daily for 8
Amoxicillin 500 mg
Scaling is the process by which biofilm and calculus are removed days
from both supragingival and subgingival tooth surfaces. No Once daily for 4 to 7
deliberate attempt is made to remove tooth substance along with the Azithromycin 500 mg
days
calculus.
Ciprofloxacin 500 mg Twice daily for 8 days
Root planing is the process by which residual embedded calculus
and portions of cementum are removed from the roots to produce a Three times daily for
Clindamycin 300 mg
smooth, hard, clean surface. 10 days
The primary objective of scaling and root planning is to restore Doxycycline or
gingival health by completely removing elements that provoke 100mg to 200 mg Once daily for 21 days
minocycline
gingival inflammation (e.g. biofilm, calculus and endotoxin) from the
Three times daily for 8
tooth surface. Metronidazole 500 mg
days
Instruments needed:
1. Scalers Combination
2. Curettes Therapy
3. Periodontal chisels, hoe, and files Metronidazole + Three times daily for 8
4. Ultrasonic scalers 250 mg of each
amoxicillin days

III. Polishing Metronidazole +

500 mg of each Twice daily for 8 days
With the use of a rubber cup and prophylaxis polishing brush on a ciprofloxacin
contra-angle hand piece running on slow speed rpm with prophylaxis
paste mixed with pumice, the teeth are polished to remove dental
biofilm and extrinsic stains.

Instruments needed:
1. Prophylactic brush
[Link] rubber cup
[Link] paste

IV. Flossing
Dental floss is the most widely recommended tool for removing
biofilm from proximal tooth surfaces. The floss must contact the
proximal surface from the line angle to line angle to clean effectively.
It must also clean the entire proximal surface including accessible
subgingival areas.

Instruments needed:
1. Waxed or unwaxed floss
2. Floss threader (for crowns, bridges, splinted teeth and
orthodontic appliances)

2018-00070 3
WEEK 2 | MODULE 3 PROFERSSOR
PERIODONTICS 1 - LABORATORY DENT 4C Ð 2ND SEM

MODULE 2: CLINICAL DIAGNOSTIC TEST

CANVAS Ð BASED Some patients suffering from periodontal disease are unaware of the
presence of their condition. However, many may report bleeding
In treatment planning, it is critical to have a proper diagnosis to be able gums, loose teeth, drifting of teeth, foul taste in the mouth, halitosis,
to identify the presence of a periodontal disease. A thorough swelling of the gums, discomfort, occasionally acute pain, or an itchy
examination of the patientÕs history and evaluation of the overall oral feeling in the gums.
health status of the patient will help the clinician identify the presence
of any periodontal diseases, its extent and severity. Ø A brief statement of a symptom(s) for which the patient is
seeking care at the moment
Periodontal diagnostic procedures should be systematic and
® Òwhat bring you to the clinic today?Ó
organized. All the findings must be pieced together to provide an
® Verbatim with quotation mark
explanation to the patientÕs periodontal problem.
3. HISTORY PRESENT ILLNESS
02/17/2022 Ð DISCUSSION
History of present illness (HPI) describes the chronological
description of the progression of a patient's present illness from the
PERIODONTAL EXAMINATION AND DIAGNOSIS: first sign and symptom to the present. In addition, pertinent questions
1. History taking Ð starts when you see the patient should be asked:
2. Diagnostic tools ¥ Are you in pain?
3. Clinical examination ¥ Where is the pain?
¥ Is it a throbbing or dull pain?
HISTORY TAKING ¥ Does the pain keep you awake?
a. Periodontal examination (history taking, diagnostic ¥ What brings on the pain Ð hot or cold beverages, sweets
tools, etc.) or upon biting?
¥ Have you had pain in the past or is this the first time?
a. Patient appraisal
¥ What treatment did you received for pain?
b. Chief complaint
¥ Do your gums ever bleed?
c. History of present illness o When you brush your teeth?
d. Medical history o When you eat hard food?
e. Dental history ¥ Did your gums bleed in the past?
f. Family history and social history ¥ What treatment did you receive?
b. Diagnosis - ¥ Do any of your teeth feel loose?
c. Periodontal treatment - ¥ Have you always had that space between your front
teeth?
LESSON 1: HISTORY TAKING ¥ Have you had any swelling in your mouth? Where, when
etc?
To understand the oral health status of the patient and its dental
needs, a health questionnaire must be fill up by the patient prior to
initial examination. This health questionnaire will help the clinician to Must know the signs (objective) and symptoms (subjective) of
design a comprehensive treatment plan for the patient. gingivitis and periodontitis
[Chief complaint à Onset à Dental History à Clinical
To assess the patientÕs history, this requires a thorough evaluation of Examination]
the following aspects: 1st sentence
¥ Chief complaint Onset Ð when did you notice/ experienced it (time: months, year)
¥ History of Present Illness Provoke/triggers/during Ð every when do the px experience it (past
¥ Medical History
tense)
¥ Dental History
Duration Ð how long do the px experience it (few seconds, mins)
¥ Family History
Factors - Other activity that causes the ÒbleedingÓ
¥ Social History
2nd sentence
1. PATIENT APPRAISAL
Dental history/treatment related to the case Ð dental treatment
While taking the history, a general appraisal of the patient should be
made, and such features as obesity, general posture, pallor, skin rash, related to perio.
heavy breathing, lip posture should be noted.
Ø Appraisal Ð assessing appearance 3rd sentence
® Mental and emotional status Upon consultation. What are the clinician observation/ examination
® Temperament Ø Clinical Examination/ Observation Ð (redness of gingiva,
® Attitude swelling, calcular deposits, halitosis, etc.)
® Physiologic age Ø Periodontal treatment that the px needs
Example: 1 year ago, the px started to experience bleeding of gums
2. CHIEF COMPLAINT during tooth brushing. The px also noticed having bad breath.
Chief complaint is important in treatment planning. Clinicians record Bleeding of gums lasts for 2-3 mins and stops upon gargling. The px
the chief complaint using the patientÕs own words to avoid replacing did not undergo any dental/periodontal treatment. Upon consultation,
the patientÕs word with their diagnostic interpretation. Usually, chief there is redness of gums, moderate to severe amount of calcular
complaints state the key symptoms that the patient is experiencing. deposits.

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WEEK 2 | MODULE 3 PROFERSSOR
PERIODONTICS 1 - LABORATORY DENT 4C Ð 2ND SEM

4. MEDICAL HISTORY 6. FAMILY HISTORY AND SOCIAL HISTORY

Although a medical history may not seem relevant to some patients, Before assessing the clinical conditions in detail, it is advantageous to
it is essential to obtain one for several reasons: elucidate the patientÕs social environment and to feel for his/her
¥ The patient may be suffering from some condition (e.g., priorities in life including the attitude towards periodontal therapy and
cardiovascular disease, renal disease, etc.), which will , potential rehabilitation with dental implants. Likewise, a family history
and will necessitate communication with the patientÕs may be important especially with respect to form of periodontitis with
physician a rapidly progressing pattern.
¥ Systemic conditions (e.g., pregnancy, diabetes), will alter
the way in which the periodontal tissues behave and may Social history
demand medical attention before periodontal treatment ® Smoking habits
can be carried out. ® Alcohol and drug use, sexual habits
¥ The mouth may be the site of some manifestation of a ® Diet, occupation, environment
systemic condition, such as anemia, which could affect ant Family history
periodontal treatment. ® Helps establish patterned and risk factors for potential
¥ The patient may be receiving medications such as diseases
antidepressants, which may conflict with medications ® Information should be related to the patientÕs correct
involved in the periodontal treatment. medical condition

A medical history should record any present illness and medication; LESSON 2: DIAGNOSTIC TOOLS
any past serious illness and medication, e.g., steroids taken in the Intraoral photographs, casts, and radiographs are important
recent past, allergies, especially any history of penicillin sensitivity, adjuncts which can be utilized to compare changes in tissue.
abnormal bleeding tendencies, in particular excessive bleeding after Photography is especially beneficial in cases where severe
injury or tooth extraction. The use of a questionnaire may be helpful. inflammation is present.
Where some systemic problem exists, communication with the Some of the adjunct devices can identify inflammation in the soft
patientÕs physician is essential. tissues but they cannot differentiate between inflammation caused by,
for example, cheek biting or lichen planus. Being able to compare
® Pertinent medical conditions that need to be considered digital images of the pre-treatment provides the dentist the added
prior to treatment benefit of actually seeing the progression of the disease. An added
® Systemic conditions that could contribute their current benefit is being able to show the patient how the disease or treatment
disease state has progressed over time. Oral photography is highly beneficial as a
key part of the patientÕs permanent record as well.
® Complete list of medications Ð for drug interactions,
contraindications, and interferences to therapy Radiographs can be used to determine the level of bone loss, adding
® Any food, drug or other allergies another dimension to the diagnostic process. Radiographs are also
important in assessing both hard and soft tissue lesions within the oral
5. DENTAL HISTORY cavity that may not be visible during the standard oral cancer exam.
Dental history should include the following: In this lesson, you will learn how to take intraoral photographs,
radiographs, as well as creating a study cast that will be useful
¥ How often do you visit the dentist?
diagnostic tools in periodontal therapy.
¥ What was the last treatment you received?
¥ When did you last have a scaling, i.e., cleaning by your
dentist? INTRAORAL PHOTOGRAPHS
¥ Do you have any dentures (false teeth that you can take Intraoral photographs are an important addition to patient records
out) Ð how long have you had them? (charting, radiographs, study models). They provide a static, in-depth
¥ Have you any false teeth that are fixed in Ð how long have look at the patient's dentition that is easily reviewed and compared
you had them? with the patient's other records.

At this stage, questioning about home care can be a waste of time. Detailed pictures showing anatomy, surgical steps, materials, and
Answers to such questions as ÔHow often do you clean your teeth?Õ completed cases can help educate patients on diagnosis and
are often suspect, as the patient is likely to say what he imagines he proposed treatment, thereby improving their understanding and case
is supposed to say, i.e., twice a day, night, and morning. Even if this acceptance.
happens to be the truth, it gives no indication of the quality of the
performance; only an examination of the mouth provides information The majority of pictures taken in periodontology are intra-oral, which
about that. includes the following:

At this time, some ideas about habits should be asked e.g., smoking,
clenching, night-grinding, biting pencils etc.
® Experiences with previous dental care
® Has the px been exposed to preventive dentistry before?
® How often does the patient brush and floss their teeth?
® Has the patient had previous periodontal cure?
® A periodontal history should be obtained Ð bleeding
gums, changes in teeth position
1. Full arch Ð frontal and occlusal

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WEEK 2 | MODULE 3 PROFERSSOR
PERIODONTICS 1 - LABORATORY DENT 4C Ð 2ND SEM

2. Quadrant - buccal, lingual

3. Magnification images for detailed analysis of teeth or
soft tissues
4. Oral mucosa

LESSON 3: CLINICAL EXAMINATION

In this lesson, we will learn how to examine the patient extraorally and
intraorally. Then we will also learn how to assess the patient
periodontally through different indices, probing, mobility, and furcation
CAST involvement. Finally, to help organize the patient information, we will
It is recommended to take a dental impression to produce a replica of record our data in the dental and periodontal chart.
the teeth and oral tissues . This will provide the clinician a 3D
representation of the patient's dentition for further evaluation. EXTRAORAL EXAMINATION
- Take note of the patientÕs gait (manner of walking),
mobility, facial asymmetries, scars or lesions
RADIOGRAPHS - Examination of the soft tissues of the head and neck
Dental radiographs are used to evaluate the dental and periodontal o Lymph nodes examination, TMJ function
health. This can help the clinician to identify problems like caries, bone - Palpation of muscles of mastication for tenderness,
loss, periapical lesions, and impacted teeth. swelling or asymmetry
Systolic Ð contraction, high pressure
Panoramic radiographs capture the entire oral cavity in a single Diastolic Ð relaxation
image, to see an overview of the whole dentition. It covers a wider
area than a conventional intraoral x-ray and, as a result, provides General physical assessment
valuable information about the maxillary sinuses, tooth positioning, The clinician needs to determine an overall impression of the general
and other bone abnormalities. It is generally used as an initial health and physical wellbeing of each patient. The general appraisal
evaluation but does not provide precise and detailed information about begins with the initial patient contact and continues during the entire
each individual tooth. appointment. The first opportunity to observe the patientÕs general
health and physical characteristics usually presents as the patient is
escorted to the operatory from the reception area. During this walk the
clinician can observe the patientÕs posture and gait and any physical
limitations which may be apparent. The general assessment continues
as the clinician obtains or updates the medical and dental histories as
learned in the previous lesson.

Head and Neck

The head and neck examination will enable the clinician to focus
attention on careful observation of the structures of the head and neck.
Complete mouth radiographic sequence (CMRS) is a full mouth The sequence used in performing the head and neck examination and
series of intraoral radiographs used to examine the dentition and subsequently the intraoral examination is not as important as
surrounding structures with more detail. It comprises of 12-14 performing each examination using the exact same sequence every
periapical radiographs in a complete set of dentition. This is a valuable time. Consistency enables the clinician to perform these examinations
tool in periodontology to detect the level of the alveolar bone including quickly and efficiently while still maintaining the highest degree of
the pattern and extent of loss of the bone. Measurements that are of awareness in order to identify abnormal versus normal conditions.
linear from the cement-enamel junction to the crest of the alveolar
bone and from the cement enamel junction to the bone defect base Symmetry and Profile
are commonly used to measure the bone height and bone defects. In Start by looking at the standing patient. Assess the symmetry of the
radiographs, the periodontal ligament space, lamina dura and face as well as the head and neck region. This can also be done if the
periapical region are seen and also helpful in identifying risk, such as patient is sat upright in the dental chair. Most of us have some
calculus and dislodged restorations. Radiographs can provide asymmetries, but significant asymmetries on comparison of one side
information for proper diagnosis and treatment planning, which can to the other should be noted. This asymmetry may be bony or soft
provide information for the assessment of accurate treatment tissue in nature. It may be acute or chronic, or it may be secondary to
outcomes. previous surgery, e.g. tumour resection or CVA. It may have occurred
following injury, such as a fall, and the patient presents to the dentist
Dental Cone Beam Computed Tomography (CBCT) is a special with deranged occlusion and facial asymmetry due to a mandibular
type of x-ray equipment used when regular dental x-rays are not fracture. Asymmetry is also associated with temporomandibular joint
sufficient. This is used to produce 3D images of the teeth, soft tissues, dysfunction and malocclusions
nerve pathways, and bone in a single scan. It provides detailed images
of the bone and is performed to evaluate diseases of the jaw, dentition, Eyes
bony structures of the face, nasal cavity, and sinuses. Looking at a patientÕs eye can give the clinician an insight into what
possible systemic conditions the patient may have. The eye may show
signs of medical conditions already known to the patient, but if they

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WEEK 2 | MODULE 3 PROFERSSOR
PERIODONTICS 1 - LABORATORY DENT 4C Ð 2ND SEM

are not known, advising the patient to seek medical attention may patientÕs record. The first step in the intraoral examination is a quick
influence their outcome. general examination of the cheeks, hard palate, tongue and gingiva
looking for any contraindications for continuing the evaluation. If there
Skin are none, start the examination.
The exposed skin of the head and neck should be examined for
suspicious lesions or discolorations. The skin of the neck and scalp During the intraoral exam, check for cavities and periodontal disease
can be examined while the clinician is palpating the occipital and and record them in the chart. The exam includes evaluating your risk
cervical nodes. The area behind and around the ear can be observed of developing other oral problems and checking your face, neck and
while palpating the auricular nodes. The patient should be questioned mouth for abnormalities. An intraoral exam might also include
about their knowledge of any lesions discovered during the radiographs and other diagnostic procedures.
examination and also any lesions that they may have noticed
themselves anywhere on the body. Lips
The lips should be examined for symmetry and tissue consistency and
Lymph nodes texture. Normally the lip tissue should be resilient, smooth and have a
The major lymph nodes of the head and neck area should be palpated homogenous pink color. The vermillion border should be distinct and
with the patient in an upright position. Findings which should be noted even. The commissures should be clear of lesions and should not
in the patient record include enlarged palpable nodes, fixed nodes, show signs of cracking or dryness.
tender nodes and whether the palpable nodes are single or present in
groups. Single or multiple non-tender, and fixed nodes are very Floor of the Mouth
suspicious for malignancy. Groups of tender nodes usually occur in The floor of the mouth is examined using direct and indirect vision
conjunction with some type of acute infection. Occasionally nodes will followed by bimanual palpation of the entire area. The patient should
remain enlarged and palpable after an infection. This is a relatively be asked to raise the tongue making direct visual examination of the
common occurrence especially within the submandibular group of tissues toward the midline of the floor of the mouth possible. The
lymph nodes. When examined, these nodes should be small (less than mirror should be used to examine the areas near the inferior border of
1 cm), non-tender and mobile. the mandible. The tissues should appear moist and very vascular.

Remember to correlate findings from the medical history and general Gingiva
appraisal of the patient to the observations made during the head and The gingiva of the maxillary and mandibular arches is visually
neck examination. examined using both direct and indirect vision. The tissues should
appear pale pink and homogenous in color and texture. Following the
TMJ visual examination, the gingiva is palpated using a digital technique.
The function of the TMJ should be evaluated using a bilateral The tissue should feel firm to touch and tightly attached to the bone.
technique. Place the fingertips over the joint and have the patient
open and close slowly, move the jaw to the left and right and jut the Palate
chin out. Look for altered opening and closing pathways, abnormal The hard palate and maxillary tuberosity areas are examined using
sounds, tenderness and limitations in opening. both direct and indirect vision and illumination. Following the visual
examination the clinician should digitally palpate the entire area
There are two basic types of altered opening pathways, deviations using firm non-sliding pressure against the bone. In general, the
and deflections. tissue is a homogenous pale pink color, firm to palpation towards the
An altered pathway on opening which comes back to the midline at anterior and lateral to the midline while more compressible towards
maximum opening is termed a deviation. the posterior and medial to the apices of the teeth.
If the greatest distance from the midline occurs at maximum opening
it is called a deflection. Tongue
The tongue is examined using both direct and indirect vision. Grasp
Abnormal sounds may be heard or felt and usually fall into one or more the tip of the tongue with a gauze square and roll the tongue over on
of three major categories, clicks, pops and crepitus. Clicks and pops one side to observe the lateral border then repeat for the other side.
are associated with articular disk derangement and crepitus is usually Use the mirror to examine the posterior lateral borders if necessary.
associated with some form of arthritis. Correlate TMJ findings with the The tissues should appear pink in color with a rough surface texture
patientÕs occlusal classification and other dental findings such as on the dorsal surface and a smoother surface texture on the ventral
missing teeth and poorly fitting partial and/or full dentures. Follow-up surface. The tongue should be symmetrical in shape and in function.
questions should focus on the history of any observed symptoms and The tissues of the tongue should feel soft and resilient with no palpable
determination of any life style or dietary modifications the patient may indurations or masses.
have made to alleviate discomfort. Examination of the TMJ provides a
perfect transition point for the intraoral examination. Teeth
Examine each tooth carefully. Check for discolorations, carious
INTRAORAL EXAM lesions, restorations, missing teeth, abrasions, erosions, prosthesis,
® Evaluate the lips, labial mucosa, buccal and vestibular and other abnormalities. Record all your findings in the dental chart
mucosa, hard and soft palate, tongue, floor of the mouth, using red ink for pathologies and blue ink for restorations.
gingiva and alveolar mucosa
® Note: color, texture, and degree of salivary flow
® Any swelling, ulceration, palpable masses or tenderness
should be noted

As with the head and neck evaluation, this examination should be

done using the same sequence every time. Areas should be visually
examined then palpated wherever possible. Findings should be
thoroughly investigated and the information should be noted in the

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WEEK 2 | MODULE 3 PROFERSSOR
PERIODONTICS 1 - LABORATORY DENT 4C Ð 2ND SEM

GINGIVAL BLEEDING INDEX

Bleeding on probing (BOP) is a widely used criterion to diagnose
gingival inflammation. To test for bleeding after probing, the probe is
carefully introduced to the bottom of the pocket and gently moved
laterally along the pocket wall. Sometimes bleeding appears
immediately after the removal of the probe; other times it may be
delayed for a few seconds. Therefore the clinician should recheck for
bleeding 30 to 60 seconds after probing. The insertion of a probe to
If OP: until mouth examination only
the bottom of the pocket elicits bleeding if the gingiva is inflamed and
PERIODONTAL INDICES if the pocket epithelium is atrophic or ulcerated.
PLAQUE INDEX
® To check the amount of plaque/ calcular deposit present Noninflamed sites rarely bleed. In most cases, bleeding on probing is
® Use of pure disclosing solution. Use swab sticks an earlier sign of inflammation than gingival color changes. If
periodontal treatment is successful, bleeding on probing will cease.
® Surfaces: labial, palatal and lingual surfaces
® Each tooth has 4 surfaces = 4x32= 128 (if complete set)
® Denominator Ð the number of teeth present x4 surfaces
® Numerator Ð number of plaques

Clinical plaque indices are used to evaluate the level and rate of
plaque formation on tooth surfaces, and to test the efficacy of oral care
products for removal and prevention of plaque deposits from these Bleeding on Probing (Ainamo & Bay 1975) As in the PI, all four
surfaces. Poor oral hygiene and inappropriate dietary behavior can surfaces of all teeth are assessed with regard to whether probing
lead to increased plaque accumulation. As dental plaque is not easily elicits bleeding or not. The severity of gingivitis is expressed as a
visible to the naked eye, its identification and removal is difficult. In percentage. Because more than 100 sites must be measured, the
order to identify dental plaque clinically, the use of disclosing agents BOP is indicated only for individual patient examinations (e.g., data
has been recommended. Disclosing agents are preparations collection, recall).
containing dye or other coloring agents which is used for the
identification of bacterial plaque that can be distinctly seen providing
a valuable visual aid and help in the maintenance of good oral health.
To use the disclosing solution, ask the patient to swish the solution
around in the mouth for about 30 seconds and spit it out. Then check
the teeth in good light for areas highlighted with the bright pink/purple
stain. These stained areas are where plaque has accumulated.

PROBING
Plaque Index simplified, PIÑPlaque Control Record, PCR (PI; ¥ Use of University of North Carolina (UNC -15) to measure
PCRÑOÕLeary et al. 1972) This precise index records the presence the periodontal pocket depth
of supragingival plaque on all four tooth surfaces. For this test, the ® 10 degrees
plaque is disclosed. The presence or absence of plaque is recorded The clinician will record six measurements for every tooth to ensure
in a simple chart, and the plaque incidence in the oral cavity is that all areas of the mouth are reviewed. Alongside these
expressed as an exact percentage. measurements, they also check for bleeding and recession.
Healthy gingiva typically has pockets measuring 0-3mm and fits
snugly around your tooth. Measurements of 4mm or greater are
concerning since plaque and bacteria could be causing the tissue to
inflamed and pull away from the tooth. Areas with higher readings are
often more sensitive to probing. In severely diseased areas, probing
depths can reach as high as 12mm. These problem areas are known

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WEEK 2 | MODULE 3 PROFERSSOR
PERIODONTICS 1 - LABORATORY DENT 4C Ð 2ND SEM

as periodontal pockets and are generally challenging to keep clean at eventually tooth loss. Increased tooth mobility is a common sign of
home. A periodontal chart helps the clinician to organize the advanced periodontal disease and is one of the main reasons patients
information about the condition and diagnose and treat the disease. seek periodontal treatment.
The goal of clinical periodontal charting is to record probing depths,
gingival recessions, and clinical attachment levels at six sites per tooth We can assess the tooth mobility by holding a tooth in between the
(mesial buccal/facial, middle buccal/facial, distal buccal/facial, mesial butt end of two instruments and gently moving back and forth or with
lingual/palatal, middle lingual/palatal, and distal lingual/palatal one instrument and one finger for support.
surfaces)
Grace And Smales Index
The Gingival Margin is the distance from the clinical gingival margin to Grade 1 - mobility <1mm buccolingually
the cemento-enamel junction. Gingival recession is the condition seen Grade 2 - mobility 1-2mm buccolingually
when the gingival margin is located apically to the cemento-enamel Grade 3 - mobility >2mm buccolingually and or vertical tooth mobility
junction. The value noted as the gingival margin should be recorded
as a negative value. This will be marked with a red ink on the
periodontal chart. FURCATION INVOLVEMENT

The Probing Depth is the distance between the gingival margin and
the base of the gingival sulcus. At some diseased sites, the cemento-
enamel junction may be located somewhat below or above the gingival
margin. The distance between the gingival margin and the base of the
periodontal pocket is then recorded as the periodontal probing depth.

Note: Periodontal pockets of > 4mm following active periodontal

therapy are called residual pockets. The site with the deepest
periodontal probing depth should be recorded for each section. This
will be marked with blue ink on the periodontal chart. A furcation is defined as ÔÔthe anatomic area of a multirooted tooth
where the roots divergeÕÕ, and furcation involvement refers to the
ÔÔpathologic resorption of bone within a furcationÕÕ. According to the
glossary of terms of the American Academy of Periodontology, a
furcation involvement exists when periodontal disease has caused
resorption of bone into the bi- or trifurcation area of a multi-rooted
tooth. Diagnosis and its correct interpretation are essential when
establishing an adequate treatment.

Diagnosis of the furcation involvement is based upon probing and

visual deteb ction. Although a straight probe may be used, detection
of subgingival furcation is facilitated by the use of the curved NaberÕs
probe. Radiographic images can also help detect furcation, but are not
completely reliable as overlapping of tooth structures can mask the
bone loss.

The Clinical Attachment Level is the distance between the cemento-

enamel junction and the base of the periodontal pocket.

Ø Each site will be calculated based on the formula:

Probing Depth (mm) Ð Gingival Margin (mm) = Attachment Level (mm)

Watch this video on how to use the naber's probe (Links to an

external site.)
Ø Furcation defects should be inspected from different
angles according to the number of roots the tooth has.
Ø Maxillary teeth: trifurcated (mesiobuccal, distobuccal,
palatal roots). Furcation entrances on the mid-buccal,
mesial, and distal aspects of the tooth.
Maxillary first premolar: can be bifurcated (buccal and palatal
roots). Furcation entrances on the mesial and distal aspects of the
tooth.
MOBILITY
The AAP defines tooth mobility as "The movement of a tooth in its Mandibular teeth: bifurcated (mesial and distal roots). Furcation
socket resulting from an applied force". entrances on the mid-facial and mid-lingual aspects of the tooth.

In health, physiological or functional mobility of the tooth exists and GlickmanÕs classification - describe the extension and main
every tooth with healthy periodontal support will have a physiologic characteristics of the furcation defect
range of mobility. However, periodontal disease can lead to the
destruction of the surrounding periodontal tissues, in particular,
alveolar bone loss. If left untreated, it may lead to tooth mobility, and

6
WEEK 2 | MODULE 3 PROFERSSOR
PERIODONTICS 1 - LABORATORY DENT 4C Ð 2ND SEM

Grade I involvement: it is the incipient or early lesion. The pocket is

supra-bony, involving the soft tissue; there is slight bone loss in the
furcation area. Radiographic change is not usual, as bone changes
are minimal.

Grade II involvement: the bone is destroyed on one or more aspects

of the furcation, but a portion of the alveolar bone and periodontal
ligament remain intact, thus allowing only partial penetration of the
probe into the furcation area. The radiograph may or may not reveal
the grade II furcation involvement.

Grade III involvement: the inter-radicular bone is completely absent,

but the facial and/or lingual orifices of the furcation are occluded by
gingival tissue. Therefore, the furcation opening cannot be seen
clinically, but it is essentially a through and through tunnel. If the
radiograph of the mandibular molars is taken with a proper angle and
the roots are divergent, these lesions will appear on the radiograph as
a radiolucent area between the roots. The maxillary molars present a
diagnostic difficulty owing to roots overlapping each other.

Grade IV involvement: the inter-radicular bone underneath the roof

of furcation is completely destroyed. The gingival tissue is also
receded apically so that the furcation opening is clinically visible. The
radiographic image is essentially the same as in grade III lesions.

Hamp, Nyman and LindheÕs classification - measure the

horizontal attachment loss

Degree I: horizontal attachment loss <3 mm of the total width of the

furcation area.

Degree II: horizontal attachment loss g3 mm but not encompassing

the total width of the furcation area.

Degree III: Òthrough and throughÓ destruction of the periodontal

tissue in the furcation area.

7
WEEK 3 | MODULE 5 DR. FREDA TAN
PERIODONTICS 1 Ð LABORATORY DENT 4C Ð 2ND SEM

MODULE 5: TREATMENT PLAN AND TREATMENT restoration and maintenance of periodontal health are the desired
outcomes of the entire treatment.
CANVAS
The success of periodontal therapy is dependent on the execution of
a well-thought out treatment plan that encompasses the management
of the entirety of the case of the patient. In this module, the rationale
behind periodontal treatment and its phases will be discussed as well
as the procedures that a clinician needs to perform for the
management of a periodontal patient. Ultimately, bringing back the
patient to an oral health and proper function.

LESSON 1: PHASES OF TREATMENT

Periodontal therapy procedures are divided into 4 phases :
Fig. 10.1 Sequence of periodontal therapy
Phase 1, Non-Surgical Phase
Phase 2 Surgical Phase The diagram above shows the proper periodontal therapy
Phase 3 Restorative Phase sequence in which the first step is the preliminary phase and not start
Phase 4 Maintenance Phase. with Phase I. Preliminary Phase attends to emergency treatments
that need to be prioritized like acute pain, abscesses, swellings, etc.
These are 4 major aspects in periodontal treatment. But and only after such emergencies are attended to, will the clinician now
a Preliminary Phase comes before these major procedures. proceed to Phase I or Non-surgical therapy. Upon completion of
The Preliminary phase treats emergencies in the oral cavity Ð dental Phase I, the next step must be Phase IV or Maintenance Phase which
or periodontal. includes re-evaluation of the periodontal tissuesÕ response to the non-
surgical treatment ideally 8 weeks after Phase I. Only then, the
Preliminary Phase decision to proceed to Phase II and Phase III can be made. So the
¥ Emergency treatment (pain, acute infections) periodontal treatment process has to be re-evaluated as maintenance
¥ Teeth requiring extraction (may be postponed to a more every 3 months before going to the next phase.
convenient time)
LESSON 2: SCALING, ROOT PLANING, POLISHING AND
Phase 1 (Non-Surgical Phase) FLOSSING
Plaque control and patient education NON-SURGICAL THERAPY (PHASE I)
¥ Diet control (patients with rampant caries)
¥ Removal of calculus and root planning Before starting this lesson, you must be ready with the different
¥ Correction of restorative and prosthetic irritational factors instruments that you need to prepare before starting with your actual
¥ Excavation of caries and restoration (temporary or final, patient in the clinics. Your professor will provide you a list of the
depending on whether a definitive prognosis for the tooth materials and instruments that you need to bring as you enter the
has been determined and the location of caries) clinics. You need to be informed of the following:
¥ Antimicrobial therapy (local or systemic)
¥ Occlusal therapy ¥ Rules in the Clinic and Rules for the Periodontics Section
¥ Minor orthodontic movement ¥ Filling up of the OD Forms
¥ Provisional splinting and prosthesis
Preparing the Dental Module Before, During and After the Procedure
*** Evaluation of Response to Non-Surgical Phase In most cases, Phase I therapy is the only set of procedures that will
¥ Pocket depth and gingival inflammation restore periodontal health, or as the preparatory procedure for
¥ Plaque and calculus, caries surgical phase.

Phase II (Surgical Phase ) Procedures:

¥ Periodontal therapy, including placements of implants 1. Plaque Control Instruction ( to be discussed separately)
¥ Endodontic therapy 2. Removal of Supragingival and Subgingival calculus
3. Recontouring Defective restorations and Crowns
Phase III ( Restorative Phase ) 4. Elimination of Carious Lesions
¥ Final restorations 5. Tissue Reevaluation
¥ Fixed and removable prosthodontic appliances
¥ Evaluation of response to restorative procedures CLINICAL PROCEDURES:
¥ Periodontal examination I. Disclosing
Disclosing determines the presence or absence of plaque with
Phase IV ( Maintenance ) the use of disclosing agents such as tablets or solutions. The first step
Periodic Re-checking : in the Scaling and Polishing Procedure is to disclose the teeth by
¥ Plaque and calculus wiping the disclosing solution on all surfaces using a cotton ball and
¥ Gingival condition (pockets, inflammation) allowing the patient to rinse to remove the excess solution. After which
you will see that the disclosed areas (colored) are those with the
¥ Occlusion, tooth mobility
presence of plaque.
¥ Other pathologic changes
Instruments needed:
1. Disclosing solution or tablet
The master plan or the treatment plan includes all aspects of the oral
2. Cotton plier
cavity. Short-term goals and long-term goals of the treatment are all
3. Cotton pellet or applicator
incorporated in the treatment plan. Overall, the total establishment,
4. Dappen dish

1
WEEK 3 | MODULE 5 DR. FREDA TAN
PERIODONTICS 1 Ð LABORATORY DENT 4C Ð 2ND SEM

2, Antiseptic - a chemical antimicrobial agent that can be applied

topically or subgingivally to mucous , wounds or intact dermal surfaces
to destroy microorganisms and inhibit their reproduction or
metabolism.

a. Disinfectant (subcategory of antiseptic) - antimicrobial agents

II. Scaling and Root Planing (SRP) applied to inanimate objects to destroy microorganisms
Scaling is the process by which biofilm and calculus are removed
from both supragingival and subgingival tooth surfaces. No deliberate Systemic administration of antibiotics is done to reduce the number of
attempt is made to remove tooth substance along with the calculus. bacteria present in the diseased periodontal pocket. This is a
necessary adjunct for controlling bacterial infection because bacteria
Root planing is the process by which residual embedded calculus can invade periodontal tissues, thereby making mechanical therapy
and portions of cementum are removed from the roots to produce a alone sometime ineffective.
smooth, hard, clean surface.
Common Antibiotic Regimens used to Treat Periodontal
The primary objective of scaling and root planning is to restore Diseases
gingival health by completely removing elements that provoke Regimen Dosage/Duration
gingival inflammation (e.g. biofilm, calculus and endotoxin) from the Single Agent
tooth surface.
Three times daily for 8
Amoxicillin 500 mg
days
Once daily for 4 to 7
Azithromycin 500 mg
days
Instruments needed: Ciprofloxacin 500 mg Twice daily for 8 days
1. Scalers Three times daily for 10
Clindamycin 300 mg
2. Curettes days
3. Periodontal chisels, hoe, and files Doxycycline or
4. Ultrasonic scalers 100mg to 200 mg Once daily for 21 days
minocycline
III. Polishing Three times daily for 8
Metronidazole 500 mg
With the use of a rubber cup and prophylaxis polishing brush on a days
contra-angle hand piece running on slow speed rpm with prophylaxis Combination Therapy
paste mixed with pumice, the teeth are polished to remove dental Metronidazole + Three times daily for 8
biofilm and extrinsic stains. 250 mg of each
amoxicillin days
Instruments needed: Metronidazole +
500 mg of each Twice daily for 8 days
[Link] brush ciprofloxacin
[Link] rubber cup
[Link] paste

IV. Flossing
Dental floss is the most widely recommended tool for removing biofilm
from proximal tooth surfaces. The floss must contact the proximal
surface from the line angle to line angle to clean effectively. It must
also clean the entire proximal surface including accessible subgingival
areas.

Instruments needed:
1. Waxed or unwaxed floss
2. Floss threader (for crowns, bridges, splinted teeth and orthodontic
appliances)

LESSON 3: PERIODONTAL MEDICINE (ANTI-INFECTIVE

THERAPY)
An anti-infective agent is a chemotherapeutic agent that acts by
reducing the number of bacteria present.

1. Antibiotic - naturally occurring, semi-synthetic or synthetic type of

anti-infective agent that destroys or inhibits the growth of select micro-
organisms

2
WEEK 4 | RADIOGRAPHIC INTERPRETATION DR. TAN
PERIODONTICS 1 Ð LABORATORY DENT 4C Ð 2ND SEM

DISCUSSION Ð MARCH 3, 2022 PARAMETERS basis to help determine final diagnosis:

RADIOGRAPHIC INTERPRETATION 1. Radiographs
The radiograph is an adjunct to the to the clinical examination---not a TYPES:
substitute. a. Periapical radiographs (Intra oral) Ð 14 pcs
b. Panoramic radiograph (extra-oral)
If a choice must be made, a more intelligent diagnosis can be made Bite wing Ð detect decay between teeth and changes in thickness of
from the patient without the radiograph, than from radiographs,
without the patient. bone caused by gum disease
2. Plaque index
-Dr. Irving Glickman, Clinical 3. Gingival Bleeding Index
Periodontology, 1953 4. Pocket probing
- To check/ evaluate the amount of bone damage/
resorption Appearance when thereÕs periodontitis
Periodontitis is precedent by gingivitis
LANDMARKS:
ALVEOLAR CREST: 1-2mm apical to the CEJ
1. Continuous and well defined lamina dura
2. Shape of alveolar crest
3. Correct level of alveolar crest
Normal: 1-2mm apical to the CEJ
Early/ mild periodontitis: > 2mm apical to CEJ
Advanced periodontitis: near the apical 3rd of root

NORMAL ANATOMICAL LANDMARKS FOR PERIO

RADIOGRAPHIC EXAMINATION:
1. INTERDENTAL BONE Ð
Significance: level of alveolar crest, tip of the interdental bone
CRESTAL BONE Ð margin of interdental bone
Anterior: triangular/ pointed, bc interproximal areas are narrower
Posterior: flat/ box, bc interproximal areas are wider

2. LAMINA DURA Ð thin layer of compact cortical bone, that

covers the trabecular/spongy bone.
- Dense. Radiopaque
- Must be continuous
Significance: the continuity of the lamina dura
Anterior Ð sharp and pyramidal
3. PERIODONTAL LIGAMENT SPACE Ð thin radiolucent
® More tapered the tooth Ð more pyramidal
line that contains the PDL fibers
- Radiolucent. 1-3mm thickness
Significance: Presence or absence of widening. Posterior Ð wide & flat
® Wider the embrasure more flat, mesiodistally &
4. CALCULAR DEPOSIT Ð but more on visual. Triangular buccolingually.
deposits.
5. SINUS APPROXIMITY (Maxillary Sinus)Ð usually from
maxillary canine to molars.
- Determine the amount of space between root surface
apical region to maxillary sinus
6. FURCATION INVOLVEMENT
7. PERIAPICAL LESIONS

2 TYPES OF BONE RESOPTION:

1. Horizontal resorption Ð parallel to CEJ but a lower level.
2. Vertical/angular resorption Ðthin longitudinal radiolucency
or triangular/vertical radiolucency

1
WEEK 4 | RADIOGRAPHIC INTERPRETATION DR. TAN
PERIODONTICS 1 Ð LABORATORY DENT 4C Ð 2ND SEM

LAMINA DURA
- Thin cortical bone anatomically represents the alveolar RADIOGRAPHIC APPEARANCE OF PERIODONTAL DISEASE
bone
- Highly mineralized Radiographic changes in periodontitis follow the pathophysiology of
- Thin radiopaque layer continuous around the roots & periodontal tissue destruction and include the following:
alveolar crest.
1. Fuzziness and disruption of the lamina dura crestal
- More radiopaque in anterior compared to posterior
cortication continuity is the earliest radiographic change in
periodontitis and results from bone resorption activated by
extension of gingival inflammation into the periodontal
bone.
2. Continued periodontal bone loss and widening of the
periodontal space resulting in a wedge-shaped
radiolucency at the mesial or distal aspect of the crest. The
apex of the area is pointed in the direction of the root.
3. The destructive process extends across the alveolar crest,
thus reducing the height of the interdental bone. As
increased osteoclastic activity results in increased bone
resorption along the endosteal margins of the medullary
spaces, the remaining interdental bone can appear
partially eroded.
4. The height of the interdental septum is progressively
reduced by the extension of inflammation and the
resorption of bone.
5. A radioopaque horizontal line can be observed across the
roots of the tooth. This opaque line demarcates the portion
of the root where the labial or lingual bony plate has been
partially or completely destroyed from the remaining bone-
supported portion.

MORPHOLOGY OF BONE LOSS

Horizontal Bone Loss:
- The bone loss is parallel with the cementoenamel
junction, usually involving more teeth.
Vertical/Angular Defects
- The bone loss is uneven and oblique, centered upon one
tooth or more than the adjacent tooth.

Bone loss at interdental sites was categorized as horizontal or

vertical bone loss. (A) If the slope angle between the root and
interdental bone wall was 90¡±10¡ on radiographs, the defect was
designated as horizontal bone loss. (B) If the angle of bone loss was
between 25¡ and 37¡, the defect was designated as vertical bone
loss.

Interdental Crater Defect:

These occurs at the crest where it is usually a two-walled defect, with
relative preservation of the buccal and lingual cortex. It is often not
appreciated on plain 2D imaging, but may appear as a focal
hypodense region at the superior aspect of the interdental bone.

Infrabony defects:
These refers to focal bone loss which extends along the root surface
apically. This defect can be:
a. Three-walled, where both buccal and lingual cortices are
preserved
b. Two-walled, where a buccal or lingual cortex is effaced
c. Single-walled, where both buccal and lingual cortices are
effaced
Look for periapical radiolucency
Abscess Ð ill defined border.

2
WEEK 5 | MODULE 4-5 DR. TAN
PERIODONTICS 1Ð LABORATORY DENT 4C Ð 2ND SEM

MODULE 4: DIAGNOSIS AND PROGNOSIS LESSON 3: 1999 CLASSIFICATION OF PERIODONTAL

CANVAS OR LECTURE/PPT -BASED DISEASES
DIAGNOSIS - the science of identifying a disease or illness based 1999 Classification of Periodontal Diseases*
from its signs and symptoms (Merriam-Webster Dictionary). Gingival diseases and conditions (including plaque-induced
PROGNOSIS - is the likely outcome or course of a disease; the gingivitis)
chance of recovery or recurrence (NCI Dictionary of Cancer Terms). Chronic periodontitis
The establishment of a well-founded diagnosis is essential in Localized aggressive period ntitis
the formulation of a good treatment plan. This in turn will deliver the
best treatment option/s for the case and leads to a better chance of Generalized aggressive periodontitis
recovery. Prognosis is good if diagnosis is made at the earlier Periodontitis as a manifestation of systemic diseases
stages of the disease because this means that disease intervention Necrotising ulcerative gingivitis and necrotising ulcerative
or interception is very possible with immediate treatment. periodontitis
Abscesses of the periodontium (including gingival and periodontal
LESSON 1: GINGIVITIS VS PERIODONTITIS abscesses)
Gingivitis is the inflammation of the gingiva or gum tissues.
Periodontitis is the inflammation of the periodontal tissues causing its Combined periodontal/endodontic lesions
damage and loss in time. Developmental/acquired conditions
*Based on Armitage 1999 and 2004 [48 (Links to an external
site.),49 (Links to an external site.)]
GINGIVITIS PERIODONTITIS
Sub-Classification according to Distribution:
1. Localized Periodontitis - is equal to or less than 30% of sites
redness and sponginess of involved.
redness and sponginess
the gingiva, but may also 2. Generalized Periodontitis - is greater than 30% of sites involved.
of the gingiva
appear normal
According to Severity:
usually presence of 1. Mild Periodontitis - characterized by 1.0 - 2.0 mm. CAL
usually presence of
plaque/biofilm and 2. Moderate Periodontitis - characterized by 3-4mm CAL, possibly
plaque/biofilm and calculus
calculus accompanied by an increase in tooth mobility and furcation
involvement.
bleeding on probing bleeding on probing 3. Severe Periodontitis - characterized by 5 mm or greater CAL,
usually accompanied by increased tooth mobility, furcation
involvement and mucogingival defects.
no pockets (probing presence of pockets and/or
pocket depths 0-3mm) attachment loss LESSON 4: 2017 STAGING AND GRADING OF PERIODONTITIS
no radiographic presence of bone loss (may
evidence of bone loss lead to tooth loss)

presence of tooth mobility in

no tooth mobility
severe cases

no crevicular fluid presence of crevicular

exudation exudation

reversible irreversible

results to periodontitis if results to tooth loss if not

not treated treated

LESSON 2: CLINICAL PARAMETERS IN PERIODONTAL

DIAGNOSIS
The following are the vital clinical parameters and tools in making a
concrete periodontal diagnosis.
1. A complete patient information profile
2. Intra-Oral photographs
3. Model casts
4. Radiographs (panoramic and periapical)
5. Oral Hygiene Index (OHI) or Plaque Index (PI)
6. Bleeding on Probing (BOP)
7. Probing pocket depth (PPD)
8. Clinical attachment loss/level (CAL)
9. Tooth Mobility (TM)
10. Furcation Involvement (FI)

1
WEEK 5 | MODULE 4-5 DR. TAN
PERIODONTICS 1Ð LABORATORY DENT 4C Ð 2ND SEM

The Preliminary phasetreats emergencies in the oral cavity Ð dental

or periodontal.

Preliminary Phase
- Emergency treatment (pain, acute infections)
- Teeth requiring extraction (may be postponed to a more
convenient time)

Phase 1 (Non-Surgical Phase) etiology phase

- Plaque control and patient education
- Diet control (patients with rampant caries)
- Removal of calculus and root planning
- Correction of restorative and prosthetic irritational factors
- Excavation of caries and restoration (temporary or final,
depending on whether a

definitive prognosis for the tooth has been determined and the
location of caries)

- Antimicrobial therapy (local or systemic)

- Occlusal therapy
- Minor orthodontic movement
- Provisional splinting and prosthesis

*** Evaluation of Response to Non-Surgical Phase

- Pocket depth and gingival inflammation
- Plaque and calculus, caries

Phase II (Surgical Phase )

- Periodontal therapy, including placements of implants
- Endodontic therapy

Phase III ( Restorative Phase )

- Final restorations
- Fixed and removable prosthodontic appliances
- Evaluation of response to restorative procedures
- Periodontal examination

Phase IV ( Maintenance )
Periodic Re-checking :
- Plaque and calculus
- Gingival condition (pockets, inflammation)
- Occlusion, tooth mobility
- Other pathologic changes

The master plan or the treatment plan includes all aspects of the oral
cavity. Short-term goals and long-term goals of the treatment are all
MODULE 5: TREATMENT PLAN AND TREATMENT incorporated in the treatment plan. Overall, the total establishment,
CANVAS OR LECTURE/PPT -BASED restoration and maintenance of periodontal health are the desired
outcomes of the entire treatment.
The success of periodontal therapy is dependent on the execution of
a well-thought out treatment plan that encompasses the management
of the entirety of the case of the patient. In this module, the rationale
behind periodontal treatment and its phases will be discussed as well
as the procedures that a clinician needs to perform for the
management of a periodontal patient. Ultimately, bringing back the
patient to a oral health and proper function.

LESSON 1: PHASES OF TREATMENT

Periodontal therapy procedures are divided into 4 phases : Phase
1, Non-Surgical Phase; Fig. 10.1 Sequence of periodontal therapy
Phase 2 Surgical Phase;
Phase 3 Restorative Phase and The diagram above shows the proper periodontal therapy
Phase 4 Maintenance Phase. sequence in which the first step is the preliminary phase and not start
These are 4 major aspects in periodontal treatment. But with Phase I. Preliminary Phase attends to emergency treatments
a Preliminary Phase comes before these major procedures. that need to be prioritized like acute pain, abscesses, swellings, etc.

2
WEEK 5 | MODULE 4-5 DR. TAN
PERIODONTICS 1Ð LABORATORY DENT 4C Ð 2ND SEM

and only after such emergencies are attended to, will the clinician now
proceed to Phase I or Non-surgical therapy. Upon completion of III. Polishing
Phase I, the next step must be Phase IV or Maintenance Phase which With the use of a rubber cup and prophylaxis polishing brush on a
includes re-evaluation of the periodontal tissuesÕ response to the non- contra-angle hand piece running on slow speed rpm with prophylaxis
surgical treatment ideally 8 weeks after Phase I. Only then, the paste mixed with pumice, the teeth are polished to remove dental
decision to proceed to Phase II and Phase III can be made. So the biofilm and extrinsic stains.
periodontal treatment process has to be re-evaluated as maintenance
every 3 months before going to the next phase. Instruments needed:
[Link] brush
LESSON 2: SCALING, ROOT PLANING, POLISHING AND [Link] rubber cup
FLOSSING [Link] paste
NON-SURGICAL THERAPY (PHASE I)
IV. Flossing
Before starting this lesson, you must be ready with the different
Dental floss is the most widely recommended tool for removing
instruments that you need to prepare before starting with your actual
biofilm from proximal tooth surfaces. The floss must contact the
patient in the clinics. Your professor will provide you a list of the
proximal surface from the line angle to line angle to clean effectively.
materials and instruments that you need to bring as you enter the
It must also clean the entire proximal surface including accessible
clinics. You need to be informed of the following:
subgingival areas.
- Rules in the Clinic and Rules for the Periodontics Section
Instruments needed:
- Filling up of the OD Forms
Waxed or unwaxed floss
Floss threader (for crowns, bridges, splinted teeth and orthodontic
Preparing the Dental Module Before, During and After the Procedure
appliances)
In most cases, Phase I therapy is the only set of procedures that will
restore periodontal health, or as the preparatory procedure for
surgical phase. LESSON 3: 1PERIODONTAL MEDICINE (ANTI-INFECTIVE
THERAPHY)
Procedures: An anti-infective agent is a chemotherapeutic agent that acts by
1. Plaque Control Instruction ( to be discussed seaparately) reducing the number of bacteria present.
2. Removal of Supragingival and Subgingival calculus 1. Antibiotic - naturally occuring, semi-synthetic or synthetic type of
3. Recontouring Defective restorations and Crowns ant-infective agent that destroys or inhibits the growth of select
4. Elimination of Carious Lesions micro-organisms
5. Tissue Reevaluation
2, Antiseptic - a chemical antimicrobial agent that can be applied
CLINICAL PROCEDURES: topically or subgingivally to mucous , wounds or intact dermal
I. Disclosing surfaces to destroy microorganisms and inhibit their reproduction or
Disclosing determines the presence or absence of plaque metabolism.
with the use of disclosing agents such as tablets or solutions. The
first step in the Scaling and Polishing Procedure is to disclose the a. Disinfectant (subcategory of antiseptic) -antimicrobial agents
teeth by wiping the disclosing solution on all surfaces using a cotton applied to inanimate objects to destroy microorganisms
ball and allowing the patient to rinse to remove the excess solution.
After which you will see that the disclosed areas (colored) are those Systemic administration of antibiotics is done to reduce the number
with the presence of plaque. of bacteria present in the diseased periodontal pocket. This is a
necessary adjunct for controlling bacterial infection because bacteria
Instruments needed: can invade periodontal tissues, thereby making mechanical therapy
1. Disclosing solution or tablet alone sometime ineffective.
2. Cotton plier Common Antibiotic Regimens used to Treat Periodontal Diseases
3. Cotton pellet or applicator Regimen Dosage/Duration
4. Dappen dish Single Agent
II. Scaling and Root Planing (SRP) Three times daily for 8
Amoxicillin 500 mg
Scaling is the process by which biofilm and calculus are days
removed from both supragingival and subgingival tooth surfaces. No Once daily for 4 to 7
deliberate attempt is made to remove tooth substance along with the Azithromycin 500 mg
days
calculus. Ciprofloxacin 500 mg Twice daily for 8 days
Root planing is the process by which residual embedded
calculus and portions of cementum are removed from the roots to Three times daily for 10
Clindamycin 300 mg
produce a smooth, hard, clean surface. days
Doxycycline or
The primary objective of scaling and root planning is to restore 100mg to 200 mg Once daily for 21 days
minocycline
gingival health by completely removing elements that provoke Three times daily for 8
gingival inflammation (e.g. biofilm, calculus and endotoxin) from the Metronidazole 500 mg
days
tooth surface.
Combination Therapy
Instruments needed: Metronidazole + Three times daily for 8
Scalers 250 mg of each
amoxicillin days
Curettes Metronidazole +
Periodontal chisels, hoe, and files 500 mg of each Twice daily for 8 days
ciprofloxacin
Ultrasonic scalers

3
WEEK 5 | MODULE 4-5 DR. TAN
PERIODONTICS 1Ð LABORATORY DENT 4C Ð 2ND SEM

MAIN DIFFERENCE between non-surgical and

surgical therapy

Non-surgical: above the gingiva; gingiva is not

involved.

Surgical therapy: gingiva is involved

Supra gingival:

-biofilm/dental biofilm/dental plaque disclosing

solution
-hard deposit/calcular deposit
seen by naked eyes
-soft deposit
seen by naked eyes
-extrinsic stains
seen by naked eyes

Curettes are used only on supragingival