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Received: 11 June 2020 Revised: 22 September 2020 Accepted: 2 October 2020
DOI: 10.1111/scd.12535
CASE H ISTORY REPORT
Insights for temporomandibular disorders management:
From psychosocial factors to genetics—A case report
Samilla Pontes Braga1 Lívia Maria Sales Pinto Fiamengui2
Virgínia Régia Souza da Silveira3 Hellíada Vasconcelos Chaves3
Bruno D’Aurea Furquim4 Carolina Ortigosa Cunha5
Carlos Eduardo Palanch Repeke6 Paulo César Rodrigues Conti7
1 Faculty of Dentistry at Sobral, Federal
University of Ceará, Fortaleza, Brazil
2 Department of Restorative Dentistry,
Federal University of Ceará, Fortaleza,
Brazil
3 Faculty of Dentistry at Sobral, Federal
University of Ceará, Sobral, Brazil
4 Private Practice, Londrina, Brazil
5 Health Science Center, Sacred Heart
University Center, Bauru, Brazil
6 Department of Dentistry, Federal
University of Sergipe at Lagarto, Lagarto,
Brazil
7 Bauru Dental School, University of Sao
Paulo, Bauru, Brazil
Correspondence
LíviaMaria Sales PintoFiamengui, Rua
MonsenhorFurtado, S/N,RodolfoTeófilo,
CEP60430-350, Fortaleza-Ceará, Brazil.
Email: livia_holanda_@hotmail.com;
liviamspf@ufc.br
Funding information
FAPESP (FundaçãodeAmparo àPesquisa
doEstadode SãoPaulo)
Abstract
Aims: This case report aimed to discuss the multifactorial etiology and also
the management of temporomandibular disorders (TMD) by addressing impor-
tant associated psychosocial and biological factors, emphasizing the interaction
between these factors and a probable genetic predisposition.
Methods and results: A 21-year-old female patient was evaluated according to
Research Diagnostic Criteria for TMD and diagnosed with arthralgia, myofascial
pain, disc displacement without reduction, and temporomandibular joint (TMJ)
degenerative disease. TMJ alterations were confirmed through magnetic reso-
nance imaging and cone-beam computed tomography. Pressure pain threshold
of masticatory structures was evaluated using a pressure algometer. Sleep brux-
ism, poor sleep quality, migraine with aura, mild anxiety, and history of facial
trauma were also identified through anamnesis and clinical examination. Fol-
lowing this, genetic analysis was performed to evaluate the presence of single
nucleotide polymorphisms (SNPs) already associated with TMD: SNP COMT
Val158Met (rs4680), MMP1-1607 (rs1799750), and tumor necrosis factor alpha-308
(rs1800629), which were all present. A personalized treatment for TMD man-
agement was performed, and it included self-management programs, occlusal
appliance therapy, pharmacotherapy, anxiety management, and stress control.
An 8-year follow-up demonstrated long-term stabilization of TMJ degenerative
disease.
Conclusion: Genetic evaluation, added to anamnesis and clinical examination,
could be useful for TMD prognosis and management.
KEYWORDS
etiology, pain, polymorphism, single nucleotide, temporomandibular joint disorders
© 2020 Special Care Dentistry Association and Wiley Periodicals LLC
Spec Care Dentist. 2020;1–7. wileyonlinelibrary.com/journal/scd 1
https://orcid.org/0000-0002-2746-2219
mailto:livia_holanda_@hotmail.com
mailto:liviamspf@ufc.br
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2 BRAGA et al.
1 INTRODUCTION
The American Academy of Orofacial Pain describes tem-
poromandibular disorders (TMD) as a group of disor-
ders involving the masticatory muscles, the temporo-
mandibular joint (TMJ), and associated structures.1 Acute
or chronic pain is the most common symptom, normally
being worsened during oral functions.1 TMD incidence is
approximately 3.5% per year,2 and its chronicity is associ-
ated with genetic risk factors,3 events of injury to the jaw,
parafunctional and overuse behaviors, and pain or other
functional disorders elsewhere in the body, among others.4
Genetic variations have been associated to different pat-
terns of pain perception and also with elevated suscepti-
bility for pain conditions.5 Genes associated with exper-
imental pain perception6 and with the increased risk of
TMD development3 have been identified. It is hypothe-
sized that genetic variants interact among themselves and
with a variety of environmental factors to influence pain
sensitivity and the expression of chronic pain conditions.7
Single nucleotide polymorphism (SNP) is a variation on
the DNA sequence due to change in a single nucleotide.8
This variation can be classified as an SNP, when it occurs
in more than 1% of a population, and can influence sus-
ceptibility to diseases or its progression and response to
therapies;9 therefore, strategies to identify genetically reg-
ulated pathways relevant to TMD have been performed.10
Catecholamine-O-methyltransferase (COMT) is an
enzyme related to regulation of catecholamines and
enkephalins levels,11 and six SNPs within the COMT gene
locus present high frequency in humans.12 One of those,
SNP rs4680, produces a change in amino acid composi-
tion, coding for a substitution of valine (val) to methionine
(met) at codon 158. This substitution produces a COMT
enzyme with decreased activity, which increases the pain
perception5,13 and TMD development.5 Polymorphims in
COMT has also been associated to anxiety.14
Individuals with TMD present heightened plasmatic15
and synovial cytokine levels16 like tumor necrosis fac-
tor alpha (TNF-α), which strongly contributes to inflam-
matory and immune responses by inducing a cascade of
various inflammatory cytokines.17 Polymorphism in the
human TNFα promoter at−308, involving the substitution
of guanine by adenosine in uncommon alleles, is a more
powerful transcriptional activator than the common allele
and is associated with high TNF-α production.18 A higher
prevalence of SNP TNFα-308 has been found in individu-
als with TMD,19,20 and it has been hypothesized that the
polymorphic rare allele comprises a risk determinant for
TMD.19
Matrix metalloproteinases (MMPs) are enzymes that
mediate the remodeling or degradation of the extracellular
matrix of the articular disc and cartilage.21 Functional
genetic polymorphisms in the promoting region of the
MMPs genes may modify basal and inducible genetic
expression of those enzymes,22 and this mechanism
may contribute to extracellular matrix degradation of
TMJ cartilage.21 MMP-1 is involved in the degradation of
collagen types I, II, and III,23 and SNP described in the
-1607 MMP1 1G/2G rs1799750 gene promoter has been
associated with increased risk of TMJ degeneration22 and
anterior disc displacement.21
The comprehension regarding the involvement of
genetic variations on TMD onset and perpetuation may
conduct to a more appropriate individualized treatment24
and prognosis.25 Thus, the present study aimed to describe
a TMD clinical case where extensive anamnesis, psychoso-
cial assessment, imaging, and genetics investigations were
made in order to perform a TMD diagnosis and personal-
ized management.
2 CASE REPORT
In 2012, a 21-year-old female presented with a chief com-
plaint of pain on the right TMJ (graded as 5 according to a
0-10 visual analogue scale), limitation on mouth opening,
and pain on masticatory muscles. During anamnesis, the
patient reported history of chin trauma at the age of 7, pre-
vious migraine with aura diagnosis made by a neurologist
and self-reported sleep bruxism.
After anamnesis and clinical examination, complemen-
tary exams and validated questionnaires were used to do a
survey of possible risk factors associated with TMD. First,
she was evaluated according to the Research Diagnos-
tic Criteria for Temporomandibular Disorders (RDC/TMD
Axis I), Beck Anxiety Inventory (BAI), Beck Depression
Inventory (BDI), and Pittsburg SleepQuality Index (PSQI).
Signs and symptoms of sleep bruxism were analyzed
according to those proposed by the American Academy of
Sleep Medicine.26
Pressure pain threshold (PPT) was also evaluated by
using a digital algometer (KRATOS, Cotia, Brazil). This
device has a 1 cm2 flat circular-shaped tip at oneendwhich
was used to apply the pressure over masticatory muscles
and TMJ. The pressure application rate was set at approx-
imately 0.5 kgf/cm2/s. The masseter belly, anterior tem-
poralis, and lateral pole of the TMJ were tested bilaterally
with the patient in a relaxed position.27
Genetic analysis was performed to evaluate the pres-
ence of three SNPs: COMTVal158Met (rs4680), MMP1-1607
(rs1799750), and TNFα-308 (rs1800629). Saliva samples
were collected according to the manufacturer’s instruc-
tions using the Oragene DNA self-collection kit. DNA was
extracted from epithelial buccal cells with sequential phe-
nol/chloroform solution and precipitated with sal/ethanol
BRAGA et al. 3
F IGURE 1 Magnetic resonance imaging revealing bilateral disc displacement without reduction. A, right TMJ, closed mouth; B, right
TMJ, open mouth; C, left TMJ, closed mouth; and D, left TMJ, open mouth
solution.28 A spectrophotometer (Nanodrop 1000; Thermo
Scientific Waltham, Mass) was used to quantify and qual-
ify the DNA samples.19 COMT Val158Met, MMP1-1607, and
TNFα-308 genotyping was performed using a TaqMan
chemistry (Applied Biosystems, Warrington, UK) held in
3μL reactions. The polymerase chain reaction (PCR) was
performed using 10 ng of sample DNA, 1X TaqMan SNP
genotyping assays, 1X TaqMan Universal MasterMix, H20
q.s.p. 5 μL. The PCR cycle conditions are as follows: 60◦C
for 30 seconds, 95◦C for 10 seconds, followed by 40 cycles
at 92◦C for 15 seconds, 60◦C for 60 seconds, and 60◦C for
30 seconds.20
During clinical examination, the patient presented a
straight opening pattern. Pain-free opening measured
34 mm while painful at maximum unassisted opening
measured 46 mm. Mandibular range of motion dur-
ing lateralization and protrusion were normal. TMJ was
assessed by magnetic resonance imaging (MRI) and cone-
beam computed tomography (CBCT). MRI revealed bilat-
eral disc displacement without reduction (Figure 1). On
CBCT, it was observed condyles flattening and osteophyte
(Figure 2).
According to RDC/TMD, the patient presented bilat-
eral myofascial pain (masseter and temporalis muscles),
right TMJ arthralgia, bilateral disc displacement without
reduction (confirmed byMRI), and bilateral TMJ degener-
ative disease (confirmed by CBCT), whichwas classified as
osteoarthritis on the right TMJ, once it was accompanied
with pain, and as osteoarthrosis on the left one.29 Accord-
ing to BAI, BDI, and PSQI, the patientwas classified as hav-
ing poor sleep quality, mild anxiety, and no depression.
The PPT values for masticatory muscles and TMJ are
shown in Table 1. Genotypes of SNPs evaluated are shown
in Table 2.
Treatment plan was based on reducing pain-related
symptoms and TMJ overload - in order to reduce
degenerative joint disease progression - and included: self-
management programs (education, thermal therapy, pain-
free diet, parafunctional behavior identification, monitor-
ing, and avoidance),30 use of occlusal appliance during
sleep, pharmacotherapy (nonsteroidal anti-inflammatory
drug and muscle relaxant), and anxiety management.
Also, the patient was informed and educated regarding the
identification of geneticmarkers that could influenceTMD
4 BRAGA et al.
F IGURE 2 Bilateral TMJ cone-beam computed tomography (initial). A and B, Sagital view in closed mouth position of right and left TMJ,
respectively. At the right and left TMJ, it can be detected flattening and osteophyte. C, Axial view of right and left TMJ, detecting sclerosis at
right TMJ. D, Coronal view of right and left TMJ, detecting flattening on both TMJs
TABLE 1 Pressure pain threshold (PPT) values (Kgf/cm2) of
TMJs and masticatory muscles
Site PPT
Right TMJ (lateral pole) 2.14
Left TMJ (lateral pole) 2.38
Right anterior temporalis 3.80
Left anterior temporalis 2.78
Right masseter 2.68
Left masseter 2.40
TABLE 2 Genes’ polymorphisms investigated with genotypes
Gene/single nucleotide
polymorphisms (SNP) Genotype
COMT Val158Met (rs4680) G>A GG
MMP1 −1607 (rs1799750) 2G2G
TNFα-308 (rs1800629) A>G AA
Abbreviations: A, adenosine; G, guanine.
predisposition and management, and that environmental
factors togetherwith the identified genetic polymorphisms
could influence pain sensitivity,12,13,20 development of
chronic pain,7 and progression of TMJ degeneration.22
During reevaluation after 1month, patient reported pain
improvement and scarce pain episodes, commonly related
to stress. Due to this information, patient self-management
education was reinforced, and the role of stress control
and improvement of coping strategies in TMD manage-
ment were emphasized. At the time of reevaluation after
6 months, patient reported great improvement in pain,
mouth opening, and psychological status, the last being
achieved by psychotherapy and physical exercise.
Recently, in 2020, 8 years after the first evaluation, the
patient was invited for a new follow-up. She declared mild
pain in both TMJ and moderate masticatory muscles pain
occurring only during stressful events, which also trig-
gers a migraine attack that is followed by pain on masti-
catory structures and neck. Overall, patient reported pre-
senting a good sleep quality, but pain episodes were also
related to events of poor sleep and periods with absence of
physical activity. Jaw mobility was normal, and no func-
tional limitation was detected. Also, the patient declared
using occlusal appliance while sleeping during this whole
period (which has been replaced three times). Another
CT was performed and revealed no progression of TMJs
degenerative disease (Figure 3). The patient was referred
to a neurologist and to a psychotherapist. The practice
of mindfulness/meditation was also suggested for stress
control.
3 DISCUSSION
The identification of specific pain phenotypes31 and
genotypes32 has been proposed as predictive for treatment
response. To our knowledge, it was the first case report
genetic-based personalized treatment for TMD manage-
ment. In the present case report, a young female patient
with history of facial trauma, poor sleep quality, sleep brux-
ism, migraine, mild anxiety, and self-reported stress pre-
sented with myofascial pain of masticatory muscles, TMJ
BRAGA et al. 5
F IGURE 3 Bilateral TMJ multidetector computed tomography for recent follow-up. A and B, Sagital view of right TMJ, in closed mouth
and open mouth position, respectively. C and D, Sagital view of left TMJ, in closed mouth and open mouth position, respectively. At the right
and left TMJ, it can be detected flattening and osteophyte. E, Axial view of right and left TMJ, detecting sclerosis at right TMJ. F, Coronal view
of right and left TMJ, detecting flattening on both TMJs
arthralgia, disc displacement without reduction, and TMJ
degenerative disease. Genetic analysis showed the pres-
ence of SNPs of COMT Val158Met (rs4680), MMP1-1607
(rs1799750), and TNFα-308 (rs1800629).
Several biological, clinical, and psychological
factors3,4,33 associated with TMD are recognized in
this clinical case. The relationship among pain-related
TMD, migraine34, stress35, anxiety,35 and sleep quality15
has already been established. Genetic variants are poten-
tial risk factors for chronic TMD due to the modulation
of central and peripheral pathways,25 and SNPs inves-
tigations reported here may corroborate with findings
previously discussed on the literature.
The SNP of COMT Val158Met (rs4680) influences pain.5
The genotypes GG (Val/Val), GA (Val/Met), and AA
(Met/Met) are associated with high, intermediate, and
low enzyme activity, respectively.5 Enzymatic reduction
activity causes elevation on catecholamines levels, such
as dopamine, epinephrine, and norepinephrine, promot-
ing increased pain sensitivity probably via β2/3-adrenergic
receptors.13 In the present study, the patient presented the
genotype GG (Val/Val), which is related to high COMT
enzyme activity, reduction on catecholamines levels, and
consequent lowered pain sensitivity.5 This finding proba-
bly explains the fact that, even presenting pain complaintand several TMD diagnoses, the patient presented PPT val-
ues compatible with those of asymptomatic individuals.27
In 2011, a pilot study demonstrated COMT gene variants
may act as genetic predictors for treatment outcomes.32
Authors found that individuals with low COMT activity
were beneficiated from a nonselective β-adrenergic recep-
tor antagonist propranolol therapy, while patients with
high COMT enzyme activity - such as in the present case
report - presented no benefit. Those findings are prelimi-
nary, and larger studies are still needed to establish COMT
genetic contributions to therapeutic responses.
The articular surface of TMJ is covered with fibrocarti-
lage that contains type II collagen and a high amount of
type I collagen, which is degraded by MMP1.23 Planello
et al22 showed association between 2G2G MMP1 geno-
type (rs1799750) and a higher risk for TMJ degeneration.
On the other hand, the authors found that 1G2G geno-
type was associated with a protective effect against TMJ
degeneration. Besides, high levels of MMP1 have been
found on TMJ’s synovial fluid with mild and severe inter-
nal derangement36 and osteoarthritis.37 In the present case
report, we hypothesize that the presence of 2G2G MMP1
genotype (rs1799750) may have influenced TMJ degenera-
tion process, especially due to the history of facial trauma,
which may explain the early onset of the disease. 2G2G
genotype has also been associated with increased suscep-
tibility to anterior disc displacement without reduction,21
which corroborates with our findings.
In the present case report, 2G2GMMP1 genotype-guided
treatment plan in terms of patient education; prescrip-
tion of nonsteroidal anti-inflammatory drug to reduce
pain, synovial inflammatory mediators, and consequent
release of MMPs; and occlusal splint therapy in order
to reduce TMJ overload due to prolonged microtrauma
(sleep bruxism). The prescription of oral supplements,
6 BRAGA et al.
such as glucosamine and chondroitin, have been sug-
gested for their chondro-protective effects, however, stud-
ies regarding theirs efficacy are still conflicting.38 When
combined to hyaluronate sodium-intra-articular injection,
oral glucosamine hydrochloride seems to provide pain
relief caused by TMJ osteoarthritis and improve TMJ func-
tions in a long term.39 In the present study, this approach
was not suggested due to the stabilization of TMJ degener-
ation (evidenced by CT) and also because of improvement
on pain and jaw mobility with the conservative treatment
proposed.
TNFα-308 polymorphism is also associated with TMD.
According to Furquim et al (2016),19 26.97 % of TMD
patients present the rare A-allele, while the same geno-
type was found in only 13.18% of healthy control, with an
odds ratio of 2.454. Subjects with TMD had a 2.87 times
greater chance of having the GA genotype than the control
group. The same study showed that individuals presenting
A-allele homozygotes had decreased pain sensitivity on
TMJ and anterior temporalis muscle, when compared to
G-allele homozygotes. Those findings corroborate with the
present case report, since the patient presented A-allele
homozygotes and TMJ low pain sensitivity measured
by the pressure algometer. Although this allele may be
related to lowered pain sensitivity, it is associated with a
higher production of TNF-α.18 Other study found higher
frequency of TNFα-308 SNP (GA+AA) in TMD patients,
but no influence on pain sensitivity.20 Future studies to
elucidate the role of SNP TNFα-308 in TMD pain are still
needed.
4 CONCLUSION
The present case report suggests that new approaches
regarding genetic polymorphisms investigations, added to
anamnesis, clinical examination, and images exams could
be useful duringTMDdiagnosis andmanagement. Genetic
analysis may be important to identify risk assessment, sus-
ceptibility, therapeutic intervention, as well as prevention
strategies.
ACKNOWLEDGMENTS
We would like to thank FAPESP (Fundação de Amparo à
Pesquisa do Estado de São Paulo) Brazil for financial sup-
port (Grant Number: 2010/19181-7).
CONFL ICT OF INTEREST
The authors declare no conflict of interest.
CONSENT APPROVAL
The patient gave permission to use clinical information
and photographic material.
ORCID
LíviaMaria Sales PintoFiamengui https://orcid.org/
0000-0002-2746-2219
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How to cite this article: Braga SP, Fiamengui
LMSP, da Silveira VRS, et al. Insights for
temporomandibular disorders management: From
psychosocial factors to genetics—A case report.
Spec Care Dentist. 2020;1–7.
https://doi.org/10.1111/scd.12535
https://doi.org/10.1111/scd.12535
	Insights for temporomandibular disorders management: From psychosocial factors to genetics-A case report
	Abstract
	1 | INTRODUCTION
	2 | CASE REPORT
	3 | DISCUSSION
	4 | CONCLUSION
	ACKNOWLEDGMENTS
	CONFLICT OF INTEREST
	CONSENT APPROVAL
	ORCID
	REFERENCES