Periodontology I
Periodontal health. Dental plaque-induced gingival
conditions
Péter Vályi D.M.D., Ph.D.
Classification of periodontal
diseases (AAP 1999)
[Link] Diseases 6. Abscesses of the Periodontium
• Plaque-induced gingival diseases*
• Gingival abscess
• Non–plaque-induced gingival lesions
• Periodontal abscess
[Link] Periodontitis • Pericoronal abscess
• Localized 7. Periodontitis Associated With Endodontic Lesions
• Generalized
• Endodontic–periodontal lesion
[Link] Periodontitis • Periodontal–endodontic lesion
• Localized • Combined lesion
• Generalized 8. Developmental or Acquired Deformities and
[Link] as a Manifestation of Conditions
Systemic Disease • Localized tooth-related factors that predispose an
individual to plaque-induced gingival diseases or
[Link] Periodontal Diseases periodontitis
• Necrotizing ulcerative gingivitis • Mucogingival deformities and conditions around the
• Necrotizing ulcerative periodontitis teeth
• Mucogingival deformities and conditions on
edentulous ridges
• Occlusal trauma
Classification of periodontal and
peri-implant diseases and conditions
2017
2018.09.17. SZTE FOK Parodontológiai Tanszék 4
Periodontal health
• 1) pristine periodontal health, defined as a total absence of
clinical inflammation and physiological immune surveillance on a
periodontium with normal support (no attachment or bone loss).
Pristine periodontal health is not likely to be observed
clinically;
• 2) clinical periodontal health, characterized by an absence or
minimal levels of clinical inflammation in a periodontium with
normal support;
• 3) periodontal disease stability in a reduced periodontium;
Stability is characterized by minimal inflammation and optimal
therapeutic response, with control of modifiable risk factors;
• 4) periodontal disease remission/control in a reduced
periodontium. not possible to fully control modifying and
predisposing factors,
Periodontal disease stability and periodontal disease
remission/control are differentiated based on the ability to
control modifying factors and therapeutic response.
2018.09.17. 5Dr. Vályi Péter Ph.D.
Periodontal health
2018.09.17. Dr. Vályi Péter Ph.D.6
Periodontal health
Periodontal health
Periodontal diseases
• Gingivitis
• Periodontitis
Course of Gingivitis
• Acute form of gingivitis can occur with sudden
onset and short duration, and it can be painful. A
less severe phase of this condition can also
occur.
• Chronic gingivitis is slow in onset and of long
duration. It is painless, unless it is complicated
by acute or subacute exacerbations, and it is the
type that is most often encountered. Chronic
gingivitis is a fluctuating disease in which
inflammation persists or resolves and in which
normal areas become inflamed.
• Recurrent gingivitis reappears after having been
eliminated by treatment or disappearing
spontaneously
Gingival inflammation
• Initial Lesion
Clinical signs: increase in the flow of
• Early Lesion gingival fluid into the sulcus
• Established Lesion • Alteration in the junctional epithelium and the
perivascular connective tissue
• response to the microbial activation of resident
leukocytes and the subsequent stimulation of
endothelial cells: vascular changes - dilated
capillaries and increased blood flow
• Changes in the connective tissue beneath the
junctional epithelium: perivascular connective
tissue matrix becomes altered, and there is
exudation and deposition of fibrin in the
affected area,loss of collagens
• PMNs soon begin to accumulate, migration into the
sulcus– increased blood flow – correlated with an
increase in the flow of gingival fluid into the
sulcus
Gingival inflammation
• Initial Lesion
Clinical signs: redness, bleeding on probing
• Early Lesion • within about 1 week after the beginning of plaque
• Established Lesion accumulation
• proliferation of capillaries and the increased
formation of capillary loops between rete pegs or
ridges
• Gingival fluid flow and the numbers of transmigrating
leukocytes reach their maximum between 6 and 12 days
after the onset of clinical gingivitis
• The amount of collagen destruction also increases; 70%
of the collagen is destroyed around the cellular
infiltrate(mainly the circular and dentogingival fiber
groups)– directly related to MMP-2 and MMP-9
production and activation
• Alterations in blood vessel morphologic features and
vascular bed patterns
• PMNs – phagocytosis, Fibroblasts show cytotoxic
alterations,40 with a decreased capacity for collagen
Gingival inflammation
• Initial Lesion
Clinical signs: changes of color, size, textura, etc.
• Early Lesion • 2 to 3 weeks after the beginning of plaque
• Established Lesion accumulation
• the blood vessels become engorged and congested,
venous return is impaired, and the blood flow becomes
sluggish: localized gingival anoxemia– bluish hue on
the reddened gingiva, extravasation of erythrocytes
into the CT, breakdown of hemoglobin: deep red color
• creation of a small gingival pocket lined with a
pocket epithelium
• Predominance of Plasma cells and B-cells (IgG1 és IgG3)
• Collagenolytic activity is increased (Collagenase
produced by some oral bacteria and by PMNs)
• Elevated enzime levels(acid and alkaline phosphatase,
stabilization or progression β-glucuronidase, β-glucosidase, β-galactosidase,
esterases, aminopeptidase, and cytochrome oxidase)-
degradation of Mx
Epidemiology of Gingivitis
• USA: adolescent 82%
• USA: adults > 50%
• Cause: dentogingival plaque and relation to the
host response
• Risk factors
Gingivitis - signs
• Redness
• sponginess of the gingival tissue
• Bleeding on probing
• Changes in gingival contour
• no radiographic evidence of crestal bone loss
• Hystology: inflamed gingival tissue reveals ulcerated
epithelium (pro-inlammatory mediators) – decreasing
protective function (barrier)– Repair of this ulcerated
epithelium depends on the proliferative or regenerative
activity of the epithelial cells
Gingivitis -Forms
• Acute
• sudden onset, short duration
• painless
• Chronic
• Onset is slow
• Painless
• Long-standing
• complicated by acute or subacute exacerbations
• most often encountered
Gingivitis - Forms
1. Localized marginal gingivitis–
affected one or more areas of the marginal 1
gingiva
2. Localized diffuse gingivitis–
extends from the margin to the mucobuccal fold in a
limited area
3. Localized papillary gingivitis–
affected one or more interdental spaces in a
limited area
2
4. Generalized marginal gingivitis–
involves the gingival margins (papilla) in relation
to all the teeth
5. Generalized diffuse gingivitis–
involves the entire gingiva. The alveolar mucosa
and the attached gingiva are affected, so the
mucogingival junction is sometimes obliterated –
Systemic conditions can be involved
5
Gingival Bleeding
• bleeding on probing may not be a good diagnostic indicator for
clinical attachment loss
• In cases of moderate or advanced periodontitis, the presence of
bleeding on probing is considered a sign of active tissue
destruction
• absence is an excellent negative predictor of future attachment loss
• Study(565 males, 26 years): sites with consistent bleeding (gingival index =
2) had 70% more attachment loss than sites that were noninflamed, persistent
gingivitis can be considered as a risk factor for periodontal attachment
loss that may lead to tooth loss
• Local factors – plaque accumulation– lead to gingivitis
• anatomic and developmental tooth variations, caries, frenum pull, iatrogenic
factors, malpositioned teeth, mouth breathing, overhangs, partial dentures,
lack of attached gingiva, and recession, orthodontic treatment and fixed
retainers
• Gingival bleedings – association with systemic changes (provoked,
spontaneously)
Gingival Bleeding
• bleeding on probing may not be a good diagnostic indicator for
clinical attachment loss
• In cases of moderate or advanced periodontitis, the presence of
bleeding on probing is considered a sign of active tissue
destruction
• absence is an excellent negative predictor of future attachment loss
• Study(565 males, 26 years): sites with consistent bleeding (gingival index =
2) had 70% more attachment loss than sites that were noninflamed, persistent
gingivitis can be considered as a risk factor for periodontal attachment
loss that may lead to tooth loss
• Local factors – plaque accumulation– lead to gingivitis
• anatomic and developmental tooth variations, caries, frenum pull, iatrogenic
factors, malpositioned teeth, mouth breathing, overhangs, partial dentures, lack
of attached gingiva, and recession, orthodontic treatment and fixed
retainers
• Gingival bleedings – association with systemic changes (provoked,
spontaneously)
Gingival Bleeding
• Bleeding on probing may not be a good diagnostic indicator for
clinical attachment loss
• In cases of moderate or advanced periodontitis, the presence of
bleeding on probing is considered a sign of active tissue
destruction
• absence is an excellent negative predictor of future attachment loss
• Study(565 males, 26 years): sites with consistent bleeding (gingival index =
2) had 70% more attachment loss than sites that were noninflamed, persistent
gingivitis can be considered as a risk factor for periodontal attachment
loss that may lead to tooth loss
• Local factors – plaque accumulation– lead to gingivitis
• anatomic and developmental tooth variations, caries, frenum pull, iatrogenic
factors, malpositioned teeth, mouth breathing, overhangs, partial dentures,
lack of attached gingiva, and recession, orthodontic treatment and fixed
retainers
• Gingival bleedings – association with systemic changes (provoked,
spontaneously)
Gingival Bleeding
• bleeding on probing may not be a good diagnostic indicator for
clinical attachment loss
• In cases of moderate or advanced periodontitis, the presence of
bleeding on probing is considered a sign of active tissue
destruction
• absence is an excellent negative predictor of future attachment loss
• Study(565 males, 26 years): sites with consistent bleeding (gingival index =
2) had 70% more attachment loss than sites that were noninflamed, persistent
gingivitis can be considered as a risk factor for periodontal attachment
loss that may lead to tooth loss
• Local factors – plaque accumulation– lead to gingivitis
• anatomic and developmental tooth variations, caries, frenum pull, iatrogenic
factors, malpositioned teeth, mouth breathing, overhangs, partial dentures,
lack of attached gingiva, and recession, orthodontic treatment and fixed
retainers
• Gingival bleedings – association with systemic changes (provoked,
spontaneously)
Gingival Bleeding
• bleeding on probing may not be a good diagnostic indicator for
clinical attachment loss
• In cases of moderate or advanced periodontitis, the presence of
bleeding on probing is considered a sign of active tissue
destruction
• absence is an excellent negative predictor of future attachment loss
• Study(565 males, 26 years): sites with consistent bleeding (gingival index =
2) had 70% more attachment loss than sites that were noninflamed, persistent
gingivitis can be considered as a risk factor for periodontal attachment
loss that may lead to tooth loss
• Local factors – plaque accumulation– lead to gingivitis
• anatomic and developmental tooth variations, caries, frenum pull, iatrogenic
factors, malpositioned teeth, mouth breathing, overhangs, partial dentures,
lack of attached gingiva, and recession, orthodontic treatment and fixed retainers
• Gingival bleedings – association with systemic changes (provoked,
spontaneously)
Gingival Bleeding
• bleeding on probing may not be a good diagnostic indicator for
clinical attachment loss
• In cases of moderate or advanced periodontitis, the presence of
bleeding on probing is considered a sign of active tissue
destruction
• absence is an excellent negative predictor of future attachment loss
• Study(565 males, 26 years): sites with consistent bleeding (gingival index =
2) had 70% more attachment loss than sites that were noninflamed, persistent
gingivitis can be considered as a risk factor for periodontal attachment
loss that may lead to tooth loss
• Local factors – plaque accumulation– lead to gingivitis
• anatomic and developmental tooth variations, caries, frenum pull, iatrogenic
factors, malpositioned teeth, mouth breathing, overhangs, partial dentures, lack
of attached gingiva, and recession, orthodontic treatment and fixed retainers
• Gingival bleedings – association with systemic changes (provoked,
spontaneously)
Gingival Bleeding- Systemic
factors
• vascular abnormalities (Henoch-Schönlein purpura, C-vitamin
deficiency)
• Platelet disorders
• Amount
• Thrombocyta dysfunction – uraemia, myeloma multiplex, postrubella
purpura
• hypoprothrombinemia
• coagulation defects (hemophilia, leukemia, Christmas disease)
• Effects of the sexual hormons
• hormonal replacement therapy, oral contraceptives, pregnancy, and the
menstrual cycle
• Endokrin – diabetes m
• Side effect of drugs– aspirin protect, drug induced hyperplasia–
secondary effect
Color changes
• Vascular changes
• Keratinization
• Thickness of the gingiva
• Pigments
• Systemic factors
• Addison’s disease
• Peutz-Jeghers’s syndrome: intestinal polyposis and melanin
pigmentation in the oral mucosa and the lips.
• Albright’s syndrome: oral melanin pigmentation
• von Recklinghausen’s disease (neurofibromatosis): oral melanin
pigmentation
• bile pigments: yellowish discoloration
• Hemochromatosis: iron – grayish
• Bleeding disorders
Gingiva – consistency
• Inflammation:
• Destructive: edematous (soft, sponginess)
• Reparative: fibrotiic, firm
Gingiva – effect of
toothbrushing
• promoting keratinization
• enhancing capillary gingival circulation
• thickening alveolar bone
• increased turnover rate and desquamation of the
junctional epithelial surfaces
• may repair small breaks in the junctional epithelium
• prevent direct access to the underlying tissue by
periodontal pathogens
Gingiva – changes in the
textura
• Healthy gingiva – orange-peel
(stippling)
• Loss of stippling
• Early signs of inflammation, but:
• pattern and extent vary in different mouth
areas, among patients, and with age
• Chronic inflammation
• Destructíive: shiny and smooth
• Reparative: firm, nodular
• Shiny and smooth due to ulceration or
desquamation too
Alteration of positon and
margin
• Irregular contour
• Traumatic Lesion
• Gingiva recession
• Stillman’s cleft, McCall festons
Grade I
Gingival enlargement
• Classification based on
distribution and localization
Grade II
• Localized or generalized
• Marginal, papilary, diffuse, Grade III
discrete
• Classification of severity
• Grade 0: no signs
• Grade I: interdental papilla
• Grade II: marginal gingiva and
papilla
• Grade III: ¾ portion of the crown
covered by gingiva
Buchner A, Hansen AS: The histomorphologic spectrum of the gingival cyst in the adult. Oral Surg. 48:532 1979
Gingival enlargement
Classification based on etiology Due to chronic or acute
I. Inflammatory enlargement inflammatory process
[Link]-induced gingival • Acute (abscesses)
enlargement • Chronic: painless, slow
[Link] Associated progression (except: acute
with Systemic Diseases infection or traumatic lesions)
• Exudative or proliferative
[Link] of gingiva
V. Hereditary
[Link]
VII.„False enlargement”
Gingival enlargement
• painless, beadlike enlargement of the interdental
papilla that then extends to the facial and
lingual gingival margins and they may develop
into a massive tissue fold that covers a
Classification based considerable portion of the crowns
on etiology • mulberry shaped, firm, pale pink, and resilient,
with a minutely lobulated surface and no tendency
I. Inflammatory enlargement to bleed
[Link]-induced gingival • Secondary inflammatory changes not only add to the
size of the lesion caused by the drug but also
enlargement produce a red or bluish-red discoloration,
[Link] Associated obliterate the lobulated surface demarcations, and
increase bleeding tendency
with Systemic Diseases
• noninflamed gingiva, fibroblasts are less active
[Link] of gingiva or even quiescent and do not respond to
circulating phenytoin, whereas fibroblasts within
V. Hereditary inflamed tissue are in an active state as a result
of the inflammatory mediators and the endogenous
[Link] growth factors that are present (Hassel)– genetic
predisposition?
VII.„False enlargement”
Gingival enlargement
Classification based on etiology • painless, beadlike enlargement of the interdental
I. Inflammatory enlargement papilla that then extends to the facial and
lingual gingival margins and they may develop
II. Drug-induced gingival enlargement into a massive tissue fold that covers a
considerable portion of the crowns
III. Enlargements Associated with
Systemic Diseases • mulberry shaped, firm, pale pink, and resilient,
with a minutely lobulated surface and no tendency
IV. Tumors of gingiva to bleed
V. Hereditary • Secondary inflammatory changes not only add to the
size of the lesion caused by the drug but also
VI. Idiopathic produce a red or bluish-red discoloration,
VII. „False enlargement” obliterate the lobulated surface demarcations, and
increase bleeding tendency
• noninflamed gingiva, fibroblasts are less active
or even quiescent and do not respond to
circulating phenytoin, whereas fibroblasts within
inflamed tissue are in an active state as a result
of the inflammatory mediators and the endogenous
growth factors that are present (Hassel)– genetic
predisposition?
Gingival enlargement
Classification based on etiology • Anticonvulsant
• Calcium-channel blockers
I. Inflammatory enlargement
• Immunosuppressant - Cyclosporin
[Link]-induced gingival
enlargement • Anticoncipiens
[Link] Associated • Erythromycin
with Systemic Diseases • Bleomycin
[Link] of gingiva
V. Hereditary
[Link]
VII.„False enlargement”
Gingival enlargement
[Link] Enlargements
1. Pregnancy
Classification based on etiology 2. Puberty
I. Inflammatory enlargement 3. C-vitamin deficiency
[Link]-induced gingival 4. Plasma-cell gingivitis
enlargement 5. Pyogenic granuloma
[Link] Associated [Link] Diseases that Cause
with Systemic Diseases Gingival Enlargement
1. Leukemia
[Link] of gingiva 2. Granulomatosus diseases (Wegener
V. Hereditary ~, sarcoidosis)
[Link]
VII.„False enlargement”
Gingival enlargement
[Link] enlargement
Classification based [Link] (marginalor tumor-
on etiology like)
I. Inflammatory enlargement [Link]
[Link]-induced gingival 3.C-vitamin deficiency
enlargement [Link]-cell gingivitis
[Link] Associated [Link] granuloma
with Systemic Diseases [Link]émás tényezők által
[Link] of gingiva okozott
V. Hereditary [Link]émia
[Link] betegség
[Link] (Wegener ~, sarcoidosis)
VII.„False enlargement”
Gingival enlargement
[Link]émás tényezők által
befolyásolt
Classification based [Link]
on etiology 2. Puberty
I. Inflammatory enlargement 3.C-vitamin deficiency
[Link]-cell gingivitis
[Link]-induced gingival [Link] granuloma
enlargement
[Link] Associated [Link]émás tényezők által
with Systemic Diseases okozott
[Link] of gingiva [Link]émia
[Link] betegség
V. Hereditary (Wegener ~, sarcoidosis)
[Link]
VII.„False enlargement”
Gingival enlargement
[Link]émás tényezők által
befolyásolt
Classification based [Link]
on etiology [Link]
I. Inflammatory enlargement 3.C-vitamin deficiency
[Link]-induced gingival [Link]-cell gingivitis
enlargement 5. Pyogenic granuloma
[Link] Associated [Link]émás tényezők által
with Systemic Diseases okozott
[Link] of gingiva [Link]émia
[Link] betegség
V. Hereditary (Wegener ~, sarcoidosis)
[Link]
VII.„False enlargement”
Gingival enlargement
Classification based • Benign
on etiology • Malignant
I. Inflammatory enlargement
[Link]-induced gingival
enlargement
[Link] Associated
with Systemic Diseases
[Link] of gingiva
V. Hereditary
[Link]
VII.„False enlargement”
Gingival enlargement
Classification based
on etiology
I. Inflammatory enlargement
•
[Link]-induced gingival
enlargement •
[Link] Associated
with Systemic Diseases
[Link] of gingiva •
V. Hereditary
[Link]
VII.„False enlargement”
Gingival enlargement
• The enlargement affects the attached
gingiva as well as the gingival margin
and the interdental papillae
Classification based on • The facial and lingual surfaces of the
etiology mandible and maxilla are generally
affected, but the involvement may be
I. Inflammatory enlargement limited to either jaw
II. Drug-induced gingival enlargement • pink, firm, and almost leathery in
III. Enlargements Associated with consistency, and it has a
Systemic Diseases characteristic minutely pebbled surface
IV. Tumors of gingiva • severe cases, the teeth are almost
V. Hereditary completely covered and enlargement
projects into the oral vestibule
VI. Idiopathic
• The jaws appear distorted as a result
VII. „False enlargement” of the bulbous enlargement of the
gingiva
• Secondary inflammatory changes are
common at the gingival margin
Gingival enlargement
Classification based
on etiology
I. Inflammatory enlargement
[Link]-induced gingival
enlargement
[Link] Associated
with Systemic Diseases
[Link] of gingiva • Underlying osseus
V. Hereditary lesions
[Link] • Underlying dental
VII.„False enlargement” tissues
Hyperplasia – Hystopathology
• Rete peg – elongated and extend deep into ct
• Acanthosis in the epithelium
• Infiltrate by lymphocytes and plasma cells
• New capillary formation
• Increase amount of fibroblasts
• Increase in the number of collagen, irregulary arranged ~
Lindhe J, Lang NP, Karring T : Clinical
• Alteration in the compositon of collagens Type III ; TypeandIImplant
Periodontology Dentistry 5th ed,
2008.
• Decraesing of collagenase activity
• Increasing in the amount of non-collagenous proteins in the CT
Matrix
• Increasing in the amount of Proteoglycans, hexosamines,
glucoseaminoglycanes
• Increasing in the number of Glucocorticoid receptors
• Increasing in the activity of mediators(TGF-β, bFGF)
PERIODONTAL DESTRUCTION
Periodontal destruction
Obligatory symptoms Secondary symptoms
• Inflammation
• Attachment loss – periodontal
pocket
• Gingival swelling or recession
• Active site – pocket
• Periodontal abscess
• Tipping, movement, elongation of
the teeth
• Tooth mobility
• Tooth loss
• Furcation involvement
PERIODONTAL POCKET
Periodontal
pocket Gingival Suprabony Infrabony
Sulcus pocket Pseudopocket Sulcus pocket
pocket
• pathologically deepened gingival sulcus
• Classification:
• Gingival pocket is formed by gingival enlargement
without destruction of the underlying periodontal
tissues. The sulcus is deepened because of the
increased bulk of the gingiva
• Periodontal pocket produces destruction of the
supporting periodontal tissues, thereby leading to
the loosening and exfoliation of the teeth
• Suprabony (supracrestal or supraalveolar) occurs when the
bottom of the pocket is coronal to the underlying alveolar
bone
• Intrabony (infrabony, subcrestal, or intraalveolar) occurs
when the bottom of the pocket is apical to the level of the
adjacent alveolar bone. With this second type, the lateral
pocket wall lies between the tooth surface and the alveolar
bone
Periodontal pocket
• Clinical signs that suggest the presence
of periodontal pockets
• bluish-red thickened marginal gingiva
• bluish-red vertical zone from the gingival
margin to the alveolar mucosa
• gingival bleeding and suppuration
• tooth mobility
• diastema formation
• Pain - localized pain or pain “deep in the
bone.”
• Diagnostic procedure: Probing by
periodontal probe
Attachment loss
SECONDARY SYMPTOMS
Mobility
Furcation involvement
A C
Periodontal abscess
