TMDs and dental occlusion relationship

QUINTESSENCE INTERNATIONAL | volume 53 • number 5 • May 2022
450
The relation of temporomandibular disorders and dental
occlusion: a narrative review
Mythili Kalladka, BDS, MSD/Andrew Young, DDS, MSD/Davis Thomas, BDS, DDS, MSD, MSc Med, MSc/
Gary M. Heir, DMD/Samuel Y.P. Quek, DMD, MPH/Junad Khan, DDS, MSD, MPH, PhD
Objective:The term temporomandibular disorders (TMDs) en-
compasses a variety of disorders of the temporomandibular
joint (TMJD) and the associated musculature (MMD). Occlusion
and its role in the genesis ofTMDs is one of the most controver-
sial topics in this arena. The objective of the narrative review
was to summarize the implications ofTMDs and its relationship
to dental occlusion in two scenarios: 1)TMD as an etiologic fac-
tor in dental occlusal changes; 2) The role of dental occlusion
as a causative factor in the genesis of TMDs. Data Sources: In-
dexed databases were searched from January 1951 to August
2021 using the termsTMJ,TMD, temporomandibular disorders,
temporomandibular joint, and dental occlusion. Conclusion:
There is lack of good primary research evaluating true associ-
ation and showing the cause-and-effect relationship between
dental occlusion andTMD. Systematic reviews suggest that the
role of occlusion as a primary factor in the genesis of TMDs is
low to very low. However, a variety ofTMDs can lead to second-
ary changes in dental occlusion. Distinction between the two
is paramount for successful management.
(Quintessence Int 2022;53:450–459; doi: 10.3290/j.qi.b2793201)
Key words: occlusion, temporomandibular disorders, temporomandibular joint
Temporomandibular disorders (TMDs) are one of the most
prevalent orofacial pain disorders, and may be arthrogenous
and/or myogenous in origin. It is estimated that 5% to 12% of
the population may be affected by these disorders.1,2
The etio-
pathogenesis of TMD has shifted from early gnathologic con-
cepts to the current biopsychosocial model.3
TMDs and occlu-
sion thus became one of the most controversial topics in
dentistry. Evidence-based dentistry today has challenged some
of the previously held views, by closely scrutinizing the studies
and clinical reports from the past. However, it is well docu-
mented that certain TMDs can lead to occlusal changes. Thus,
many occlusal changes, especially those that manifest with
acute changes in occlusion, may be sequelae to TMDs rather
than the causation of TMDs.4,5
These changes may be subse-
quent to developmental, degenerative, systemic, adaptive, be-
nign, and malignant disorders. These patients may often pres-
ent to the dental practitioner with subjective, and sometimes
objective, signs and symptoms of a change in occlusion. Deter-
mination of the underlying TMD responsible for the occlusal
changes is crucial for treatment planning and successful man-
agement.
The objective of this narrative review was to familiarize oral
health care providers with the scientific evidence on: 1)TMD as
an etiologic factor in dental occlusal changes; and 2) the role of
dental occlusion as a causative factor in the genesis of TMD.
Data source and resource selection
Indexed databases (PubMed, EMBASE, Scopus, ISIWeb of Knowl-
edge, Medline, OVID, Scopus, Cochrane Library) were searched
from January 1951 to August 2021 using the terms (“dental oc-
clusion”[MeSHTerms] OR (“dental”[All Fields] AND“occlusion”[All
Fields]) OR “dental occlusion”[All Fields]) AND (“temporoman-
dibular joint disorders”[MeSH Terms] OR (“temporomandibu-
lar”[All Fields] AND “joint”[All Fields] AND “disorders”[All
Fields]) OR“temporomandibular joint disorders”[All Fields] OR
(“tem
poromandibular”[All Fields] AND “disorders”[All Fields])
OR“temporomandibular disorders”[All Fields]).
GENERAL DENTISTRY

QUINTESSENCE INTERNATIONAL | volume 53 • number 5 • May 2022 451
Kalladka et al
Changes in occlusion secondary to TMD
Changes in occlusion may occur secondary to TMDs of the
temporomandibular joint (TMJD) or the associated muscula-
ture (MMD). The DC-TMD is the most commonly accepted clas-
sification for TMDs.6
It subclassifies TMJD into joint pain, joint
disorders, joint diseases, fractures, and congenital or develop-
mental disorders. MMDs include muscle pain, contracture, hy-
pertrophy, neoplasm, movement disorders, and masticatory
muscle pain attributed to central or systemic pain disorders.7,8
In addition, certain TMD-related conditions like bruxism (sleep
and awake) may also cause changes in occlusion.
Changes in occlusion secondary to TMDs may be acute
(when it develops suddenly) or chronic (when occlusal changes
are gradual over a period of months to years). The changes in
occlusion include posterior open bite, anterior open bite, facial
asymmetries, midline deviations, crossbites, and miscellaneous
(such as loss of vertical dimension, and heavier occlusal con-
tacts).These changes may occur as a consequence ofTMJ-related
pathologies or muscle-related conditions, and may manifest as
acute or chronic changes in occlusion. Changes in occlusion may
follow increased intraarticular pressure, loss of bone support or
MMD resulting from muscle fatigue, electrolyte imbalance, or
deep pain inputs. Muscle contraction may also cause positional
changes in the jaw, which may vary depending on the muscle
involved.9
The subsequent section discusses changes in occlusion
secondary to TMDs. The specific types of occlusal changes are
listed as categories, and the causative TMDs are listed as sub-
categories, following the taxonomic classification and diagnos-
tic criteria of TMDs (DC-TMD). Additional causes of occlusal
changes, such as iatrogenic causes, have also been included
wherever applicable. A list of the TMDs and the changes in
occlusion secondary to TMDs are shown in Table 1.
Posterior open bite
This may be seen in TMJD subcategories such as joint pain
(arthritis), joint disorders (disc disorders such as acute anterior
disc displacement without reduction), joint diseases (synovial
chondromatosis), fractures, and MMD subcategories.7,10
Joint pain
Arthralgia
Terms such as synovitis or capsulitis have been previously used
to describe this condition.The expanded taxonomy of DC-TMD
describes it as pain originating in the TMJ accompanied with
clinical features of localized infection/inflammation and not
associated with any systemic condition.7
On clinical examination, palpation of the lateral aspect of
the TMJ and range of movements may result in reproduction
of the pain complaints. This may be accompanied by signs of
inflammation such as redness, swelling, or increased tempera-
ture in the area of theTMJ.The intraarticular swelling, and effu-
sion of the inflammatory exudate may result in a unilateral
ipsilateral/ bilateral posterior open bite with deep anterior
teeth contacts depending on whether the condition is unilat-
eral or bilateral.7
Since this condition is localized to theTMJ and excludes sys-
temic arthritides and rheumatologic diseases, blood tests/lab
studies including rheumatoid panel, erythrocyte sedimenta-
tion rate (ESR), complete blood count (CBC) with differential,
C-reactive protein (CRP), and anti-nuclear antibody (ANA) may
be advised to rule out these conditions.
Joint disorders
Disc disorders
Disc displacement without reduction with limited opening
(DDW/O R) is an intracapsular biomechanical disorder involving
the disc condyle complex. In in
stances of acute DDW/O R the
articular disc is most commonly displaced anteriorly and medi-
ally, and less commonly laterally and posteriorly.6,11
On clinical examination, the maximum assisted mouth
opening is less than 40 mm. Contralateral excursive move-
ment is also limited. Loading test may be positive for pain on
the same side. In instances of acute anterior DDW/O R, the disc
is dislocated anteriorly and the condyle sits heavily on the ret-
rodiscal tissue immediately. This may cause mild changes in
occlusion which may manifest as heavier occlusal contacts on
the affected side. Subsequently, the retrodiscal tissue may
become inflamed, which may cause posterior open bite on the
affected side.7
The diagnosis is confirmed through magnetic resonance
imaging (MRI). A systematic review correlating clinical findings
to MRI reported low to moderate correlation in diagnosing in-
ternal derangements through the clinical examination, and
suggested that the clinical examination may be utilized for
screening, and advanced imaging like MRI should be reserved
for accurate diagnosis in cases that are symptomatic12
and not
responding to treatment. A systematic review and meta-analy-
sis suggested that ultrasound, especially high-resolution dy-
namic and static ultraosund, may be used as adjunct tools to
the clinical examination and prior to MRI to enable a fast, sim-
ple, and cost-effective option for diagnosis.13,14

452
GENERAL DENTISTRY
Table 1 Changes in dental occlusion secondary to TMDs
Condition
Occlusal presentation
Onset Diagram
Anterior
occlusion
Posterior
occlusion Midline shift
Spasm of masseter, medial pterygoid,
and/or temporalis muscles
Unaffected Ipsilaterally feels
heavy to patient.
Not usually
measurable.
Unaffected Rapid
TMJ condylar
hypoplasia:
Degenerative joint
disease; Arthritis;
Idiopathic condylar
resorption
Mild Unaffected Hyper occlusion on
ipsilateral
distalmost tooth
Unaffected Gradual
Advanced Open Occlusion only on
ipsilateral
distalmost tooth
Toward side of
condition (if
unilateral)
Lateral pterygoid shortening: Spasm;
Contracture
Hyper-occlusion Ipsilateral
hypo-occlusion or
no occlusion
Away from side of
condition (if
unilateral)
Rapid
Disc displacement Unaffected Ipsilateral hyper
occlusion
Unaffected Rapid
TMJ inflammation Unaffected Ipsilateral
hypo-occlusion or
no occlusion
Unaffected Rapid
Dislocation May occlude on
some teeth
May occlude on
some teeth
Markedly (if
unilateral) away
from the side of
the condition
Rapid

Kalladka et al
Joint diseases
Synovial osteochondromatosis
This is a benign lesion characterized by numerous calcifications
within the joint subsequent to cartilaginous metaplasia occur-
ring in the synovial membrane.7,11
On clinical examination, the patient may exhibit preauricu-
lar swelling, and reproduction of the pain complaints with TMJ
palpation.15
MRI or CBCT may be used for diagnosis. Histopathologic
examination reveals cartilaginous metaplasia.7
Fractures
A displaced or non-displaced fracture may involve the bony
components of the joint and may cause occlusal changes such
as contralateral posterior open bite.
On clinical examination, the patient may exhibit preauricu-
lar swelling, and reproduction of the pain complaints with TMJ
palpation.
Orthopantomography may be used for initial evaluation.
CT/CBCT may be used for diagnosis.7
Masticatory muscle disorders
Myalgia
This is pain of muscular origin affected by function, parafunc-
tion, and jaw movement. Myofascial pain may be characterized
by trigger points, which are hyperirritable spots in taut bands
of muscle. Trigger points in the inferior lateral pterygoid may
cause mild occlusal changes presenting as disoccluded ipsilat-
eral posterior teeth and premature contact of the contralateral
anterior teeth.7
Chairside tests such as loading tests, and tests of provocation,
may be used. In addition, diagnostic local anesthetic blocks can
be used if necessary to distinguish the source and site of pain.
Spasm/myositis/contracture
Spasm is a sudden, reversible, involuntary tonic contraction of a
muscle. Myositis is a pain of muscular origin, generally second-
ary to infection, inflammation, or autoimmune conditions. Con-
tracture occurs secondary to trauma, infection, or radiation ther-
apy, and may result in fibrosis of muscle fibers, tendons, and
ligaments. These conditions may alter the postural position of
jaws; the type of occlusal change produced depends on the
muscle involved.16
The most common masticatory muscles in-
volved are the medial and lateral pterygoid, and the masseter.
Complete spasm of the elevator muscles causes limitation of
opening. Partial spasm causes acute malocclusion, which may
sometimes not be visible clinically, but has the potential to
cause patient discomfort and a report of their bite “feeling dif-
ferent.”Occasionally occlusion is detectably heavier on the ipsi-
lateral side. Unilateral inferior lateral pterygoid spasm/contrac-
ture causes loss of contact on the ipsilateral posterior teeth and
heavy contact on the contralateral canines. Bilateral inferior
lateral pterygoid spasm/contracture may manifest as bilateral
posterior open bite and heavy anterior occlusal contacts. Unilat-
eral medial pterygoid spasm/contracture may result in slight
ipsilateral posterior open bite and contralateral accentuated ver-
tical overlap (overbite). Unilateral superficial masseter spasm/
contracture may result in mild posterior open bite on the con-
tralateral side. Myostatic contracture, or shortening of the rest-
ing length, of lateral pterygoid muscles (causing posterior open
bite) may also occur as a consequence of mandibular advance-
ment device usage, or a protrusive night guard. An early form of
open bite is hypo-
occlusion.16
Additional chair side tests such as loading tests, tests of
provocation, and diagnostic blocks can be used as necessary.
Intramuscular electromyography (EMG) may be elevated in
myospasm.17
Serologic tests may be advised for myositis and
may reveal elevated inflammatory markers and elevated creat-
inine kinase. Serological testing may also be advised to rule out
autoimmune disorders.7
Iatrogenic
The immediate postoperative period ofTMJ surgeries may also
exhibit changes in occlusion.
Anterior open bite/inability of anterior teeth to occlude
This may occur secondary to joint diseases (including degener-
ative joint diseases, systemic arthritides, condylysis/idiopathic
condylar resorption, osteonecrosis), bilateral degenerative
changes secondary to rheumatoid arthritis/ other autoimmune
arthritis, and bilateral idiopathic condylar resorption. Anterior
open bite secondary toTMD must be distinguished from anter-
ior open bite due to non-TMD causes such as tongue thrusting
habit.
Joint diseases
Degenerative joint disease
The expanded taxonomy of DC-TMD describes degenerative dis-
orders not associated with rheumatologic diseases and affecting
the joint with damage/degradation of the articular tissues and
changes in the osseous structures such as the articular eminence
and condyle. Progressive open bite may occur due to resorption
of condylar structures.7,11,18

454
GENERAL DENTISTRY
Systemic arthritides
These conditions are attributed to an underlying systemic in-
flammatory/rheumatologic disease resulting in pain, inflam-
mation, and structural changes to the TMJ.
Systemic arthritic disorders include inflammatory arthritis
(eg, rheumatoid arthritis, juvenile rheumatoid arthritis, psori-
atic arthritis, ankylosing spondylitis), degenerative arthritis
(osteoarthritis), infectious arthritis (Lyme associated, gonococ-
cal arthritis, syphilitic arthritis, tuberculous arthritis), meta-
bolic arthritis (pseudogout, gout), and traumatic arthritis.19
Among these, juvenile rheumatoid arthritis and rheumatoid
arthritis are most commonly associated with anterior open
bite. Children with juvenile idiopathic arthritis present with a
remarkable prevalence of condylar destruction, which is cor-
related to the type and duration of the disease.20,21
Patients
with rheumatoid arthritis often present with rapid onset anter-
ior open bite and often present with class II occlusion. This is
secondary to destruction of the mandibular condyles resulting
in progressive loss of ramus height.11
CBCT has been shown to
have high diagnostic accuracy in detection of bony changes
and may be helpful in evaluating progression of DJD over
time. However, care should be exercised owing to radiation
exposure, and it should not be used as a screening tool in
healthy individuals.22
Positron emission tomography (PET)
scan in combination with CT is the most reliable modality to
determine active rheumatoid TMJ arthritis.23
Laboratory stud-
ies include serologic testing for various systemic conditions
such as arthritis, and may include rheumatoid panel, CBC with
differential, ESR, C-reactive protein, anti-
nuclear antibody
(ANA), and complete metabolic panel with electrolytes. These
should be advised only when necessary, keeping in mind radi-
ation exposure and financial implications.17
Idiopathic condylar resorption
This idiopathic condition is seen in adolescents and young fe-
males and leads to degeneration of the TMJ condyle with pro-
gressive loss of condylar height. It is associated with progres-
sive anterior open bite.24
Other occlusal changes: facial asymmetries, deviated
midline, crossbites
Benign and malignant neoplasms
A variety of benign and malignant neoplasms may affect the TMJ
and cause a variety of occlusal changes such as facial asymmetry
and midline shift. Primary benign and malignant neoplasms of
the TMJ are rare. In these instances, the malignancy may affect
the hard and soft tissues of the TMJ including cartilage and
bone. Metastasis to the condyle is rare and mainly involves ma-
lignancy from the lung. Peripheral osteoma of the mandibular
condyle can cause anterior cross bite and mandibular devia-
tion.25
Benign and malignant neoplasms and cysts may cause
unilateral open bite.26
MRI or CT/CBCT may be used to aid diagnosis. PET scanning
may be used to rule out distant metastasis. Biopsy may be used
for definitive diagnosis.11
Fractures
Untreated condylar fracture secondary to trauma results in
lower midline deviation coinciding with the side of the unilat-
eral fractured condyle.27
In general, plain radiographs serve as
basic screening aids to rule out gross morphologic changes in
the osseous structure and fractures. Advanced radiographic
aids such as CBCT or CT may be advised for accurate diagnosis.
Congenital/developmental disorders
This grouping includes aplasia, hypoplasia, and condylar hyper-
plasia. Aplasia is a congenital condition characterized by the
absenceofthemandibularcondyleandhypoplasiaoftheglenoid
fossaandarticulareminence.Itmaybeassociatedwithsyndromes
such asTreacher Collins or Goldenhar syndrome, and has associ-
atedchangesinocclusionincludingcrossbite,openbite,posterior
open bite, and facial asymmetry. Hypoplasia is a less severe form
of aplasia and may be congenital or secondary to trauma. It may
be associated with facial asymmetry, occlusal changes such as a
non-horizontalocclusalplane,andposterioropenbiteonthecon-
tralateral side. Bilateral cases may result in anterior open bite.7,11
Hyperplasia is a developmental disorder characterized by
facial asymmetry as a result of continued growth of the man-
dibular condyle.11
Iatrogenic
Occlusal changes commonly occur after TMJ arthroscopic disc
repositioning and suturing. It may be characterized by heavier
contacts or premature contacts, posterior open bite on the sur-
gery side, mandible midline deviations, and incisal prematurity.
One study suggested that the majority of the changes in occlu-
sion resolve in 28 days, and treatment should be considered in
cases that do not resolve in this time.28
Injection of contrast agent during arthrography
Heavier contact may occur on contralateral posterior teeth.16
Intracapsular edema subsequent to early-stage arthritis also
results in premature occlusion of teeth on the opposite side.

Kalladka et al
Chronic unilateral bruxism
This often causes ipsilateral collapsed bite with severe attrition.
Limitation of mouth opening
This may be seen in conditions such as acute disc displacement
without reduction (as previously described), ankylosis, hypo-
plasia, and adhesions.
Hypomobility disorders
This includes adhesions and ankylosis (bony or fibrous). Adhe-
sions are conditions are associated with limitation of opening
due to restriction of disc condyle movement by fibrous adhe-
sions. Ankylosis may be bony or fibrous and there may be com-
plete or partial limitation of mouth opening. When unilateral,
both conditions cause uncorrected jaw deviation to the involved
side on opening.11,12
Inability to close mouth
TMJ hypermobility allows the disc condyle complex to slide be-
yond the articular eminence. In dislocation, the disc condyle
complex cannot return to the fossa (often referred to as an
“open lock”) without maneuver either by the patient or by a
clinician. In subluxation, such manual reduction is not neces-
sary to return to closure.11,12
Occlusion and TMD
Controversy has existed for decades on the role of occlusion in
TMDs.The current review summarizes the evidence from system-
atic reviews and meta-analysis on the role of occlusion in TMD.
An early systematic review (2004) on population-
based
studies in adults, addressing the association of malocclusion,
functional occlusion parameters (such as nonworking-side oc-
clusal contacts and occlusal interference), and TMDs, con-
cluded that there were very few associations.29
The associations
were not uniform, and the authors found no particular func-
tional occlusal or malocclusion feature to be apparent. The
strength of correlation was not mentioned in studies in two
positive associations (number of rotated lateral teeth, excessive
abrasion, and signs and symptoms of TMD). In addition, pa-
tients with Angles Class II malocclusion, anterior crossbite and
deep bite had fewer symptoms of clinical dysfunction. In view
of the limited number of RCTs, methodologic quality, and dis-
crepancies in study design, the authors suggested confirmation
of results through validated representative studies in future.29
In 2005, a systematic review by the Swedish Council on
HealthTechnology Assessment concluded that the scientific evi-
dence until then was insufficient to enable definite conclusions
on the correlation betweenTMD and specific untreated maloc-
clusion.30
There was also limited scientific evidence to show the
connection of TMD with orthodontic treatment.30
A systematic
review by Mohlin et al31
in 2007 reconfirmed these findings,
reporting a lack of association between specific malocclusion or
orthodontic treatment and signs and symptoms of TMD.
A systematic review on attrition, occlusion, and masticatory
system dysfunction reported that few studies reported a cor-
relation between anterior spatial relationships and attrition.32
One study reported that a smaller number of teeth may lead to
higher tooth wear index, but no study reported loss of poster-
ior teeth contributing to enhanced attrition; it instead ap-
peared to be co-existent with self-reported bruxism. However,
there was no definite conclusion regarding the relationship
between TMD and attrition.32
A systematic review on posterior crossbite and functional
changes on the masticatory muscles in the primary and mixed
dentition concluded that the malocclusion in these instances
could lead to asymmetric muscle function.33
There was also a
significant association between posterior crossbite in primary
and mixed dentition and TMD that deserved further investiga-
tion.33
A study by Iodice et al34
suggested that it was not possible
to draw an association between posterior crossbites, muscle
pain, and disc displacement with reduction because the distri-
bution of studies supporting and refuting were similar, and
hence the authors suggested more rigorous scientific studies
were needed to draw conclusions. Another systematic review in
2018 onTMJ positional and dimensional changes following cor-
rection of posterior crossbites in children concluded that there
is insufficient evidence for a firm conclusion.35
A systematic review by Abduo et al36
concluded that there
was no association between lateral occlusal schemes and TMD
development. Another systematic review on centric relation–
intercuspal position discrepancy and TMD concluded that due
to the low quality of articles and varied methodology, it was
difficult to establish definite correlations.37
Further well-de-
signed longitudinal studies with validated diagnostic criteria
and strict, standardized methodology were required.37
Manfredini et al38
conducted a systematic review on associ-
ation studies to determine if there is an association between
TMD and features of occlusion, and concluded that there was
no disease-specific association between the two, and that
there is no role of dental occlusion in the pathogenesis ofTMD.

456
GENERAL DENTISTRY
Table 2 Diagnosis and management of TMDs causing changes in dental occlusion
Condition Presentation Diagnostic aids Treatment
Joint pain Arthralgia Pain in jaw, ear, temple, or preauricular area, and
changed with jaw function. Pain with TMJ
palpation
CBCT or MRI. Blood
tests to rule out
systemic arthritis/
systemic
inflammatory
disease
Conservative measures, including patient
education, physiotherapy, pharmacotherapy,
intraoral appliance therapy, behavioral therapy
Disc disorders Disc
displacement
without
reduction with
limited opening
Limitation in mouth opening significant enough to
interfere with ability to eat.
MRI Gentle range of motion exercises. Optional manual
manipulation for reduction; may be facilitated by
use of nerve blocks. Pharmacotherapy for pain, tem-
porary intraoral appliance therapy, physiotherapy
Hypermobility Luxation Inability to close without specific maneuver by
clinician. Protruded or laterotruded mandible
Panoramic
radiograph
Manual reduction
Joint disease Degenerative
joint disease
Crepitus, and subchondral cyst(s), erosion(s),
generalized sclerosis, or osteophytes
CBCT or MRI Conservative measures, including patient
intraoral appliance therapy, behavioral therapy
Systemic
arthritis
Diagnosis of systemic inflammatory joint disease
and TMJ pain or noises. Subchondral cyst(s),
erosion(s), generalized sclerosis, or osteophyte(s)
CBCT, MRI,
laboratory studies
(including ANA, RF,
ESR, CRP)
Pharmacotherapy
Neoplasm Swelling, pain during function, limited mouth
opening, crepitus, occlusal changes, facial
asymmetry, and/or sensory-motor changes
MRI Medical and surgical management
Synovial
chondromatosis
Preauricular swelling, TMJ pain, progressive
limitation in mouth opening, or joint noises.
Multiple chondroid nodules, joint effusion and
amorphous iso-intensity signal tissues within the
joint space and capsule, or loose calcified bodies in
the soft tissues
MRI, arthroscopy Arthroscopy or open surgery
Fracture Trauma, preauricular swelling, TMJ pain, or limited
mouth opening. May have malocclusion
CBCT, panoramic
radiograph
Open or closed reduction
Congenital/
developmental
disorders
Aplasia/
hypoplasia
Progressive mandibular asymmetry or micro
gnathia from early childhood. Development of
malocclusion. Hypoplasia or aplasia of condyle and
hypoplasia of fossa and eminence in imaging
CBCT No treatment if minor. Distraction osteogenesis,
autologous reconstruction, total alloplastic joint
replacement
Hyperplasia Progressive mandibular or facial asymmetry.
Asymmetry in ramus height in imaging. Increased
uptake of technitium-99-hydroxy diphosphonate
CBCT No treatment if minor. Osteotomy
Muscular
conditions
Local myalgia Pain in jaw, ear,
temple, or
preauricular area,
and changed with
jaw function
Pain confined to site of
palpation
Diagnostic criteria
do not involve
laboratory studies
or imaging
Conservative measures, including patient
intraoral appliance therapy, trigger point
injections, anesthetic nerve block, behavioral
therapy
Myofascial pain Pain spreads beyond site of
palpation, but within same
muscle
Myofascial pain
with referral
Pain spreads beyond
muscle palpated
Myositis Trauma, infection, or
autoimmune disease.
Erythema, edema, and/or
increased temperature over
muscle. Serologic testing
may reveal elevated
inflammatory markers or
indicators of autoimmune
diseases
Laboratory studies
(including ANA,
CK, ESR)
Pharmacotherapy, physiotherapy, management
of underlying, infection, autoimmune condition
Myospasm Acute involuntary contraction. Sudden onset of
myalgia and limitation of mouth opening.
Decreased range of motion. Function of muscle
aggravates pain. Increased activity of muscle in EMG
EMG Education, physiotherapy, appliance therapy,
pharmaceutical agents, anesthetic nerve blocks,
behavioral therapy
Contracture Progressive loss of range of motion. Opening
limited with hard end-feel
Diagnostic criteria
do not involve
laboratory studies
or imaging
Physiotherapy
ANA, anti-nuclear antibody; CK, creatine kinase; CRP, C-reactive protein; EMG, intramuscular electromyography ; ESR, erythrocyte sedimentation rate; RF, rheumatoid factor

Kalladka et al
Management
The shift in the role of occlusion from one of causation to being
one of sequelae warrants a change in management. Targeting
the pathologic process through mechanism-based approaches
is necessary for long-term success, especially in instances where
changes in occlusion are secondary to TMDs.
The leading professional societies across the world concur
on the use of conservative measures as the first line for most
TMJD and MMD.10,39
Since most TMDs are self-limiting, the first
line of management should begin with conservative, reversible
procedures.These include home care, pharmacotherapy, short-
term splint therapy, physiotherapy, psychologic counselling,
and behavioral modification techniques.17,40
These modalities
are applicable to several TMDs including arthralgia, arthritis,
DDW/O R, DJD, and MMDs. The diagnostic criteria, diagnostic
aids, and management of changes in occlusion secondary to
TMDs has been detailed in Table 2. The clinical presentation is
based on Peck et al.7
Manual reduction may be attempted in cases of acute DDW/
O R with auriculotemporal or twin block nerve blocks. System-
atic reviews on various treatment modalities (conservative,
minimally invasive, and surgical) for DDW/O R found heteroge-
neity in the included studies and unclear risk of bias, and sug-
gested that the different modalities had comparable therapeu-
tic effects. Therefore, the simplest, least invasive modalities
should be tried first for initial management of DDW/O R, espe-
cially in simple cases without major psychologic symptoms.41
Hypoplasia/aplasia may require distraction osteogenesis,
autologous reconstruction, or total alloplastic joint replacement
if the jaw function or esthetics are not acceptable to the patient.
Condylar hyperplasia may be treated with high condylec-
tomy (preferred in unilateral condylar hyperplasia) or propor-
tional condylectomy in active condylar hyperplasia. However
further studies are needed on the efficacy.42
In TMJ luxation, manual reduction may be used chairside,
followed by physiotherapy strengthening modalities/exercises.
In recurrent cases, dextrose prolotherapy may cause significant
reduction in mouth opening and pain.43
Autologous blood in-
jection alone and in combination with intermaxillary fixation
has been reported to be effective in recurrent TMJ luxation.
However, concerns on its effect on articular cartilage and pos-
sibility of ankylosis have yet to be studied in detail.44,45
Surgical
interventions for management of TMJ luxation are still unclear
and have low quality of evidence for recurrent luxation.46
Regarding joint diseases (DJD, systemic arthritides, ICR),
management of underlying systemic disorders is critical in
managing systemic arthritides. Interdisciplinary management
is often required in complex cases.47
A majority ofTMJ neoplasms and cysts require surgical pro-
cedures.11,48
Accurate diagnosis and distinguishing the original
source is critical to success.49-51
TMJ chondrosarcoma has been
studied systematically and is associated with lower recurrence
and higher survival in comparison with other chondrosarco-
mas. Local recurrence and distant metastasis may be associ-
ated with poor prognosis.52
Synovial chondromatosis cases may be managed by ar-
throscopy or open surgery. Open surgery is the recommended
modality of treatment. Arthroscopy may be effective in cases
less than 3 mm or without extra articular extension.53
Adultcondylarfracturesmaybetreatedbyopenreductionand
rigid internal fixation (ORIF) and closed treatment. A systematic
review comparing the two modalities suggested ORIF may have
better clinical and functional outcomes. In unilateral displaced
subcondylar fractures both modalities provide si
milar results
for protrusive and maximum mouth opening. However closed
treatment resulted in better lateral excursive movements.54,55
Managementofunderlyinginfectionorsystemicautoimmune
disordermayberequiredinadditiontoconservativemodalitiesfor
management of myositis. Physiotherapy modalities may be re-
quiredinmanagementofMMDcontractureandmyofascialpain.56
Current evidence is insufficient to suggest irreversible pro-
cedures like extensive oral rehabilitation for preventative or
management purposes of TMDs. A systematic review by Man-
fredini and Poggio57
suggested there was an absence of RCTs on
the topic related to TMD, bruxism, and prosthodontic planning,
and based on the best available current evidence suggested
that prosthetic changes in occlusion as a management strategy
for TMD and bruxism were not yet acceptable. Another system-
atic review concluded that at present there was insufficient evi-
dence to demonstrate a cause-and-effect relationship between
orthodontics and occlusion, and that orthodontics may not pre-
vent or treat TMDs.58
Conclusion
Systematicreviewssuggestthattheroleofocclusionastheprimary
factorinthegenesisofTMDislowtoverylow.However,avarietyof
TMDs can lead to secondary changes in occlusion. Distinction
between the two is paramount for successful management.
Disclosure
The authors deny any conflicts of interest.

458
GENERAL DENTISTRY
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Mythili Kalladka
Mythili Kalladka Adjunct Assistant Professor, Orofacial Pain and
Temporomandibular Disorders, Eastman Institute for Oral Health,
Rochester, NY, USA
Andrew Young Assistant Professor, Arthur A. Dugoni School of
Dentistry, University of the Pacific, San Francisco, California, USA
Davis Thomas Assistant Clinical Professor, Rutgers School of
Dental Medicine, Newark, NJ, USA
Gary M. Heir Professor, Program and Clinical Director, Center for
Temporomandibular Disorders and Orofacial Pain, Rutgers School
of Dental Medicine, Newark, NJ, USA
SamuelY.P. Quek Professor, Department of Diagnostic Sciences,
Rutgers School of Dental Medicine, NJ, USA
Junad Khan Associate Professor, Program Director, Orofacial
Pain andTemporomandibular Disorders, Eastman Institute for Oral
Health, Rochester, NY, USA
Correspondence: Mythili Kalladka, Adjunct Assistant Professor, Orofacial Pain and Temporomandibular Disorders, Eastman Institute for
Oral Health, Rochester, NY, USA. Email: dr.mythili@gmail.com

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