See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/355040608

Trauma From Occlusion -Periodontal Traumatism

Article in Annals of the Romanian Society for Cell Biology · January 2020

CITATIONS READS
0 6,218

3 authors, including:

Jaideep Mahendra
Meenakshi Ammal Dental College and Hospital
306 PUBLICATIONS 1,236 CITATIONS

SEE PROFILE

All content following this page was uploaded by Jaideep Mahendra on 04 October 2021.

The user has requested enhancement of the downloaded file.

Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

Trauma From Occlusion - Periodontal Traumatism

Jaideep Mahendra1*,AbiramiNayaki Rao P2, Dr Janani M3

1
Director of Postgraduate Studies and Research, Professor,Department of Periodontology, Meenakshi
AmmalDental College, Faculty of Dentistry, Meenakshi Academy of Higher Education and Research,
Chennai, India.
2,3
Postgraduate students, Department of Periodontics, Meenakshi Academy of Higher Education and
Research, Faculty of Dentistry, Meenakshi Ammal Dental College and Hospital, Chennai, India.

Corresponding Author: Dr Jaideep Mahendra*, E mail: [email protected]

ABSTRACT
Patients suffering from occlusal trauma may experience tooth mobility, temperomandibular joint pain,
masticatory pain, and periodontal disease. An early diagnosis, a proper treatment plan, and malocclusion
correction can all lead to a successful outcome. In patients with occlusal trauma, a lack of awareness of
orthodontic treatment can result in tooth structure loss. The effects of occlusal trauma and excessive
occlusal forces on the periodontium are investigated in this narrative review, which includes the onset and
progression of periodontitis, abfraction, and gingival recession.

Keywords: trauma from occlusion, jiggling forces, coronoplasty, splinting, peri-implant occlusal load

INTRODUCTION
The periodontal ligament acts on forces applied to the teeth as a way of accommodating the
forces exerted on the crown because of the elastic character of the periodontal ligament and all
the teeth that have a regular bone support with physiological movement in all directions, when
occlusal strength increases. Thus, it has a cushioning effect on forces exerted on the tooth in all
directions. It is primarily determined by the magnitude, direction, duration, and frequency. 1
When occlusal forces are increased in magnitude, the periodontium responds by widening the
periodontal ligament space, increasing the number and width of periodontal ligament fibres, and
increasing the density of alveolar bone. Changing the direction of occlusal forces causes the
stresses and strains within the periodontium to reorient. The principal fibres of the periodontal
ligament are arranged to best accommodate occlusal forces along the tooth's long axis. Lateral
(horizontal) and torque (rotational) forces are more likely to cause periodontal injury. The
duration and frequency of occlusal forces affect the response of alveolar bone, with constant
pressure being more damaging than intermittent forces. The more frequently an intermittent
force is applied, the more damaging it is to the periodontium.1

TRAUMA FROM OCCLUSION

Whenocclusal forces exceed the adaptive capacity of the tissues, tissue injury results. The
resultant injury is termed trauma from occlusion. Trauma from occlusion refers to the tissue
injury, not the occlusal force. The term trauma from occlusion is generally used in connection
with injury in the periodontium.An occlusion that produces such injury is called a traumatic

1224
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

occlusion.Excessive occlusal forces may also disrupt the function of the masticatory musculature
and cause painful spasms, injure the temperomandibular joints, or produce excessive tooth wear.2

ETIOLOGY
The etiology of occlusion-related trauma includes both intrinsic and extrinsic factors. Intrinsic
factors include the orientation of the teeth's long axis in relation to the forces to which they are
subjected, the morphology of the roots, and the morphology of the alveolar process. Extrinsic
factors include plaque, the fabrication of long span bridges on a few teeth, injudicious bone
resection during surgical procedures, parafunctional habits, food impaction, overhanging fillings,
poorly contoured crowns and bridges, and ill-fitting dentures.1

CLASSIFICATION OF TRAUMA FROM OCCLUSION

There are four main classification of trauma from occlusion discussed in the article which
include, Box et al classification (1930) who classified into Physiologic occlusion was defined by
Box et al as a condition in which the systems of forces acting on the tooth during occlusion are in
a state of equilibrium and do not and cannot change the normal relationship between the tooth
and its supporting structures and traumatic occlusion - The periodontium suffers damage as a
result of the occlusion's overstress.3 The second one being Glickman’s classification
(1953)1Trauma from occlusion can be classified as acute or chronic depending on the duration of
the cause. It can be divided into primary and secondary trauma from occlusion based on the
nature of the cause.3The third classification being Hamp, Nyman, and Lindhe’s classification
(1975), in this classification is based on a horizontal component of tissue destruction in the inter-
radicular area, such as the degree of horizontal root exposure or attachment loss.
Degree I refer to horizontal loss of periodontal tissue support that is less than one-third the width
of the tooth. Degree II refers to horizontal loss of periodontal support that is greater than one-
third the width of the tooth. Degree III refers to horizontal through and through destruction of
periodontal tissue in the area of the furcation.4
The fourth and final classification being the latest2017 AAP classification5 where the occlusal
trauma is classified into three types: primary occlusal trauma, secondary occlusal trauma, and
orthodontic force trauma.5

ACUTE TRAUMA AS A RESULT OF OCCLUSION

The result of an abrupt occlusal impact, such as biting on a hard object (e.g., olive pit) is termed
as acute trauma from occlusion. Acute trauma can also be caused by restorations or prosthetic
appliances that interfere with or change the direction of occlusal forces on the teeth. Acute
trauma can also cause cementum tears if the force is dissipated by a shift in tooth position or by
wearing away or correcting the restoration and the injury heals and the symptoms go away.
Otherwise, periodontal injury may worsen and progress to necrosis, accompanied by the
formation of a periodontal abscess, or it may persist as a symptom-free, chronic condition.1

1225
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

Tooth pain, sensitivity to percussion, and increased tooth mobility were all observed in cases of
acute trauma. While it is more common and significant in cases of chronic trauma. Gradual
changes were observed, such as tooth wear, drifting movement and extrusion, and parafunctional
habits (bruxism, clenching).1

Occlusal disharmony, functional imbalance, and occlusal dystrophy are all terms used to describe
traumatic occlusal relationships. When trauma from occlusion is caused by changes in occlusal
forces, it is referred to as "primary trauma from occlusion." It is referred to as "secondary trauma
from occlusion" when it occurs as a result of the tissues' reduced ability to resist occlusal forces.1

I. Primary trauma from occlusion

Primary occlusal trauma can occur due to following reasons which include inclusion of a "high-
filling", inclusion of prosthesis replacement that creates excessive force for abutment and
antagonistic teeth; movement or extrusion of teeth into spaces created by missing teeth; primary
trauma changes do not alter the level of connective tissue attachment and do not initiate pocket
formation. This is most likely due to the fact that the supracrestal gingival fibres are unaffected,
preventing apical migration of the junctional epithelium.1

II. Secondary trauma from occlusion

Secondary trauma from occlusion occurs when bone loss caused by marginal inflammation
impairs the tissues' adaptive capacity to withstand occlusal forces. This reduces the area of
periodontal attachment and changes the leverage on the remaining tissues. The periodontium
becomes more prone to injury, and previously tolerable occlusal forces become traumatic.1
Traumatic forces can occur on the following surfacesnormal periodontium with normal bone
height, normal periodontium with reduced bone height, or marginal periodontitis with reduced
bone height. The first case is an example of primary occlusion trauma, while the last two are
examples of secondary occlusion trauma.

STAGES OF TISSUE RESPONSE TO INCREASED OCCLUSAL FORCES

Stages of tissue response to increased occlusal forces include 3 stages. They are Injury, Repair
and Adaptive remodelling of the periodontium.

I. Stage I: Injury

Tissue injury is produced by excessive occlusal forces. The body then attempts to repair the
injury and restore the periodontium. If the offending force is chronic, the periodontium is
remodelled to cushion its impact. The ligament is widened at the expense of the bone, resulting

1226
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

in angular bone defects without periodontal pockets, and the tooth becomes loose. Under the
forces of occlusion, a tooth rotates around a fulcrum or axis of rotation, which in single rooted
teeth is located in the junction between the middle third and the apical third of the clinical root.
This creates areas of pressure and tension on opposite sides of the fulcrum. Different lesions are
produced by different degrees of pressure and tension.1

Occlusion trauma causes vascular changes in the periodontium within 30 minutes. Within 2-3
hours, stasis and vasodilation occur. Between 1 and 7 days, the blood vessel walls disintegrate
and the contents are released into the surrounding tissue, accompanied by pain and
hypersensitivity. Later changes result in bone loss lining the socket, widened periodontal
ligament, and increased tooth mobility. Furthermore, increased alveolar bone resorption and
tooth surface resorption occur.1

TISSUE DESTRUCTIVE CHANGES INDUCED BY TRAUMA FROM OCCLUSION

Occlusion trauma causes vascular changes in the periodontium within 30 minutes. Within 2-3
hours, stasis and vasodilation occur. Between 1 and 7 days, the blood vessel walls disintegrate
and the contents are released into the surrounding tissue, accompanied by pain and
hypersensitivity. Later changes result in bone loss lining the socket, widened periodontal
ligament, and increased tooth mobility. Furthermore, increased alveolar bone resorption and
tooth surface resorption occur. Frontal resorption of cortical bone begins in the area of pdl
compression and progresses to spongy bone tissue, resulting in periodontal ligament widening
(24-38hrs).1

MOLECULAR MECHANISMS OF BONE RESORPTION INDUCED BY FORCE

APPLICATION

Traumatogenic occlusal forces that slightly exceed the tissue adaption threshold cause very rapid
circulatory changes in the periodontal ligament, resulting in platelet aggregation and
prostaglandin release, which activates osteoclasts. During orthodontic movement, there is a
significant increase in the levels of IL-1 and PGE2 in gingival crevicular fluid in 10 patients,
which returns to baseline within 7 days (Grieve et al 1994).6

Mechanical stimuli on teeth generate free proteins within the periodontal ligament, which are
induced either by cell compression and mechanical stress or by cellular destruction and collagen
fibredisorganisation following blood vessel collapse. These proteins cause mast cell
degranulation in the periodontal ligament. It takes about 90 minutes after applying force to the
periodontal ligament for an inflammatory infiltrate to form, eliciting an acid pH that promotes
the attraction and accumulation of osteoclasts. Bone resorption began 12 hours after the
application of orthodontic force and reached a peak 48 hours after the start of orthodontic
movement.1

1227
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

RANKL expression on endothelial cells, inflammatory cells, and periodontal ligament cells is
linked to inflammatory bone resorption. According to Walker et al2008, occlusal trauma causes
an increase in osteoclasts, which is related to the expression of RANKL.7 Traumatogenic
occlusion resulted in the expression of both RANKL and osteopontin in the hyperocclusion
mouse model. According to Passos et al2009, osteopontin and RANKL in bone resorption are
related to trauma from occlusion.8

II. Stage II: Repair

Normal periodontium is constantly repairing itself, and trauma from occlusion stimulates
increased reparative activity. In an attempt to restore the injured periodontium, the damaged
tissues are removed, and new connective tissue cells and fibres, bone, and cementum are formed.
When bone is resorbed by excessive occlusal forces, the body attempts to reinforce the thinned
bony trabeculae with new bone, a process known as buttressing bone formation. It can also
happen when bone is destroyed by inflammation or osteolytic tumours that are buttressing the
bone.1The formation of buttressing bone occurs both within the jaw (central buttressing) and on
the bone surface (peripheral buttressing). Endosteal cells deposit new bone, which restores the
bony trabeculae and reduces the size of the marrow spaces, resulting in central buttressing.
Peripheral buttressing occurs on the alveolar plate's facial and lingual surfaces. Peripheral
buttressing can cause a shelf-like thickening of the alveolar margin, known as "lipping," or a
pronounced bulge in the contour of the facial and lingual Bone, depending on its severity.1

III. Stage III: Adaptive Remodeling of the Periodontium

If the repair process is unable to keep up with the occlusion's destruction. The periodontium is
remodelled to form a structural relationship that results in a thickened periodontal ligament, a
funnel-shaped crest, and angular defects in the bone, but no pocket formation. Increased
vascularization has also been reported as the involved teeth become loose. The relative amounts
of periodontal bone surface undergoing resorption or formation have been used to differentiate
the three stages in the evolution of traumatic lesions. The injury phase is characterised by
increased resorption and decreased bone formation, whereas the repair phase is characterised by
decreased resorption and increased bone formation after adaptive remodelling of the
periodontium, when resorption and formation return to normal.1

CLINICAL AND RADIOGRAPHIC SIGNS OF TRAUMA FROM OCCLUSION

The clinical signs include increased tooth mobility; destruction of periodontal fibres in the injury
stage; fractured tooth; widening of the periodontal ligament in the final stage, which also leads to
increased tooth mobility; thermal sensitivity; fremitus; wear facets; occlusal discrepancies; tooth
migration; discomfort/pain on chewing and cemental tear. The radiographic signs
include:1periodontal space width, frequently associated with thickening of the lamina dura along
the lateral aspect of the root, in the apical region, and in bifurcation areas, interdental septum

1228
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

destruction that is “vertical” rather than “horizontal”,alveolar bone radiolucency and

condensationand resorption of the roots.1

EFFECTS OF INSUFFICIENT OCCLUSAL FORCE

Inadequate occlusal force can also be harmful to the supporting periodontal tissues. Inadequate
stimulation causes periodontal ligament thinning, fibre atrophy, alveolar bone osteoporosis, and
bone height reduction. Hypofunction can be caused by an open-bite relationship, a lack of
functional antagonists, or unilateral chewing habits that ignore one side of the mouth.1

REVERSIBILITY OF TRAUMATIC LESIONS

Occlusion-related trauma is reversible. If the teeth are unable to escape or adapt to excessive
occlusal force, periodontal damage will persist and worsen. Inflammation in the periodontium
caused by plaque accumulation may impair the reversibility of traumatic lesions.1

RELATIONSHIP BETWEEN PLAQUE-INDUCED PERIODONTAL DISEASES AND

TRAUMA FROM OCCLUSION
he bacterial plaque accumulation that causes gingivitis and periodontal pocket formation affects
the marginal gingiva, but trauma from occlusion occurs in the supporting tissues and has no
effect on the gingiva. Human mobile teeth contain significantly more Campylobacter rectus and
Peptostreptococcus micros than nonmobile teeth. Plaque-induced inflammation enters the zone
of co-destruction when it spreads from the gingiva into the supporting periodontal tissues. There
have been other theories proposed to explain the interaction of trauma and inflammation.1

In 1974, the Eastman Dental Center group in Rochester, New York examined squirrel monkeys
that had been subjected to trauma caused by repetitive interdental wedging and mild to moderate
gingival inflammation; the experiments lasted up to 10 weeks. Periodontitis-induced attachment
loss was not exacerbated by the presence of trauma.9

The University of Gothenburg group in Sweden experimented with beagle dogs in 1974,
inducing severe gingival inflammation by placing cap splints and orthodontic appliances.
Periodontal destruction caused by periodontitis is exacerbated by occlusal stresses.10

Trauma from occlusion may alter the pathway of gingival inflammation extension to the
underlying tissues, according to other theories proposed to explain the interaction of trauma and
inflammation. The bone loss that results would be angular, with pockets that could become
intrabony. Deeper lesions may develop as a result of trauma-induced areas of root resorption
revealed by apical migration of the inflamed gingival attachment. Supragingival plaque can
become subgingival if the tooth is tilted orthodontically or if it migrates into an edentulous area,
causing a suprabony pocket to become an intrabony pocket. Increased mobility of traumatised
weakened teeth can pump metabolites of plaques, boosting their dispersion.1

1229
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

INFLUENCE OF TRAUMA FROM OCCLUSION ON PROGRESSION OF MARGINAL

PERIODONTITIS
The clinical impressions of early investigators and clinicians assigned an important role to
trauma from occlusion in the aetiology of periodontal lesions.1Numerous studies have since been
performed to determine the mechanisms by which TFO may affect periodontal disease.

These studies can be classified broadly into three categories: - Human autopsy material, Clinical
trials and Animal experiments

I. Human Autopsy Material:

Certain criteria were evaluated using human autopsy material. They were based on
histopathology of the lesions, presence of apical extension of microbial deposits, mobility and
occlusion. Based on these findings, two concepts were proposed: Glickmans concept 1965 and
Waerhaug concept 1979

Glickmans concept, 1965

If forces of an abnormal magnitude occur in the form of subgingival plaque, the path of
spreading the plaque-related gingival lesion may shift. The periodontal structures can be split
into two zones, irritation zone and co-destruction zone, on the basis of this notion. The marginal
and interdental gingiva comprise the irritation zone. Only on the side of the soft tissue in this
zone are hard tissues bounded, and the occlusion forces do not influence this area. Gingival
inflammation is therefore caused not by trauma of occlusion but by irritation from microbial
deposits.11
The PDL, root cement and alveolar bone are included in the co-destruction zone. The transeptal
and the dentoalveolar fibre bundles are coronally defined. There are two possible pathways for
fibre bundles separating the two areas: alterations in the co-destruction area caused by the
inflammatory lesion maintained by the plaque in the irritation zone and by trauma. The bundle of
fibres can be disintegrated and/or parallel to the surface of the root. Altering the normal
propagation path results in angular osteoarthritis.11
Waerhaugs concept, 1979

The distance between the subsidingives plate and the associated inflammatory periphery of the
infiltrate cell on the surface of the adjacent bone was measured by Waerhupp, and he concluded
that angular ion defects and infrastructural pockets are equally observed which are not affected
by a TFO as in the case of traumatised loss of teething tissue and resorption of the teeth of the
bone. Corner ossic deficiencies and infrabony pockets occur once the subgingival plaque of the
tooth is more than the microbiota of the surrounding tooth and the volume of the root alveolar
bone is relatively high.12

1230
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

II. Clinical trials

In human patients, various writers have performed clinical studies. Rosling et al 1976
demonstrated that hypermobile teeth had the same level of healing as those near to hard teeth in
the infrabony pocket.13Fleaszar et al1980 showed that clinically mobile teeth with the same
disease activity as hard teeth do not respond to periodontal treatments.14 The teeth of enhanced
mobility and extended PDL widening had in fact more pockets, more attachment and less bone
support than the teeth with no these symptoms (Philstrom et al 1986).15Burgett et al 1992
showed that patients who underwent scaling and occlusal adjustment, the probability of an
attachment increase was on average approximately 0.5mm higher than in patients who did not
receive an occlusal adaptation.16Neiderud et al1992 substantiated tissue changes with clinically
healthy gingiva in movable teeth may lower the resistance to testing supplied by periodontal
tissue.17

III. Animal experiments

The positioning of high crowns or restorations on the teeth of dogs or monks leading in one
direction to a continuous and intermittent stress. When a tooth is exposed to unilateral forces that
do not withstand and disperse its periodontal tissue while keeping the tooth stability in such
magnitude, frequency or duration, certain well-defined reactions occur in periodontal structures
in accordance with changed functional demand. The tooth tilts towards the force when
horizontally oriented pressures are applied, causing pressure and tension zones inside the
marginal and apical regions of the tooth to grow briefly and migrate to new positions and heals.2

When horizontally directed pressures are applied, it tilts towards the force that causes the
development of pressure and stress zone in the marginal and apical areas, and the tooth is briefly
hypermobile. In experimental animals with jiggling force, traumas of occlusion were examined,
usually induced with the help of a high crown paired with an orthodontic instrument. In another
way, the teeth were inter-proximally separated by wooden or elastic material to move a tooth to
the opposite side. It took 48 hours to remove the wedge and repeat the procedure on the other
side.2

Alternative traumatic forces are administered orally and lingually or mesially and distally. The
PDL space increases on each side, leading to inflammatory alterations, active sound resorption
and increasing movement, and there are combinations of pressure and tension zones. At one
stage, when the rising breadth is equal to strength, the teeth are hypermobile yet mobility is not
progressive any more. A healthy periodontium with low height is capable of adapting to
modified functional requirements within specific limits, like that of a periodontal with a normal
height.

1231
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

Due to the removal ("occlusal adjustment") of the giggling forces, the width of the periodontal
ligament will be normalised in this circumstance. The tissue could not adjust in the area of
pressure/tension in the presence of plaque-associated periodontal disease and the harm in the
areas of co deterioration had an increasingly permanent character. The following alterations were
noted: continual destruction of alveolar bone, steady mobility of teeth, fusion of the irritant area
and co-destruction zone, apically proliferating dentogingival epithelium, and periodontal
disease.2

TRAUMAFROM OCCLUSIONPERI-IMPLANT TISSUES

Trauma from occlusion in peri – implant tissues can occur due to various reasons which
includeorthodontic loading and alveolar bone,bone reactions to functional loading, excessive
occlusal load on implants, static and cyclic loads on implants, load and loss of osseointegration,
masticatory occlusal forces on implants
and tooth-implant supported reconstructions

I. Orthodontic loading and alveolar bone

Excessive loading was studied in Adell et al 1981, a prevalent cause of implant loss.18 Early
charging seen by Sagara et al 1993 may hinder osseointegration.19Isidor et al 1997 studied non-
axial implant forces as an osseointegration risk factor.20 The bone surrounding an implant –
biological reaction to mechanical stress below the threshold in Asikainen et al 1997, whereas loss
of the marginal bone or osseointegration due to mechanical stress outside the threshold.21

II. Bone reactions to functional loading

After long term functional load, Berglundh et al 2005 discussed the reactivity of the peri-implant
bone in comparison to unloaded controls.22AstraTech implants are implanted on the one hand
after extraction and Branemark on the other. Results demonstrated that functional implant
loading may improve osseointegration.22

III. Excessive occlusal load on implants

Heitz-Mayfield et al2004 studied on dogs using 2 titanium plasma sprayed implant and 2
sandblasted acid etched implants on each side of the mandible.23 In the test side, implants were
placed after 6months gold crowns are placed in supraocclussion. Result showed that occlusal
overload does not result in loss of implant stability.23

IV. Static and cyclic loads on implants

Scheppers1977 demonstrated bone tissue reaction to axial loading and was evaluated using
conventional three‐unit FDPs in the mandible of Beagle dogs, and compared with that to
non‐axial loading provoked by installing a distal cantilever of two implants.24Gotfredsen et
al2001analyzed bone reactions around osseointegrated implants to static load in three studies in
dogs.25 Results showed that lateral static load resulting in an adaptive remodeling of the

1232
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

periimplant bone.25Duycket al2001 showed that dynamic load on implants resulted in the
establishment of marginal crater defects.26

V. Load and loss of osseointegration

Isidor et al1997 studied excessive occlusal load leading to osseointegration along the entire
length of implant that causes implant mobility.20Lindhe et al 1992 used cotton ligatures for
increased plaque retention placed around implants. It resulted in mucositis and later peri-
implantitis.17

VI. Masticatory occlusal forces on implants

Lundgren et al1989 examined 8 strain gauge tranducers mounted bilaterally in maxillary
complete denture to occlude with mandibular implant suported fixed cantilever
prosthesis.27Larger closing and chewing forces were measured over the cantilever than implant
supported areas.27

DIAGNOSIS
Increased tooth movement is cardinal symptom of primary TFO. The mechanical and electronic
equipment can assess mobility. Mobility subjective evaluations are carried out as allocated from
0 to 3 in the Miller classification. Tilting and migration of single teeth or whole segments. If
there's primary TFO in a fixing device, the pounding of the teeth with an unobtrusive instrument
changes from the resonating note with a healthy support structure to a dull note careful
examination of chewing muscles to see whether hypertrophy or hypertonic signs are present with
probable spasm of a muscle group.TMJ palpation and observation on numerous routes for
closure of any deviation from the mandible. The fremitus test is a measurement of the vibrational
patterns of the teeth when the tooth is placed in the position and motion of the contact.1

MANAGEMENT OF TRAUMA FROM OCCLUSION

Occlusal therapy should concentrate primarily at building stable functional links, including
periodontium, favorable to dental health in patients.1For the management of TFO the following
procedures are used:occlusal adjustment – coronoplasty andorthodontic treatment.
Occlusal analysis is done by using occlusal registration steps, occlusal indicator wax, marking
ribbon, red, green, blue nylon ribbon and using articulating paper.

Coronoplasty
Coronoplasty is a selective reduction in occlusal areas with the main objective of affecting
mechanical contact and sensory input neuronal pattern.
Objectives of coronoplasty includes changes in the pattern and degree of afferent impulses,
lessening of excessive tooth mobility, multiple simultaneous contact spread over the occlusal
scheme to effect occlusal stabilization, beneficial change in the pattern of chewing or swallowing

1233
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

function, multidirectional mandibular moving patterns and verticalization of occlusal forces on

implants.1

The following are the steps followed in coronoplasty. The first stepbeing the removal of
extensive prematurities and eliminate the deflective shift from retrudedcuspal position (RCP) to
intercuspal position (ICP). The second step indicates adjustment of ICP to achieve stable
simultaneous, multi-pointed, widely distributed contact . The third Step involves thetest for
excessive contact on the incisor teeth. The fourth step codes for the removal of posterior
protrusive super contacts and establish contacts that are bilaterally distributed on the anterior
teeth. The fifth step ensures removal of lessen mediotrusive interferences. The next following
step involves reduction of excessive cusp steepness on the laterotrusive contacts. The seventh
step involves elimination of gross occlusal disharmonies. The eighth step being rechecking of
tooth contact relationships The last and final step involves polishing of all rough tooth surfaces. 1

Invasive, irreversible intervention and no reduction in mobility or pocket depth are the
disadvantages of coronoplasty. Time for tissue healing must be allowed to take precautions and
periodic reassessment should be carried out.

ORTHODONTIC TREATMENT
The orthodontic treatment indications include anterior functional crossbit, tapped teeth and single
rooted extruded teeth. Timing of orthodontic treatment: 1) Until the teeth are completely scaled,
planned and the patient is trained in oral hygiene, should be commenced. 2) Completed before
full correction of the occlusal and periodontal operations. 3) Bonded orthodontic retainers that
stabilise the teeth can ensure ideal health and bone regeneration conditions for periodontal
treatment.1

I. Temporary and Provisional Splinting:

A splint is a rigid appliance used to stabilize and protect an injured part. A temporary splint is
used to reduce occlusal forces and stabilize teeth for a limited period of time. A provisional
splint is used in borderline cases in which the final results of the periodontal treatment cannot be
predicted with certainty at the time of the initial treatment planning. It is beneficial in cases of
progressive TFO during the post-operative healing phase.2

II. Biteplanes:
A flat maxillary biteplane with cuspid rise is the best universal appliance for prompt
temporary elimination of TFO. It is especially useful in patients with bruxism and advanced
periodontal disease, since it will induce muscle relaxation and eliminate the bruxism.1
CONCLUSION
The primary management is the elimination of abnormal occlusal forces as well as the
stabilization of the involved tooth/teeth. Except in the presence of periodontitis, when TFO is

1234
http://annalsofrscb.ro
Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

removed, bone loss is reversed. The elimination of periodontal inflammation as well as TFO is
critical for complete periodontal health and improving tooth prognosis.

REFERENCES
1. Newman MG, Takei H, Klokkevold PR, Carranza FA. Newman and Carranza's Clinical
periodontology E-book. Elsevier Health Sciences; 2018.
2. Lindhe J, Karring T, Lang NP. Clinical periodontology and implant dentistry. Blackwell;
2003.
3. Singh DK, Jalaluddin M, Rajeev R. Trauma from occlusion: The overstrain of the
supporting structures of the teeth. Indian Journal of Dental Sciences. 2017;9(2):126-32.
4. Hamp SE, Nyman S, Lindhe J. Periodontal treatment of multi rooted teeth. Results after 5
years. Journal of clinical periodontology. 1975(3):126-35.
5. Fan J, Caton JG. Occlusal trauma and excessive occlusal forces: Narrative review, case
definitions, and diagnostic considerations. Journal of periodontology. 2018 ;89:S214-22.
6. Grieve III WG, Johnson GK, Moore RN, Reinhardt RA, DuBois LM. Prostaglandin E
(PGE) and interleukin-1β (IL-1β) levels in gingival crevicular fluid during human
orthodontic tooth movement. American Journal of Orthodontics and Dentofacial
Orthopedics. 1994;105(4):369-74.
7. Walker CG, Ito Y, Dangaria S, Luan X, Diekwisch TG. RANKL, osteopontin, and
osteoclast homeostasis in a hyperocclusion mouse model. European journal of oral
sciences. 2008 :6(4):312-8.
8. Passos SP, Zamboni SC, Takahashi FE, de Macedo NL. Trauma oclusal x
tecidosperiodontais: ação da osteopontina e do receptor ativador do fator nuclear kappa
B. Periodontia. 2009:75-81.
9. Polson AM, Meitner SW, Zander HA. Trauma and progression of marginal periodontitis
in squirrel monkeys: IV. Reversibility of bone loss due to trauma alone and trauma
superimposed upon periodontitis. Journal of Periodontal Research. 1976;11(5):290-8.
10. Lindhe J, Svanberg G. Influence of trauma from occlusion on progression of
experimental periodontitis in the beagle dog. Journal of Clinical Periodontology.
1974;1(1):3-14.
11. Glickman I, Smulow JB. Effect of excessive occlusal forces upon the pathway of
gingival inflammation in humans. The Journal of periodontology. 1965;36(2):141-7.
12. Waerhaug J. The infrabony pocket and its relationship to trauma from occlusion and
subgingival plaque. Journal of periodontology. 1979;50(7):355-65.
13. Rosling B, Nyman S, Lindhe J, Jern B. The healing potential of the periodontal tissues
following different techniques of periodontal surgery in plaque‐free dentitions: A 2‐year
clinical study. Journal of clinical periodontology. 1976;3(4):233-50.
14. Fleszar TJ, Knowles JW, Morrison EC, Burgett FG, Nissle RR, Ramfjord SP. Tooth
mobility and periodontal therapy. Journal of Clinical Periodontology. 1980;7(6):495-505.

1235
http://annalsofrscb.ro
 Annals of R.S.C.B., ISSN: 1583-6258, Vol. 24, Issue 1, 2020, Pages. 1224 -1236
Received 15 April 2020; Accepted 23 June 2020

15. Pihlstrom BL, Anderson KA, Aeppli D, Schaffer EM. Association between signs of
trauma from occlusion and periodontitis. Journal of periodontology. 1986 ;57(1):1-6.
16. Burgett FG, Ramfjord SP, Nissle RR, Morrison EC, Charbeneau TD, Caffesse RG. A
randomized trial of occlusal adjustment in the treatment of periodontitis patients. Journal
of clinical periodontology. 1992 l;19(6):381-7.
17. Neiderud AM, Ericsson I, Lindhe J. Probing pocket depth at mobile/nonmobile teeth.
Journal of clinical periodontology. 1992;19(10):754-9.
18. Adell R, Lekholm U, Rockler BR, Brånemark PI. A 15-year study of osseointegrated
implants in the treatment of the edentulous jaw. International journal of oral surgery.
1981 1;10(6):387-416.
19. Sagara M, Akagawa Y, Nikai H, Tsuru H. The effects of early occlusal loading on one-
stage titanium alloy implants in beagle dogs: a pilot study. The Journal of prosthetic
dentistry. 1993 r 1;69(3):281-8.
20. Isidor F. Histological evaluation of peri-implant bone at implants subjected to occlusal
overload or plaque accumulation. Clinical oral implants research. 1997 1;8(1):1-9.
21. Asikainen P, Klemettil E, Vuilleminz T, Sutter F, Rainio V, Kotilainen R. Titanium
implants and lateral forces. An experimental study with sheep. Clinical Oral Implants
Research. 1997;8(6):465-8.
22. Berglundh T, Donati M. Aspects of adaptive host response in periodontitis. Journal of
clinical periodontology. 2005t;32:87-107.
23. Heitz‐Mayfield LJ, Schmid B, Weigel C, Gerber S, Bosshardt DD, Jönsson J, Lang NP,
Jönsson J. Does excessive occlusal load affect osseointegration? An experimental study
in the dog. Clinical oral implants research. 2004;15(3):259-68.
24. Barbier L, Schepers E. Adaptive bone remodeling around oral implants under axial and
nonaxial loading conditions in the dog mandible. International Journal of Oral &
Maxillofacial Implants. 1997 1;12(2).
25. Gotfredsen K, Berglundh T, Lindhe J. Bone reactions adjacent to titanium implants
subjected to static load: a study in the dog (I). Clinical oral implants research.
2001;12(1):1-8.
26. Duyck J, Naert I, Rønold HJ, Ellingsen JE, Van Oosterwyck H, Vander Sloten J. The
influence of static and dynamic loading on marginal bone reactions around
osseointegrated implants: an animal experimental study. Clinical oral implants research.
2001;12(3):207-18.
27. Lundgren D, Falk H, Laurell L. The Influence of Number and Distribution of Occlusal
Cantilever Contacts on Closing and Chewing Forces in Dentitions with Implants-
Supported Fixed Prostheses Occluding with Complete Dentures. International Journal of
Oral & Maxillofacial Implants. 1989 1;4(4).

1236
http://annalsofrscb.ro

View publication stats