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Review Article

Timing interventions in relation to temporomandibular joint closed lock duration: a systematic review of ‘locking duration’

M . A L - B A G H D A D I * , J . D U R H A M * & J . S T E E L E

*Department of Oral and Maxillofacial Surgery, School of Dental Sciences, Newcastle University, Newcastle upon Tyne, andDepartment of Restorative Dentistry, School of Dental Sciences, Newcastle University, Newcastle upon Tyne, UK

ABSTRACT

Temporomandibular joint (TMJ) ‘closed lock’ (CL) is a clinical condition causing TMJ pain and limited mouth opening (painful locking) that is mostly attributed to disc displacement without reduction (DDwoR), or less commonly to anchored disc phenomenon (ADP). Both conditions are described clinically as CL that can be ‘acute’ or

‘chronic’ depending on the duration of locking.

There is, however, no consensus about the duration of locking that defines the acute state and its effect on the success of interventions. This review paper, therefore, aims to provide: (i) a narrative review of the pathophysiological need for early intervention in DDwoR and the clinical implications of acute/chronic CL stages on the management pathway; (ii) a systematic review investigating the effects of locking duration on the success of interventions for CL management.

Electronic and manual searches until mid-August 2013 were conducted for English-language studies of any design investigating the effects of non- surgical and surgical interventions for acute or

chronic CL (DDwoR or ADP). A total of 626 records were identified, and 113 studies were included. Data extraction and quality assessment were completed for all included studies. Included studies were, however, heterogeneous and mostly of poor-quality leading to contradictory and inconsistent evidence on the effect of the duration of locking on treatment outcomes. Future high- quality trials investigating the effect of CL duration on treatment outcome are needed. At present, early intervention by ‘unlock’ mandibular manipulation seems to be the most practical and realistic approach that can be attempted first in every CL patient as an initial diagnostic/

therapeutic approach.

KEYWORDS:

acute closed lock, chronic closed lock, disc displacement without reduction, jaw locking, locking duration, temporomandibular joint

Accepted for publication 29 November 2013

Introduction

Temporomandibular joint (TMJ) disc displacement without reduction (DDwoR) is a specific subgroup of temporomandibular disorders (TMDs) where the disc is permanently displaced, most frequently anteriorly or anteromedially, to the condyle resulting in a ‘pain- ful locking’ (1–4). This condition of TMJ pain and locking is known clinically as ‘closed lock’ (CL) (5 –8).

The ‘TMJ closed lock’ term does not, however, always exclusively, refer to TMJ DDwoR because another condition suggested in the literature to have the same

‘hypomobility’ symptoms (i.e. anchored disc phenom- enon ‘ADP’) (9). In this review, the ‘closed lock’ term has only been used to describe the clinical symptoms of the ‘two’ conditions (DDwoR and ADP).

Depending on duration of locking, CL can be acute or chronic (7, 10 –13). The definition of acute and

Journal of Oral Rehabilitation 2014 41; 24--58

J o u r n a l o f

O ral Rehabilitation

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chronic CL stages in relation to locking duration and its implications on ‘early’ management is, however, con- troversial (13, 14). This controversy is related mostly to unproven effect of locking duration on CL treatment outcomes. This paper, therefore, aims to provide:

1 A narrative review of:

a the evidence from a pathophysiological perspec- tive of the need for early intervention in the DDwoR management pathway

b the clinical definition and implications of acute and chronic CL stages.

2 A systematic review of the effects of locking dura- tion on the success of therapeutic interventions in CL. It is explicitly restricted to examining the evi- dence for the effect of duration of symptoms on treatment outcome as the evidence for the effect of different treatments on DDwoR would require a systematic review of randomised clinical trials which is the subject of another review currently coming to completion (15).

Materials and methods

Search methods

A systematic search in Medline database via Ovid for TMJ CL studies was conducted (last update was on:

15th August 2013). The Medline search strategy is available in Appendix S1. Additional searches were also conducted using other sources including hand- searching the reference lists of the included studies and relevant review articles, as well as searching the Google Scholar using ‘disc displacement without reduction’ and ‘closed lock’ keywords.

Criteria for considering studies for the systematic review Inclusion criteria. Studies of any design investigating the effects of any form of non-surgical and/or surgical interventions on patients with clinical and/or radio- logical diagnosis of acute or chronic DDwoR were considered in this review as long as the duration of symptoms were reported. Diagnostic criteria accepted were as follows: American Association of Orofacial Pain (AAOP) (acute or chronic DDwoR) (16); research diagnostic criteria for temporomandibular disorders (RDC/TMD) (IIb or IIc) (17); Wilkes stages III or IV (18); or any other bespoke study criteria that were

compatible with, or comparable to, the aforemen- tioned criteria. Studies involving CL patients with a

‘static’ or ‘fixed’ disc (i.e. anchored disc phenomenon

‘ADP’) (9, 19) were also included.

Studies that involved other heterogeneous groups of TMD patients (e.g. osteoarthritis, myofacial pain, disc displacement with reduction ‘DDwR’) in addition to patients with DDwoR were considered only if: sep- arate data (e.g. success rate and/or locking duration) were provided in the study for DDwoR patients, or if the sample consisted of ≥ 80% DDwoR patients. Stud- ies involving patients with a confirmed diagnosis of DDwoR disorder with comorbid disorders were also included.

Exclusion criteria. Studies were excluded if they did not report the duration of symptoms of their sample or if they addressed diagnoses other than ‘closed lock’

(DDwoR or ADP). Studies were also excluded if they addressed subject matter other than CL treatment.

Data collection and extraction

Selection of studies. The first reviewer (MA) selected eligible studies based on the inclusion/exclusion crite- ria with those identified as clearly irrelevant from their title/abstract being excluded. The full texts of all potentially eligible studies were retrieved and exam- ined. Throughout the selection process, any doubt about a study’s inclusion meant it was examined by the second reviewer (JD) and the decision to include or exclude the study was made by discussion with the first reviewer to reach a consensus.

Data extraction and management. A standardised table was used for data extraction. The data from eligible studies were extracted and recorded by the first reviewer (MA). The second reviewer (JD) cross- checked the extracted data’s validity. The data on duration of symptoms and follow-up period were standardised in months and the data for Visual Ana- logue Scale (VAS) pain successful outcome were stan- dardised, when possible, to (0–100) scale. If not provided, the mean patient age and locking duration was calculated from the raw data using SPSS statistics version 19.0 for windows*.

*SPSS Inc., Armonk, NY, USA.

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Quality assessment. Two independent reviewers (MA &

JD) assessed the quality of study design in the included studies using the National Health and Medi- cal Research Council (NHMRC) level of evidence guidelines for intervention trials (20) with slight mod- ification (Appendix S2). The level of evidence in each study was judged by its design as: (I) highest, (II-1), (II-2), (III-1), (III-2), (III-3), or (IV) lowest. Any dis- agreements concerning the assessment were resolved by discussion to reach a consensus.

Results

Search results

The search strategy identified a total of 626 records from electronic and manual searches (426 from MED- LINE and 200 from other sources). Of these, the full texts of 395 potentially eligible papers were retrieved and examined. Eventually, 113 studies (of 122 reports) were found eligible and included in the sys- tematic review. The study flow diagram is available in Appendix S3.

Narrative review of DDwoR pathophysiology, and the clinical definition and implications of acute and chronic CL stages

Pathophysiology and progression of DDwoR. Patients with DDwoR are often characterised by distinct combina- tions of signs and symptoms: history of clicking fol- lowed by sudden onset of pain and limited mouth opening (locking without clicking) and impaired con- tralateral movement (2, 5, 7, 17, 21, 22). These char- acteristic symptoms are usually present in ‘acute’

DDwoR [CL] (painful limited opening) as opposed to

‘chronic’ DDwoR (decreased pain-improved opening), which makes the clinical diagnosis of the former more readily achievable. The latter may be difficult to diag- nose clinically without magnetic resonance imaging (MRI) (11, 23). The incidence of DDwoR among TMDs is not fully determined but is estimated to occur in about 2–8% (24–27). DDwoR is, however, also diagnosed by MRI in people without any clinical signs or symptoms with a reported prevalence of 3%

among the asymptomatic general population (23, 28 – 30).

The two predominant biomedical complaints in DDwoR are TMJ pain and limitation of jaw move-

ments. The exact cause of pain associated with DDwoR is still not fully understood (31). The dis- placed disc is thought to play an important role in the pain process (32–34), but it is unlikely to be the only source of pain as disc displacement alone is not always associated with pain (29, 35–40). In addition to alteration in disc position, other factors have been suggested in the development of pain: joint effusion and inflammatory reactions (e.g. synovitis, capsulitis or retrodiscitis), and capsule impingement and/or ret- rodiscal tissue compression (31, 41–50).

The other predominant biomedical complaint in DDwoR is the abrupt restriction in jaw movements.

This is usually attributed to mechanical obstruction by the displaced disc to the translating condylar move- ment (1, 2, 5, 21, 51). This condition is often, almost colloquially, termed as ‘closed lock’ (CL) (5 –8). The

‘closed lock’ term, however, describes a clinical symp- tom and not an anatomic diagnosis and the condition of CL is not always exclusively attributed to DDwoR.

Anchored disc phenomenon (ADP) has also been sug- gested as potentially responsible for some of the cases of CL (9, 52). The putative pathogenic processes underpinning ADP are as follows: direct mechanical injury from joint overloading, hypoxia-reperfusion injury, release of free radicals into the synovial fluid, causing degradation of hyaluronic acid and eventually a vacuum effect (suction cup effect). The end result of these proposed pathological processes leads to disc adherence to the roof of the glenoid fossa. The adhered or ‘stuck’ disc then totally prevents the con- dylar sliding movement producing a more pro- nounced lock but that responds better to arthrocentesis than DDwoR (9, 52–55). Whether ADP is a distinct entity from DDwoR, or a differing stage of the same clinical entity, is still debatable (56) due to the degree of similarity between the signs and symp- toms of the two conditions. This similarity makes the differentiation of the two conditions based on clinical diagnosis alone virtually impossible and differentiation on the basis of MRI (19) is doubtful as all bar one ADP study (57), involve patients with displaced discs as well as normally positioned discs (55, 58, 59). Fur- ther studies with MRI evidence of a normally posi- tioned disc in CL patients are required to gain a better understanding of ADP and whether it is a separate entity within the ‘closed lock’ category (57, 60).

The course of DDwoR disorder has been shown to

be ‘favourable’ (14, 61 –66). Studies on the natural

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course of ‘chronic’ DDwoR have shown that in about two-thirds of patients, the clinical signs and symp- toms tend to resolve or improve over a period of (6–30 months), while the other one-third did not improve or became worse during the observation per- iod (14, 61, 63, 67). A recent study on the short-term natural course of ‘acute’ DDwoR demonstrated that signs and symptoms resolved in 95% of patients over 3 months of observation (68).

The improvement over the time in some patients with DDwoR may be attributed to stretching and remodelling of the retrodiscal tissues and ‘pseudo’ disc adaptation (44, 69–74). Despite the increased range of jaw motion and decreased pain, several studies have demonstrated that the displacement of the disc and the deformation of the disc/condyle complex increases (14, 61, 63, 65, 75 –81). There are also some indica- tions that the permanently displaced disc may be cor- related with alterations in maxillofacial skeletal morphology in the long term (82–88).

The TMJ is a load-bearing joint and its articular tis- sues have a remarkable adaptive capacity to mechani- cal loading (89 –91), but this capacity is not infinite.

Sustained overloading may increase the susceptibility to degenerative joint disease (31, 71, 92–94) and other risk factors may adversely influence the adap- tive capacity of the articular tissues including age, sys- temic illness, hormonal, nutritional, traumatic, mechanical and genetic factors (91, 92, 95–99). A degenerative state can, therefore, ensue if functional demands surpass the adaptive capacity or if the affected individual is susceptible to maladaptive responses (92). In general, the molecular events that underlie TMJ remodelling and adaptation are still not fully understood (92), and the molecular and cellular basis of DDwoR pathophysiology is still unclear, but there is some biochemical evidence of increasing sus- ceptibility to osteoarthritic degeneration in ‘chronic’

CL patients (100–107).

Three models have been proposed that may be involved in the pathogenesis of degenerative TMJ dis- eases: the direct mechanical trauma model, the hypoxia-reperfusion model and the neurogenic inflammation model (108). The molecular events and cascades in response to mechanical stress in these models may ultimately lead to an imbalance between catabolic and anabolic events leading to catabolism (degeneration) of the articular tissues in the affected joints (91, 92). The risk of degenerative changes in

joints with DDwoR was shown to be four times greater than in joints with normal disc position (109), and suggestions were made that the propensity for degenerative disease was mediated by an imbalance in the patient’s adaptive capacity and functional load- ing of the TMJ. The study concluded that a careful, individualised, assessment of each DDwoR patient was required to evaluate the various factors that might contribute towards the progression to degenera- tive disease (109).

At present, the line separating normal adaptive responses from responses that result in (degenerative) disease is ill-defined. It may, therefore, be difficult to predict the DDwoR prognosis in an individual patient (71). In fact, TMJ DDwoR is a disorder with two pos- sible scenarios. On one hand, it is a benign self-limit- ing disorder in which most of patients’ symptoms improve with the passage of the time and do not nec- essarily progress to degenerative joint disease (69, 77, 110, 111). On the other hand, DDwoR can be also a debilitating disorder causing significant pain and dys- function that disturbs the patient’s quality of life with the potential for persistence of symptoms and degen- erative progression in susceptible patients in the longer term (71, 109, 112–115). Both scenarios are possible in DDwoR patients, and it is still not clear which patients have, or which biomechanical and bio- chemical factors predict, the greatest risk of progress- ing to the more advanced stages (116). This means that it is important to treat all patients early in the time course of DDwoR to prevent disease progress in susceptible patients (117–119). This ‘early’ manage- ment will also prevent progression from an acute to a chronic condition, thereby avoiding the possibility of developing chronic pain and its psychosocial conse- quences in symptomatic DDwoR patients (120–122).

Any initial active intervention, however, should be simpler and less invasive than waiting for possible symptomatic resolution during the ‘favourable’ natu- ral course of the DDwoR disorder (68).

Clinical definition and implications of acute versus chronic CL stages. The term ‘acute’ is usually related to a tem- porary state or condition which may or may not be severe, while the term ‘chronic’ is related to a state or condition that is persistent or long lasting and again does not imply anything about severity (123, 124).

Both medical terms are often used as measures of the

time scale of a disease rather than its severity. In pain

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conditions, ‘acute pain’ usually refers to pain of recent onset with a duration ≤1 month (≤30 days), while

‘chronic pain’ usually refers to a persistent pain with a longer duration (≥3 months or ≥90 days) (125, 126). In a CL condition, the terms ‘acute closed lock’

(ACL) and ‘chronic closed lock’ (CCL) are widely used in the CL literature usually describing the chronicity of DDwoR. The most reliable diagnostic criteria for TMDs (17, 22, 127 –129) depend, however, primarily on the patients’ signs and symptoms rather than the duration of symptoms to classify acute versus chronic DDwoR (Appendix S4). In clinical trials involving patients with DDwoR, however, most authors usually define their samples based on the duration of symp- toms (i.e. locking duration or time since DDwoR onset), although there is considerable variation in the threshold that defines acute and chronic stages rang- ing from 1 to 6 months (Appendix S5). In the authors’ opinion, a more appropriate clinical classifi- cation of acute and chronic CL could be based on the time scale for the possibility of recapturing the displaced disc to return the DDwoR to its previ- ous condition (i.e. DDwR) with a non-invasive inter- vention.

In DDwoR (CL), both patient and management fac- tors have been suggested to predict the outcomes. The predictors suggested include the following: age, gen- der, level of pain, range of mandibular motion, dura- tion of locking, joint inflammation, disc mobility, severity of disc displacement, stage and degree of morphological and pathological changes in disc/con- dyle complex, and type, frequency, and duration of therapy (114, 130 –144). The role of these factors in predicting CL treatment outcome is, however, still debatable. In fact, these ‘prognostic’ factors may inter- relate or interact with each other to a greater or lesser degree and there are still not significant data on the role psychosocial factors may have in predicting out- come in CL. To give an example, the severity of intra- articular pathological changes and the stage of inter- nal derangement may increase with the age of the patient and/or duration of locking. Some of the afore- mentioned predictive factors are, however, easily accessible through standard history and clinical exam- ination, whereas others require either more advanced imaging (e.g. MRI) or investigations (e.g. arthros- copy). Duration of locking is very simply estimated by self-report, although the accuracy of report may be influenced by several factors including recall bias.

The possible mechanism for jaw locking and DDwoR progression from ‘acute’ to ‘chronic’ has been proposed to begin as a displaced disc obstructing the forward condylar translation resulting in restricted mouth opening (acute stage); the repeated attempts to increase mouth opening then displace the disc gradually farther forward to an anterior position, so the condyle can slide forward, and the mouth open- ing range increases with the ‘time’ (chronic stage) (2, 116, 145). From a clinical perspective, the progression from an acute to a chronic DDwoR over the time can affect treatment outcome as patients may respond dif- ferently to a similar therapeutic intervention depen- dent on locking duration (114, 146). This coupled with the fact that the two most frequently measured outcomes to assess treatment effectiveness tend to improve over time (increased opening and decreased pain) (131), may be one of the reasons for confusing outcomes reported in the literature around the man- agement of DDwoR: the effectiveness of treatments and authors’ findings in their studies may vary because of varying levels of chronicity in their sample.

A systematic review of CL studies was, therefore, con- ducted to investigate the effects of locking duration on the success of therapeutic interventions.

Systematic review of effects of interventions in relation to CL duration

Multiple different non-surgical and surgical treatment modalities have been used for CL management. The interventions identified from the studies included in this review were defined according to their main treatment components: mandibular manipulation (MM); self-management (SM); physiotherapy (PT);

splint therapy; combination therapy of splint + PT  SM; arthrocentesis (AC); arthroscopy (AS); open sur- gery (OS). A detailed description of each treatment strategy is available in Appendix S6.

To investigate the effects of interventions in relation

to locking duration, the characteristics and quality of

the included studies were tabulated and summarised

in Tables 1 –6. The interventions’ success rates pro-

vided in the tables are based on the success criteria

used by each included study. The definition of success

was, therefore, highly variable involving both objec-

tive and subjective factors with the most frequent

measures being mouth opening and pain levels

(Tables 1–6).

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Table1.Characteristicsofincludedmandibularmanipulation(unlockmanipulation‘UM’orpumpingmanipulation‘PM’)studies Study(Year) Study design Participants’characteristics MainIntervention assessed Longest follow-up duration (months)Successcriteria Studyfindingsinrelation toCLduration Overallsuccess rate%(ITTuse)

Study design quality

Samplesize (drop/exc) Study diagnosis GenderAge(years)Lockingduration(months) MFRangeMeanRangeMeanSD ChibaandEchigo (2005)(117)

CR1DDwoR (ACL) 121033Farrar’sUMaunder LA+ARS

137Decreasedpain, cMMO40mm,&DR onMRI

––IV Correaetal.(2009) (147)

CR1DDwoR11836UMunderLA+ARS, NSAIDs,cryotherapy 24cMMO>40mm––IV Fosteretal.(2000) (148)

PNCoSt55(19)22CL (DDwoR) &14IL 74815–52243–4813ForcedUMunderGA+ Self-careSplint 3MMO35mm& subjective improvement Therangeoflocking duration(6–48)was similarinSG&UG.

CL:409% (noITT)

III-3 Helkimoand Hugoson(1988) (149)

PCS10DDwoR3717–632941–36122Farrar’sUMunderN2O/ O2sedation+SS 6Improvementin:pain, jawdysfunction (Di:I–II),LM,& MMO40mm Longerlockingduration inUG20(12–36)than inSG108(1–30).

60%IV Hernandezand Karibe(2004)(150)

CR1DDwoR128025UMunderLA+Med, PT(US),SS, Self-exercises 1MMO40mm––IV Jagger(1991)(151)PCS12DDwoR4815–432181–93UM(owntechnique)MMO35mmLockingDurationisnot animportantfactorfor UMsuccess

667%IV Kaietal.(1993) (152)

PCS12bDDwoR11111–61303301–205053UMorPM+ARS1Improvementinclinical symptoms& MMO40mm 583%DRon arthrography.

667%IV Kuritaetal.(1999) (132)

PNCoSt74/215 assessed byMRI DDwoR767325114Farrar’sUM+ARSor NSAIDorSS FewwksDRonMRINosignificantdifference inlockingduration betweensuccessfulDR (10191)andnoDR (128246).

18%(noITT) 9%(ITT)

III-3 Liuetal.(2012) (153)

RNCoSt3623CL (DDwoR) &13IL 63013–31198<3UMunderLA+ARS6Improvementin:pain, MMO,&jaw dysfunction.

DDwoR:696%IV Martinietal.(1996) (154)

PCS13/1500 reported DDwoR––19–56314023–18036025347UM(owntechnique)+ ARS,PT 2–24Absenceofpain, MMO35mm,&DR onMRI Lockingdurationisnot relatedtoUMsuccess.

997%IV Minagietal.(1991) (135)

PCS35DDwoR23312–683594025–18326409UM(owntechnique)MMO40mmNodifferenceinsuccess ratebetween<1mo (50%)&>1mo(53%) duration.

514%IV (continued)

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Table1.(continued) Study(Year) Study design Participants’characteristics MainIntervention assessed Longest follow-up duration (months)Successcriteria Studyfindingsinrelation toCLduration Overallsuccess rate%(ITTuse)

Study design quality

Samplesize (drop/exc) Study diagnosis

GenderAge(years)Lockingduration(months) MFRangeMeanRangeMeanSD Monginietal. (1995;1996) (113,155)

PCT75(7)DDwoR76813–43278025–1201332184Extra-oralUMunder LA+ARS,SS,Med,PT 18–147Nopainorpainpresent onlyonjaw movement& MMO35mm Nodifferenceinlocking durationbetweenSG& UG.44%DRonMRI.

868%(noITT)IV Muhtarogullarietal. (2013)(156)

PNCoSt22DDwoR31914–48271325UM+ARSif unsuccessfulDR: SS+Self-exercises 6Nopainonpalpation, MMO40mm,normal LM&PrM 159%DRonMRI100%III-3 Murakamietal. (1987)(157)

PCS10DDwoR1914–462891–947PM+CS+ARS6AAOMScriteria: increaseincMMO Nodifferenceinlocking durationbetweenSG& UG.PMhelpstounlock theCLuptoabout6mo

70%IV Murakamietal. (1995)(12)c

PCoSt108W:III(CL)208831435088 5669 68102 NS:Med/UM/PS, N=63;AC,N=20 AS,N=25 6VASpain<20, MMO>38mm,LM& PrM>6mm,& improvedDAL Patientswith>7mo lockingdurationdidnot respondtoarthrocentesis NS:556% (Med:159% UM:189% PS:333%) AC:70% AS:91%

III-2 Ohnukietal. (2006)(137)c

RCoSt85DDwoR97613–734185168 104131 668 142222

SS,N=11 PM,N=33 AC,N=9 AS,N=32

12VASpain<20& MMO>38mm

Nosignificantdifference betweenSGregarding lockingduration.10% DRonMRIamongall groupswithno differencebetween groups.

Med:0% SS:129% PM:446% AC:22% AS:100%

III-3 Ozawaetal. (1996)(158)

RCS40DDwoR43616–68381501–12019583399PM ACL(01–027), N=5;CCL(2–120), N=35 007–3 (ACL:2–3dy CCL:2–3mo) Improvementinpain& MMO35mm Highersuccessratein ACL(100%)thanin CCL(371%).PMable toreleaseacutelocking only.

686%IV Segamietal. (1990)(139)

PCS28DDwoR32514–57254007–2447Farrar’sUMorPM+ ARS&NSAIDs 2Noorslightpain& MMO40mm NorelationbetweenMM technique(UMorPM)& lockingduration.367% DRonarthrography.

100%IV (continued)

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Table1.(continued) Study(Year) Study design Participants’characteristics MainIntervention assessed Longest follow-up duration (months)Successcriteria Studyfindingsinrelation toCLduration Overallsuccess rate%(ITTuse)

Study design quality

Samplesize (drop/exc) Study diagnosis GenderAge(years)Lockingduration(months) MFRangeMeanRangeMeanSD Simmons (2002)(159)

CR1DDwoR11405PMunderIV-sedation+ ARS 24Improvementin: cMMO,LM,PrM, subjective improvement,&DR onMRI

––IV Singh(2010)(160)CR1DDwoR (Chronic)

13224UMunderLAwith CS+IMFscrews& elastics+ARS 025Improvementin:VAS pain,cMMO

––IV VanDykeand Goldman(1990) (161)

PCS41DDwoR (Acute) ––15–2UMunderIM-LA (owntech)+ARS MMO40mm927%IV Yoshidaetal.(2005) (141)

RCT305DDwoR7622918–740033–<12UM(owntechnique)+ NSAID,N=204 NSAIDonly,N=101 025VASpain<20, MMO36mm, LM6mm,&DR onMRI

UMsuccessratedrops significantlywiththe increaseinlocking duration:1-2dy(100%), <1wk(983%),<2wk (946%),<3wk(90%), <1mo(571%),<2mo (167%),<6mo(0%).

UM:843% NSAID:0%

II-2 Yoshidaetal. (2011;2013) (114,162)

RCT148DDwoR14819–75400033–9 0067–11

157 173

Self-UM,N=74 Notreatment,N=74 10minutesAbsenceofpain& MMO>38mm Lockingdurationwas shorterinSG(118) thaninUG(292).

S-UM:68% Ctrl:4%

II-2 TOTAL19studies 6studies

DDwoR DDwoR

003–180 007–120

893 798

UM PM

DRaveragesuccess rate:44% (range:44%–997%) 676% 699%

RCT,randomisedcontrolledtrial;Q-RCT,quasi-randomisedcontrolledtrial;PCoSt,prospectivecomparativestudy;RCoSt,retrospectivecomparativestudy;PCCSt,prospectivecase–controlstudy;PNCoSt,prospectivenon-comparativestudy;RNCoSt,retrospectivenon-com- parativestudy;FSt,follow-upstudy;PCS,prospectivecaseseries;RCS,retrospectivecaseseries;BACS,before-aftercaseseries;BACR,before-aftercasereport;CR,casereport;AAOMS,Americanassociationoforalandmaxillofacialsurgery;ACL,acuteclosedlock;ARS, anteriorrepositioningsplint;CCL,chronicclosedlock;Ch,chronic;CMI,CranioMandibularIndex;cMMO,comfortable‘painless’maximummouthopening;CS,corticosteroids;Ctrl,control;DAL,dailyactivitylimitation;DDwoR,discdisplacementwithoutreduction;DR, discrecapturing;drop,drop-outs;dy,day;exc,excluded;Exr,exercises;F,female;GA,generalanaesthesia;ID,internalderangement;IL,intermittentlocking;ITT,intention-to-treatanalysis;IV,intravenous;j,joint;LA,localanaesthesia;LDF,limitationindailyfunction; LM,lateralmovement;M,male;Med,medication;MFIQ,mandibularfunctionimpairmentquestionnaire;mm.millimetres;MMO,maximummouthopening;mo,month;MR,musclerelaxant;MRI,magneticresonanceimaging;N,numberofpatients;NS,non-surgical; NSAIDs,non-steroidalanti-inflammatorydrugs;OS,opensurgery,PrM,protrusivemovement;PM,pumpingmanipulation;PS,pivotsplint;PT,physiotherapy;Reh,rehabilitation;S&S,signsandsymptoms;SD,standarddeviation;SG,successfulgroup;SH,sodiumhyaluro- nate;SM,self-management;SS,stabilisationsplint;Sub-ac,sub-acute;S-UM,self-unlockmanipulation;UG,unsuccessfulgroup;UM,unlockmanipulation;US,ultrasound;VAS,VisualAnalogueScale;W,Wilkesstagingofinternalderangement;wk,week;yr,year. aDescriptionofFarrar’sUMtechnique(2)isavailableinAppendixS7(figure). bSeparatedataprovidedareforDDwoRpatientsonly. cStudydataarealsoprovidedinothertablesaccordingtomaintreatmentmodalityassessed.

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Table2.Characteristicsofincludedself-management(SM)andphysiotherapy(PT)studies Study(Year) Study design Participants’characteristics Main interventions assessed Longest follow-up duration (months)Successcriteria Studyfindingsin relationtoCL duration Overallsuccess rate%(ITTuse)

Study design quality

Sample size (drop/exc) Study diagnosis GenderAge(years)Lockingduration(months) MFRangeMeanRangeMeanSD Braun(1987)(163)CR1DDwoR171075Self-exercises+ Iontophoresis

15Absenceofpain, MMO>40mm, LM>7mm,improved jawfunction,& eatingnormaldiet

––IV ClelandandPalmer (2004)(164)

BACR1DDwoR12419SM+PT3VASpain<20, MMO40mm,& improvedjaw function

––IV Craaneetal.(2012) (165)

RCT49(7)DDwoR247366wks–yrsExercises,N=23 Educationonly, N=26 13Improvementin: VASpain,MMO, &MFIQ

––(ITT)II-1 Haketaetal.(2010) (145)a

RCT52(14)DDwoR646376Over05Self-care+SS, N=25;Self-care+ Self-exercise, N=19 2Improvementin: VASpain,MMO, &LDF

––(ITT)II-1 Minakuchietal. (2001;2004) (166,167)a

RCT69(8)DDwoR76234389556 281509 312503 Educationonly, N=21 Self-care/NSAIDs, N=23 SS+Exercises+Self- care/NSAIDs, N=25 2Improvementin: VASpain,MMO, &DAL

––(ITT)II-1 Nicolakisetal. (2001)(136)

BACS20(2)51537312–60156Active&passive jawexercises 6Improvementin: VASpain,MMO, &DLA

85%(ITT)III-3 Schiffmanetal. (2007;2013) (168,169)a

RCT108(12)W:III–IV (DDwoR) 8983172Non–ch <6ch6SM+Med,N=29 SS+PT+CBT, N=25 AS+CS,N=26 OS,N=26 60Self-reportedsuccess (Patientsatisfaction)SM:72% Reh:81% AS:762% OS:833%(ITT)

II-1 Srisintorn(1992) (170)

CR1DDwoR1292Self-care/NSAID+ Self-exercises

12cMMO40mm––IV (continued)

(10)

Table2.(continued) Study(Year) Study design Participants’characteristics Main interventions assessed Longest follow-up duration (months)Successcriteria Studyfindingsin relationtoCL duration Overallsuccess rate%(ITTuse)

Study design quality

Sample size (drop/exc) Study diagnosis GenderAge(years)Lockingduration(months) MFRangeMeanRangeMeanSD YuasaandKurita (2001)(142)

RCT60(NR)DDwoR (15ACL, 45CCL) 124816–69Median28053–2507 063–418

Median233 Median327

NSAIDs+self- exercise,N=30 Notreatment, N=30 1AAOMS&IAOMS modifiedcriteria: VASpain33& MMO35mm CCL(>1mo) respondedbetterto treatmentthan non-treatmentin comparisonwith ACL(≤1mo) SM:60% Ctrl:33%(ITT)

II-1 Total2studiesDDwoR–––PT(Stretching exr.)–– 7studiesDDwoR–––SM(self-care/ Med/Exr)––66% RCT,randomisedcontrolledtrial;Q-RCT,quasi-randomisedcontrolledtrial;PCoSt,prospectivecomparativestudy;RCoSt,retrospectivecomparativestudy;PCCSt,prospectivecase–controlstudy;PNCoSt,prospectivenon-comparativestudy; RNCoSt,retrospectivenon-comparativestudy;FSt,follow-upstudy;PCS,prospectivecaseseries;RCS,retrospectivecaseseries;BACS,before-aftercaseseries;BACR,before-aftercasereport;CR,casereport;AAOMS,Americanassociationof oralandmaxillofacialsurgery;AC,arthrocentesis;ACL,acuteclosedlock;ARS,anteriorrepositioningsplint;AS,arthroscopy;CBT,cognitivebehaviouraltherapy;CCL,chronicclosedlock;Ch,chronic;CMI,CranioMandibularIndex;cMMO, comfortable‘painless’maximummouthopening;CS,corticosteroids;Ctrl,control;DAL,dailyactivitylimitation;DDwoR,discdisplacementwithoutreduction;DR,discrecapturing;drop,drop-outs;dy,day;exc,excluded;Exr,exercises;F, female;GA,generalanaesthesia;ID,internalderangement;IL,intermittentlocking;ITT,intention-to-treatanalysis;IV,intravenous;j,joint;LA,localanaesthesia;LDF,limitationindailyfunction;LM,lateralmovement;M,male;Med,medi- cation;MFIQ,mandibularfunctionimpairmentquestionnaire;mm.millimetres;MMO,maximummouthopening;mo,month;MR,musclerelaxant;MRI,magneticresonanceimaging;N,numberofpatients;NS,non-surgical;NSAIDs,non- steroidalanti-inflammatorydrugs;OS,opensurgery,PrM,protrusivemovement;PM,pumpingmanipulation;PS,pivotsplint;PT,physiotherapy;Reh,rehabilitation;S&S,signsandsymptoms;SD,standarddeviation;SG,successfulgroup; SH,sodiumhyaluronate;SM,self-management;SS,stabilisationsplint;Sub-ac,sub-acute;UG,unsuccessfulgroup;UM,unlockmanipulation;VAS,VisualAnalogueScale;W,Wilkesstagingofinternalderangement;wk,week;yr,year. aStudydataarealsoprovidedinothertablesaccordingtomaintreatmentmodalityassessed.

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