predisposing and precipitating.pdf

7/23/2019 Predisposing and Precipitating.pdf

http://slidepdf.com/reader/full/predisposing-and-precipitatingpdf 1/20

Predisposing and PrecipitatingFactors in Temporomandibular DisordersRoss H. Tallents, S. Stein, D. J. Macher, R. W. Katzberg, and W. Murphy

The hyperdivergent facial profile presents the orthodontist, oral surgeon,and restorative dentist with problems that might not be solvable withany one or all of our specialties. This article will review the literature onthe possible predisposing and precipitating factors that might contributeto hyperdivergent facial profiles. We will attempt to correlate facialmorphology as it might relate to disk displacement (DD) and degenera-tive joint disease (DJD). Human and animal studies will be reviewed thatsupport these observations. Our hypothesis is that this hyperdivergent

facial profile is often associated with bilateral DD and/or DJD. The effectof DD/DJD in animal and human studies and the effect of cartilagedegeneration on hard and soft tissues will be reviewed. The presence ofcatabolic biological markers of joint degeneration (interleukin-1, inter-leukin-6, matrix metalloproteinases, tumor necrosis factor-, C-reactiveprotein, synovial fluid proteins) and anabolic markers (tissue inhibitors ofmetalloproteinases, interleukin-4, interleukin-10, interleukin-13) will bediscussed. Epidemiologic studies suggest that in patients presentingwith temporomandibular joint pain, there is a strong correlation between

the disorder and severe mandibular retrognathia in adult women (oddsratio, 6.3). Human cephalometric studies will demonstrate that bilateralDD/DJD is highly correlated with the hyperdivergent facial profile. Fol-low-up orthognathic surgery studies suggest that correction might beunstable. This review will present a compelling case that the hyperdiver-gent facial profile is strongly correlated with bilateral DD and/or DJD.Clinicians should be aware of these findings and convey this information

to patients presenting for dental treatments. (Semin Orthod 2012;18:10-29.) © 2012 Elsevier Inc. All rights reserved.

T emporomandibular joint disorder (TMD)is a collective term embracing several

clinical problems that involve the masticatory musculature, the temporomandibular joint

(TMJ) and associated structures, or both.1

Disk displacement (DD) and osteoarthritis(OA) or degenerative joint diseases (DJDs) areoften associated with TMJ pain. DD with re-duction (DDR) is frequently associated with aclicking sound, and DD without reduction(DDN) is often associated with limitation of jaw opening.2 OA can be recognized radiolog-ically, surgically, and pathologically by find-ings such as mandibular condyle flattening,deformity, sclerosis, and osteophytes on thearticular surface margins.3,4 There are degen-eration of the disk and areas of erosion of thearticular cartilage of the condyle and temporalbone.3,4 Females are more commonly affect-ed.5-8 It has been suggested that DD alters

Professor of Dentistry, Eastman Institute for Oral Health, Divi-

sions of Orthodontics and Prosthodontics, Rochester, NY; Clinical Professor, Eastman Institute for Oral Health, Division of Orthodon- tics, Rochester, NY; Clinical Professor, Eastman Institute for Oral Health, Division of Orthodontics, Rochester, NY; Professor, Depart- ment of Radiology, Davis Medical Center, Sacramento, CA; Com- puter Programmer, Howard Proskin Associates, Rochester, NY.

Address correspondence to Ross H. Tallents, DDS, Eastman Institute for Oral Health, 625 Elmwood Avenue, Rochester, NY 14620. E-mail: [email protected]

© 2012 Elsevier Inc. All rights reserved.1073-8746/12/1801-0$30.00/0 doi:10.1053/j.sodo.2011.09.003

10 Seminars in Orthodontics, Vol 18, No 1 (March), 2012: pp 10-29

mailto:[email protected]

mailto:[email protected]



mandibular growth, sometimes resulting in aretrognathic facial profile.9-12

Some authors suggest that the prevalence of TMD begins to rise in late adolescence and in-creases through middle age and is associated

with female sex, facial trauma, and specific ana-tomical and occlusal relationships.13 For exam-ple, abnormal mandibular morphology 10-14 orincreased horizontal overlap15 are potential cor-relates with mandibular morphology. In fact,subjects with TMD with horizontal overlap 4mm significantly differ from controls.16 It is not clear whether the disharmony of the facial skel-etal structure is caused by the TMJ disorder or vice versa.

This review will examine the skeletal featuresof subjects (asymptomatic volunteers) with bilat-

eral normal joints (controls), compared withsymptomatic subjects with bilateral TMJ DD andDJD.9 The contribution of internal derange-ment of the TMJ will be evaluated and the pos-sible effect on treatment outcomes and cranio-facial form. Data from animal and humanstudies (magnetic resonance imaging [MRI],cephalometrics, lavage) will be used to developthis hypothesis. An explanation of the chain of events that might occur resulting in a change incraniofacial form will be discussed. We will thenpose questions that the clinician should consider

when treatment planning for patients with ret-rognathia and/or hyperdivergent facial profile. All subjects in this study (control and experi-mental) had bilateral MRI scans in the sagittalclosed and open and coronal closed positions toevaluate for the presence of internal derange-ment.9 Rheumatoid and psoriatic arthritis wereruled out by using findings from bilateral MRI.

Why should there be a concern? First concernis poor results for nonsurgical and/or surgicaltreatment with or without pain (lack of potentialor expected growth). Second concern is post-

treatment pain, and third concern is both sce-narios. Fig. 1 shows a patient treated with anocclusal splint. There were no presplint recordsto compare, but the patient stated that her “bitegot worse” after wearing an occlusal splint. Thehorizontal overlap was 7 mm. The second case isa postorthodontic treatment female patient whohas developed an open bite (Fig. 2). This casedemonstrates instability with the original out-come.

These 2 cases demonstrate a moderate openbite, which should pique our curiosity of why this skeletal feature is present. The followingsections will elucidate why we might have mini-mal control of the underlying, preexisting con-

ditions in children and/or adults.

Background: Prevalence ofDD in Humans

DD of the TMJ has been suggested to be com-mon in symptomatic and asymptomatic subjects.Recent studies have used arthrography and MRIto evaluate asymptomatic volunteers.17,18 Theprev alence of displacement ranged from 0%-32%.17-19 Other joints (knee, cervical spine, andlumbar spine) have been studied in asymptom-

atic volunteers. Abnormalities in the absence of pain ranged from 16%-33%.20-25 A more recent study compared MRI findings in 82 asymptom-atic v olunteers and 263 symptomatic adult pa-tients.26 DD was observed in 33% of the asymp-tomatic volunteers and 84% of the symptomaticpatients. These data suggest that DD is morecommon in symptomatic subjects but empha-sizes that DD is common in adult volunteers.26

Ribeiro et al27 found that the prevalence of DD in asymptomatic children and young adults was 34%, whereas the prevalence of DD was 86%in symptomatic children. Their results showed

that 13.8% had bilateral symptomatic but nor-mal joints, 28% had unilateral DD, and 58% hadbilateral DD. These 2 studies26,27 suggest that DDs in symptomatic children and young adultsand adults are equal, suggesting that the poten-tial for joint remodeling (OA) might start at a young age. In asymptomatic volunteers t he prev-alence of DDN/DJD was 2% in adults26 and 1%in children and young adults.27 It is important tonote that these volunteers (adults and children) were screened for the absence of joint sounds,limited jaw motion, locking, and facial symme-

try, therefore a low pre valence of DJD.Nebbe and Major28 have evaluated consecu-

tive and nonconsecutive subjects entering anorthodontic department. They have suggestedthat in a consecutive sample there were 8.8% onthe right and 3.3% on the left of boys with fullDD with loss of morphology. For girls there were23.8% on the right and 18% on the left with fullDD with loss of morphology. These percentagesmight seem to be high, but these are patients

11Predisposing and Precipitating Factors in TMD



seeking orthodontic treatment; they are not asymptomatic volunteers.

In the nonconsecutive sample28 there were9.1% on the right and 40% on the left of boys with full DD with loss of morphology. For girlsthere were 36% on the right and 40% on the left with full DD with loss of morphology. We areassuming that DD with loss of morphology issynonymous with DDN. These percentagesmight seem high, but these are patients present-

ing for orthodontic treatment and not screenedfor the presence of TMD symptoms.

In another study evaluating condyle positionfrom their preorthodontic sample, 45% of thesubjects had DD.29 The above data suggest inter-nal derangement is common in children as wellas adults.13,27-29 The following review will evalu-ate the potential effects of DD, specifically bilat-eral DJD, on the facial skeleton in animal mod-els and in human subjects.

Animal Studies

Strategies to study the effects of unilateral andbilateral DD on facial growth (mandibular andmaxillary) have been performed in rabbits.30-34

Unilateral DD in Animals

Hatalla et al32 evaluated the skeletal effect of unilateral DD in the young New Zealand Whiterabbit. The gross appearance of the condyles

demonstrates shortening and flattening of thearticulating surface in the experimental group(Fig. 3). No significant shortening and flatten-ing were found in the control group (no surgi-cally induced DD), suggesting that surgically cre-ated DD can induce remodeling in the TMJresulting in altered morphology and growth of the maxilla and mandible. The histologic ap-pearance of the control and experimentalgroups is seen in Fig. 4.

Figure 1. This cephalometric x-ray (A) represents a 10-year-old girl with TMJ pain and locking. We can assumethat she has bilateral DDN by history. Note the Class II molar relationship, anterior open bite, and horizontaloverlap of 7 mm. (B) Panorex film. There does not seem to be small or flattened condyles or antegonialnotching. Still this patient has some features of patients with chronic DJD, high mandibular plane angle, andhorizontal overlap 4 mm, convex facial appearance, and short posterior face height as demonstrated by Gidarakou et al.9

12 Tallents et al



In fact, superimposition of the normal side of the rabbit and human over the experimentalside demonstrates the tipped back sagittal pro-file of the mandibular ramus,31 which has beenalso suggested by Gidarakou et al9 and Dib-

bets.12,14 In the human and rabbit tracings there were 5 subjects in each group used to produce abest-fit comparison (Fig. 5).31

Several authors have suggested that early carti-lage degeneration caused by OA is primarily re-

Figure 2. This clinical presentation represents a 24-year woman who had orthodontics as a teenager. Note theopen bite that extends posterior to the first molar area. The Panorex demonstrates small deformed condyles.

With this clinical presentation the suspicion of bilateral degenerative joint is evident, associated with condyle/ramus shortening. (Color version of figure is available online.)

Figure 3. The skull and mandible of the rabbit have been de-fleshed. Note the flattening of the condylar head(superior arrows) on the displaced side (right) compared with the contralateral side (left). Note also that thereis remodeling of the coronoid process (inferior arrows) on the right side compared with the left.




lated to changes in the proteoglycans (PGs) and inthe collagen network.35-41 Mechanically, cartilagedegeneration is characterized by an increase inthickness, decrease in stiffness, increase in perme-ability, and increased water content. In severely damaged cartilage, cracks initiate at the articularsurface and extend downward into the superficial,middle, and eventually deep zone.35-41

Hatala et al32 demonstrated that there was lossof PGs in the experimental animals. PGs give car-tilage its tensile stiffness and compressive strength,allowing the disk to distribute the load. Loss of PGs

allows the disk to fragment and deform.Qadan et al33 investigated the effect of unilat-

eral TMJ DD on the mandibular condyle, mid-face, and cranial base. The occlusal radiographdemonstrated that the glenoid fossa on the ex-perimental side was located more anterior and was remodeled (Fig. 6). The oblique radiographdemonstrated that the root of the zygomaticarch on the experimental side was inferior.33

This suggests an alteration of the cranial base

Figure 4. The 4 histologic sections (A-D) represent a normal joint (A), immediate DD (B), 2-week DD (C), and4-week DD (D). In (A) the posterior band, intermediate zone, and anterior band can be visualized (black arrows). In(B) the anteriorly displaced disk can be seen flexed anterior to the condylar head. In (C) the eminence (E) andcondyle (C) are flattened and eroded. The articular covering is gone, and the medullary bone is exposed at 2 weeks.

Also the morphology (anterior, intermediate, and posterior zones) is lost. In (D) (4 weeks) there is a return of thearticular covering (E, C), the disk is deformed, and there is synovial hyperplasia (open arrow). The articular coveringhas hypertrophied on the condylar head (open arrow). (Color version of figure is available online.)

Figure 5. Superimposition on left is of the rabbit, andthe right is the human. Five rabbits with unilateralsurgically created DD and 5 humans with unilateralDDR were included in the study. Superimposition of anormal side of the rabbit and human over the exper-imental side demonstrates the tipped back sagittalprofile of the mandibular ramus similar to that pres-ent in subjects with high mandibular plane angles.(Color version of figure is available online.)

14 Tallents et al



that is induced by DD, resulting in an asymmet-ric cranial base.

Puzas et al42 suggested that rabbit TMJ diskcells appear to undergo changes seen in OA.Furthermore, disk and articular cells express ma-trix metalloproteinase (MMP)-9 and interleukin(IL)-1, which are present in OA in humans. We will evaluate the presence of proinflammatory cytokines and metalloproteinases from joint lavage studies later in this article.

Bilateral DD in Animals

Bryndahl et al34 have suggested that in rabbits,bilateral nonreducing TMJ DD retarded man-dibular growth, similar to the mandibular ret-rognathia seen in humans. Displacement of therabbit TMJ disk during the growth period in-duced condylar cartilage adaptive reactions that were associated with an adverse amount anddirection of mandibular growth, manifesting ina retrognathic mandibular growth pattern.

Ribeiro et al,27 Katzberg et al,2 and Nebbeand Major28 have suggested that DD is commonin asymptomatic children. DD in young rabbitsalters growth of the mandible, which was similarto the observations in children. In a condyleposition study, Kamelchuk et al29 also suggestedthat 45% of patients presenting for orthodontictreatment have DD. This probably representssubjects who are asymptomatic and some of whom have asymptomatic clicking and lockingand/or some with possible pain.

Induced Arthritis in Transgenic Mice

In an effort to study the histology and immunohis-tochemistry of OA, Lai et al43 examined the effectsof genetically induced intra-articular induction of IL-1 expression in adult transgenic mice. They demonstrated that induction of IL-1 expressionin the TMJ of adult mice led to development be-havioral changes, including increased orofacialgrooming and decreased resistance to mouth

Figure 6. The left skull (control) and right (experimental) are demonstrated. Note in the control animal (A)that the glenoid fossa (left arrow) are symmetric and foramen ovale (right arrow) are symmetric. In experimentalanimal (B) the glenoid fossa (left arrow) and foramen ovale (right arrow) are asymmetric, suggesting a lack of growth on the experimental side.




opening. Orofacial grooming and resistance to jaw opening were used as measures of nociception anddysfunction, respectively. There was significant in-crease in expression of the pain-related neu-rotransmitter calcitonin gene-related peptide

(CGRP) in the sensory ganglia as well as the aux-iliary protein CGRP receptor component proteinof the calcitonin-like receptor in the brainstem, which further substantiated the induction of pain.This somatic mosaic model induces joint changes

similar to OA and also altered condyle morphol-ogy (Figs. 7, 8).

Biological Markersfor Joint Degeneration

Molecular Markers

Molecular markers are used for the detection of osteoarthritic changes in joints in an early stageof the disease. These different markers are cru-

Figure 7. (A) TMJ from a control. (B) TMJ from an experimental mouse where arthritis has been inducedgenetically by using IL-1, a proinflammatioy cytokine. Note the irregular surface and depth of the articularsurface compared with (A). (C) Higher-magnification view of (A). (D) Abnormal cartilage architecture withcellular disorganization and chondrocyte hypertrophy are evident (brace indicates cartilage erosion). (E)Higher-magnification view showing signs of surface erosions (arrows indicate lacunae forming on the surface of TMJ condyle in experimental mice). (F) Higher magnification of (D) with microscopic fibrillations throughout the surface of the articular cartilage. (Color version of figure is available online.)

16 Tallents et al



cial for understanding the pathophysiology of OA, whether the knee or TMJ is being studied.For this review we used these studies to support the contention that this neuroinflammatory cas-cade is responsible for loss of articular cartilageand degeneration as well as pain. In the TMJ thismight also contribute to the shortening of ramalheight or a disturbance in cranial facial growth.For a review of catabolic and anabolic molecularmarkers for stimulation and inhibition, see the

review in Bonnett and Walsh.44

Synovitis

Chronic synovitis is associated with markedchanges in the central connections of sensory nerves and changes in their synthesis and releaseof neurotransmitters and neuromodulators.45

Inflammation might exacerbate cartilage degra-dation in OA. Patients with OA in whom radio-

logic scores progress rapidly tend to have higherserum concentrations of C-reactive protein at baseline than do those whose disease progressesslowly.46,47 Tumor necrosis factor-alpha (TNF-)and IL-1 stimulate chondrocytes to produceMMPs and plasminogen activator, which de-grade matrix PG and collagen.48,49 Chondro-cytes also produce further IL-1 that acts in anautocrine manner and further stimulates MMPand plasminogen activator production.50

OA, which represents tissue injury in joints, isassociated with proinflammatory cytokines andgrowth factors (IL-1, TNF-). They regulate car-tilage remodeling as catabolic (IL-1, TNF-),acting on target cells to increase products that enhance matrix degradation (MMPs) and anti-catabolic (IL-4, IL-10, IL-13), tending to inhibit orantagonize the activity of the catabolic cytokineson chondrocytes to increase synthetic activity.50

Figure 8. PG content was evaluated by safranin O fast green histochemistry (purple stain on green background).(A) Control mouse (purple stain represents PGs). (B) In the experimental mouse the purple stain has decreased,

which represents loss of PGs. Articulator cartilage changes were also evaluated by type II collagen (CII)immunohistochemistry in control (C) and (D) experimental mice. Overall, we observed an induction of CIIstaining (brown) (D) in the hypertrophic articular zone of TMJs in experimental mice not seen in controls.(Color version of figure is available online.)




Lavage Studies

Lavage studies support these observations in theknee51 and TMJ.52-57 Smith et al51 found evi-dence of thickening of the lining layer, in-

creased vascularity, and inflammatory cell infil-tration in synovial membranes from patients with all grades of OA in the knee. The most marked changes seen in synovial tissue werefrom patients with advanced grades of OA. Pro-duction of IL-1, IL-1, and TNF- was present in synovial membranes from all patients withOA, irrespective of the degree of articular carti-lage damage. They suggested that low-grade sy-novitis results in the production of cytokines andcontributes to the pathogenesis of OA.

Similar findings have been demonstrated in

the TMJ and will be discussed below.Mizui et al52 examined MMP-2 activity in sy-novial lavage fluid of patients with disorders of the TMJ and explored the possible correlationbetween MMP-2 activity and radiologic changes.They studied 86 patients and 10 healthy volun-teers. Symptomatic patients were divided into 3groups on the basis of arthrographic findings:no abnormality (n 36), internal derangement (n 39), and OA (n 11). Active MMP-2 insymptomatic subjects was detected in 9 of 36 with no abnormality (25%), 14 of 39 with inter-

nal derangement (36%), and 5 of 11 with OA (45%). No active form of MMP-2 was detected inthe healthy volunteers. The incidence of activeMMP-2 was high in the internal derangement group and highest in the OA group, which sug-gests that active MMP-2 plays an important rolein joint degeneration (DJD). An interesting find-ing was that patients with normal but painful joints had a 25% detection rate for MMP-2. Pre- vious studies26,27 have demonstrated that pa-tients with normal findings on MRI or arthrog-raphy have symptomatic but painful joints. This

might suggest that catabolic/stimulators of car-tilage breakdown (MMPs, IL-1, and TNF-)might be present in the absence of DD.

Segami et al53 found evidence of joint effu-sion (JE) on MRI, suggesting synovial inflamma-tory activity. This confirms the common consen-sus that JE probably reflects synovitis (cellscapable of producing proinflammatory cyto-kines) especially because synovial hyperplasiahas a key role in the pathogenesis of JE.

Ijima et al54 injected IL-1 into the joint of the rat to study MMP activity of cultured rat TMJchondrocytes and disk cells. They found that MMP-9 and MMP-3 were predominantly pro-duced by disk cells, and these might be consid-

ered to play a pivotal role in extracellular matrixdegradation during pathologic conditions of theTMJ, such as IL-1–induced TMJ arthritis. Thesefindings are supported in the transgenic modelof Lai et al.43

Ishimaru et al55 measured MMPs and tissueinhibitor of metalloproteinases (TIMP) in pain-ful and nonpainful subjects. They found that synovial fluid (SF) concentration of MMP-3 wassignificantly increased in the painful group com-pared with controls.

Kubota et al56 used SF from 22 symptoma-

tic joints in 25 patients with internal derange-ment or osteoarthritis (TMJ-OA). There were 15asymptomatic controls from 11 normal volun-teers and 10 osteoarthritic knee joints. Theirfindings suggest increased levels of cytokines(IL-1 and IL-6) and SF protein. SF from patients with internal derangement showed higher (P .05) levels (330.1 347.7 pg/100 g SF protein)of IL-l than the asymptomatic control TMJs(76.7 95.3 pg/l00 g SF protein). SF fromTMJs with OA contained significantly (P .05)higher levels of IL- (531.8 379.6 pg/100 gSF protein) and IL-6 (979 552 pg/l00 g SF

protein) than those with DD (IL-l: 216.7 280.1 pg, IL-6: 293 434 pg). The findings that IL-, IL-6, and total SF protein are increased aresimilar to other joints as suggested by other au-thors.44,51

Lohmander et al57 reported that concentra-tions of MMPs, TIMPs, and PG fragments from SFof the knee joint were significantly elevated inpatients with OA, when compared with volunteers with healthy knees. MMP concentrations in diseasegroups averaged 15-45 times those of the controls.

The above studies suggest that IL-1, IL-6,

TNF-, MMPs, TIMPs, IL-4, IL-6, IL-10, IL-13,and total SF protein43,50-57 are present in joints with pain and/or OA (ie, the knee and TMJ)and are credible markers for cartilage break-down. Interestingly, Mizui et al52 found MMP-2activity in 9 of 36 (25%) symptomatic but nor-mal joints studied with arthrography. Bilaterally normal but painful joints have been found inclinical studies in adults (42 of 263, 16%)26 andchildren (25 of 181, 14%).27

18 Tallents et al



Condylar Resorption

Condylar resorption has been associated withrheumatoid arthritis, TMJ internal derange-ment, condylar fractures, connective tissue orautoimmune diseases, orthodontic treatment,and orthognathic surgery. In most cases, how-ever, there is no identifiable precipitating event,hence the term idiopathic condylar resorption .58

This would have a diagnosis of OA associated with DD in the TMJ. We would suggest that thelavage studies provide evidence associated withcartilage degeneration. It is rapid and unex-pected in some patients. An example of severeresorption is seen in Fig. 9. This patient wasseronegative for rheumatoid arthritis.

Arnett et al 59 suggested that there is consistent osseous resorption of the postglenoid spine and

posterior condylar surface when the condyle is

posterior and compressed in the glenoid fossa.Because of the prevalence of DD in asy mptomaticand symptomatic children and adults,26-28 thesefindings are not surprising. Whether the posteriorcondyle is related or unrelated could only be eval-

uated with longitudinal studies. A recent article by Gunson et al60 suggested that condylar resorptionmight be a result of low estrogen levels. The use of birth control (ethinyl estradiol) or prematureovarian failure induces low circulating 17-estra-diol and makes it impossible for the natural repar-ative capacity of the condyle to take place in theface of local inflammatory factors.

Human Cephalometric Studies

Several studies by Gidarakou et al9,61-65 in hu-

mans have compared the effects of DD on

Figure 9. The cephalogram (A) represents a patient with bilateral TMJ pain. The arrow points to the anteriorteeth; note the horizontal overlap prior to splint treatment. Maxillary occlusal splint was constructed, and at 1-week follow-up the mandible has been displaced posteriorly and vertically (B). There is now an anterior openbite. The arrow points to the anterior teeth; note the increase in the horizontal overlap. The Panorex (C)demonstrates a small flattened mandibular condyle on the left (right arrow) and a severely degenerated condyleon the right side (left arrows). This patient was seronegative for rheumatoid arthritis. The mandible retruded,has an anterior open bite, and is only occluding on the molars, and there is condylar resorption.




craniofacial morphology, particularly symptom-atic bilateral DD patients with DJD.9 Cranialbase, profile analysis, denture base patterns, and vertical relationships were compared in asymp-tomatic volunteers and symptomatic patients

(Fig. 10).Gidarakou et al9 demonstrated that subjects

with bilateral DJD were shown to have bimaxil-lary retrusion (Frankfort Horizontal [FH] to Na-sion – Point A [Na-A]), (FH to Nasion-Pogonion[Na-Pg]). Maxillary and mandibular denturebases were also shown to be more retrusive (Sella-Nasion – Point A [SNA] and Sella-Nasion –Point B [SNB]) in subjects with bilateral DJD,and the maxillary and mandibular denture basesdiffered from each other significantly (Point A-Nasion-Point B [ANB]) as compared with con-

trols. The maxilla was found to be shorter (An-terior nasal spine [ANS] – Posterior nasalspine[PNS]) in bilateral DJD subjects as com-pared with controls. These data suggest that thesagittal position and horizontal projection of themaxilla, mandible, and their respective denturebases might be affected in patients with bilateralDJD.

The denture pattern of subjects with DJDshowed differences in the relation of the oc-clusal plane ([FH]-Occlusal Plane [OP] wasincreased), maxillary incisor position (U1 to[Point A] A-Pg [Pogonion] was increased), and

lower incisor position (L1 to OP was decreased),as compared with normal subjects.

The 2 groups were found to have several ver-tical relationships that differed significantly.Subjects with bilateral DJD had increased man-

dibular plane angle (MP to FH, [Sella] S-Gn[Gonion] to FH), shorter ramal height (Ar [Ar-ticulare] – [Gonion] Go), and increased gonialangle (Ar-Go-Gn [Gnathion]) as compared withnormal subjects. Facial proportions also differedsignificantly, with bilateral DJD subjects showingincreased lower face height (ANS – Me [Men-ton]) and a decreased upper face height/totalface height ratio (UFH:TFH). The bilateral DJDsubjects also showed significant increases in Pal-atal Plane (PP) to FH, PP to OP, and PP to MP.The antegonial notch was shown to be more

acute in subjects with DJD as well.These findings suggest that patients with DJDhave more hyperdivergent relationships of theirmaxillo-mandibular skeleton and increasedlower anterior facial proportions. Their mandib-ular morphology showed lack of vertical devel-opment, a possible disturbance in the growthand development of the TMJ (which is recog-nized as a secondary center for facial growth),and/or condylar degeneration with correspond-ing mandibulo-maxillary changes. The resultssuggest that maxillary incisors were more pro-truded and mandibular incisors were more ret-

roclined, resulting in an increased overjet rela-tionship as compared with controls. This loss of condylar height and/or growth because of DDcauses or worsens the horizontal and verticaloverlap and shortens the ramus, producing amandibular deficiency. Bryndahl34 has demon-strated that bilateral DD in the rabbit results ininhibition of mandibular growth and a moreretrognathic facial profile.

Ferrario et al66,67 demonstrated that normo-divergent and hyperdivergent mandibles dif-fered mostly at gonion, the coronoid process,

sigmoid notch, alveolar process, posterior bor-der of the ramus, and along the mandibularplane. A significant size effect was also found, with smaller mandibles in the hyperdivergent girls. Each experimental subject with DJD had ahyperdivergent facial profile, more lingual tilt-ing of the maxillary incisors, and a steeper in-clined occlusal plane. The conclusions were that there was a significant correlation between thestructure of the lower face and TMD.

Figure 10. This graphic compares the control (black)and experimental (red in the online version) sub-

jects.9 These data suggest that there is a cant of thepalatal plane, points A and B are retruded, the Frank-fort plane is more obtuse, and the ramus height isreduced. (Color version of figure is available online.)

20 Tallents et al



Other authors have found bony changes onthe articular surface of the mandibular condylein patients with TMJ internal derangement.68-70

Oberg et al71 also suggested that deviations inform and morphology are more common in the

lateral third of the condyle.

OrthognathicSurgery and TMD Symptoms

Kerstens et al72 have demonstrated that patientsundergoing orthognathic surgery, with no priorsymptoms, might exhibit TMD after surgicaltreatment. Open bite or large horizontal over-lap of the incisors should be viewed as a riskfactor before the initiation of orthodontics,prosthodontics, routine oral surgery (ie, third

molar extraction), or orthognathic surgery. Theskeletal features of these subjects might suggest an increased risk for mandibular pain and dys-function. This might be an expression of condy-lar changes (OA) producing arthrosis (remodel-ing), which has been suggested in severalstudies.9,73-77

Several authors have examined orthognathicsurgery patients both preoperatively and postoper-atively and have found that patients presenting with high mandibular plane angles, Class II mal-occlusion featuring retrognathia, or open bite with vertical maxillary excess and retrognathia are

more likely to have TMJ signs and symptoms pre-operatively and are more likely to develop and ormaintain them postoperatively.78-84

Kahnberg85 studied 13 patients who had max-illary impaction for correction of open bite and vertical maxillary excess. None had clinical oranamnestic TMJ signs or symptoms preopera-tively. More than 60% of the patients developedTMJ symptoms during the 6- to 30-month fol-low-up period.

Kerstens et al72 studied 480 orthognathic sur-gery patients both preoperatively and postoper-

atively. Preoperative TMJ symptoms were seen in16.2% of the 480 patients. After surgery 66% of the preoperatively symptomatic patients re-ported fewer or no TMJ symptoms. Contrary tothis finding, 11.5% preoperatively asymptomaticpatients developed TMJ symptoms after surgery.They suggested that the chance of developingTMJ symptoms in high angle, absolute mandib-ular retrognathism patients, operated on by means of bimaxillary surgery, is considerable.

Kerstens et al82 studied 206 patients who un-derwent orthognathic surgery in combination with orthodontic treatment. They found that 12patients suffered condylar atrophy during post-surgical follow-up. All 12 had a high mandibular

plane angle, Class II retrognathia, with openbite, and they were all treated with bilateral sag-ittal split ostoetomy and Le Fort I osteotomy.Nine of these patients (75%) had TMJ signs orsymptoms presurgically. Four of the original 12(33%) complained that their pain was worseafter surgery, 6 (50%) found no improvement,and 2 (16%) reported that their pain was better.

Wolford et al86 evaluated 25 patients withMRI for the clinical verification of preoperativeTMJ articular DD. These subjects underwent double-jaw surgery for the treatment of their

disorders. They were retrospectively evaluated, with an average follow-up of 2.2 years. Beforesurgery, 16% of the patients had only TMJ pain,64% had only TMJ sounds, and 20% had bothTMJ pain and sounds. After surgery, 24% of thepatients had only TMJ pain, 16% had only TMJsounds, and 60% had both TMJ pain andsounds. The authors concluded that patients with preexisting TMJ dysfunction undergoingorthognathic surgery, particularly mandibularadvancement, are likely to have significant wors-ening of the TMJ dysfunction after surgery.

Wolford et al87

suggested that any clinical orradiographic evidence of TMJ dysfunction, re-gardless of the severity of clinical symptomatol-ogy, warrants comprehensive assessment. Con-sideration should be given to surgical correctionof preexisting TMJ pathology as part of the or-thognathic surgical correction plan. They sug-gested that the clinician routinely perform con-comitant TMJ and orthognathic surgery forcorrection of patients with coexisting dentofa-cial deformities and TMJ internal derangement.If the surgeon prefers, the TMJ surgery might be

done as a separate procedure, but they believe it should be done as the first procedure. Wolfordet al also suggested that concomitant TMJ andorthognathic surgery had an overall success rateof 91.4% based on a 35-mm vertical openingand a decrease in pain. Strong considerationshould be given to early surgical interventionbecause the success rate decreases significantly with preexisting TMJ dysfunction of 48-monthduration.




Fig. 11 represents a patient who has had conventional orthodontic treatment in conjunction with a Herbst appliance (Fig. 11A, B). One yearlater there has been significant relapse (Fig.11C). Orthognathic surgery was done to correct

the malocclusion (Fig. 11D). Approximately 2 years later (Fig. 11E) the case had relapsed, andthere was considerable pain (pain of 6 on a visual analog scale of 0-10).

Craniofacial Morphology

Dibbets and van der Weele12 and Boering88 haveshown the effect of TMJ remodeling on cranio-facial development and morphology in adoles-cent and adult patients. Patients showing x-ray deformities of the TMJs had distinct morpholo-

gies featuring shorter corpus, smaller posteriorfacial heights, and a profile that appeared to bemore Class II Division I. When these mandibles were studied to assess their growth pattern, it wasshown that they were backwardly rotating and

had antegonial notching.Bjork and Skieller89 conducted a 25-year lon-

gitudinal study on normal and abnormal growthof the mandible. Mandibles that had normalgrowth showed a forward rotation. Nearly every mandible showing a backwardly rotation fea-tured some form of condylar problem. It is in-teresting to note that Bjork and Skeiller alludedto the fact that these mandibles might have aneffect on the morphology of other parts of thedeveloping face when they state “It is not knownto what extent maxillary growth is primarily af-

Figure 11. Initial cephalometric film of patient presenting for orthodontic treatment. (A) Pretreatment ceph-alometric film. Treatment consisted of Herbst appliance, followed by conventional orthodontic treatment. (B)Completed treatment. One year later (C) the patient presents for a retention check with an anterior open bite.The patient had subsequent orthognathic surgery to close the anterior open bite (D). Approximately 2 monthsafter surgical treatment there has been relapse. Note the horizontal overlap of the maxillary incisors hasincreased (E).

22 Tallents et al



fected. It is obvious however from the maxillary implants and from the inclination of the ante-rior surface of the zygomatic process that there was increasing backward rotation of the maxil-lary corpus, probably secondary to the rotation

of the mandibular corpus.”Schellhas et al90 evaluated 100 subjects with

visible mandibular deformity and no histories of previous extra-articular mandibular fracture and were selected for retrospective analysis. All subjects had MRI to evaluate the joints. They sug-gested that there were radiologically distinct processes: (1) OA, (2) avascular necrosis, and(3) regressive remodeling. This involved themandibular condyle and temporal bone in jointsmost often exhibiting disk derangement. Theirconclusions were that TMJ degeneration is the

principal cause of both acquired facial skeletonremodeling and unstable occlusion in patients with intact dentition and without previous man-dible fracture. This would suggest preexistingconditions (DD, DDN/DJD) might be responsi-ble for the deformities.

Stringert and Worms10 compared cephalo-metric data from a group of 62 subjects withstructural changes in the TMJ with a sample of 102 subjects from a normative sample. All subjects had arthrography to document the pres-ence or absence of internal derangement. Theresults documented an increased proportion of

“high plane” or hyperdivergent subjects in theexperimental group and a decrease in the pro-portion of “low plane” or hypodivergent subjects.

Link and Nickerson84 examined 39 patientsreferred for orthognathic surgery. Patients hadClass I open bite, Class I on one side and Class IIcontralaterally, or Class II bilaterally, with or without open bite. Patients who were evaluatedby arthrography (n 35) or who had clearly deformed condyles as seen on transpharyngealradiographs (n 4) were included in the study.

The mean age was 29 years. Condylar morphol-ogy was defined by transpharyngeal radiography and classified as being normal, small, or de-formed. The 24 deformed joints evaluated by arthrography had DDN. Condyles with smallmorphology and 80% of condyles with normalmorphology also had an internal derangement.The 6 patients with mandibular deviation hadeither small or deformed condyles with internalderangement on the side to which the mandible

deviated. The 6 contralateral joints had normalbony morphology. In the patients with deviation,those who had normal morphology and a nor-mal disk position were Class I on the ipsilateralside and Class II on the contralateral joint with

internal derangement. The other 3 patients withdeviation all had bilateral internal derangement,but the more advanced derangement was on theside that demonstrated the greater degree of Class II molar relationship and the small or de-formed condyle. Of the 30 symmetric Class II(with or without open bite) patients, 43% hadbilateral deformed condyles or a combination of deformed and small condyles. All open-bite pa-tients and 88% of the patients with Class II mal-occlusion had bilateral derangements. The pa-tients with facial deviation offered the greatest

support for the hypothesis that internal derange-ment has a significant influence on craniofacialmorphology. The 3 patients with unilateral DDhad mandibular deviation to the side with DD.The patients with bilateral DD had mandibulardeviation toward the side with a more adv anceddisplacement. Nickerson and Moystad91 statedthat pain-free, nonclicking TMJs might have in-ternal derangements that might be the cause of skeletal remodeling.

By using MRI, Schellhas et al92 studied 128consecutive children who were suspected of hav-ing TMJ disease because of inflammatory (pain),

mechanical, or structural symptoms such as ret-rognathia and mandibular asymmetry. Resultsshowed that lateral deviation of the chin wasalways toward the smaller and more degeneratedTMJ. MRI findings showed 112 of 128 childrenexhibited at least one joint with internal de-rangement. Eighty-five had bilateral derange-ments. Fifty-six of 60 retrognathic patients werefound to have joints with internal derangement. Advanced stages of TMJ derangement were al-most invariably noted in cases of severe retrog-nathia or lateral asymmetry (mandibular asym-

metry, deviation to the affected [shorter] side).These previously presented studies suggest a

link between craniofacial development and in-ternal derangement of the TMJ, particularly subjects with DJD (mandibular asymmetry, retrog-nathia). Furthermore, they suggest that internalderangement might lead to specific types of craniofacial morphology that include a highmandibular plane angle, mandibular retrog-nathia with or without open bite, and facial




asymmetry in both the growing and nongrowingpatient and that these types of patients fre-quently will present for dental care (prosthodon-tics, orthodontics, and/or orthognathic sur-gery). It should be clearly pointed out that these

previously presented studies represent a simplestatic snapshot in time; they do not show actualdynamic change with time.

Epidemiologic Studies

Kaiser Permanente recruited 160 women, aged18-70 years seeking treatment for TMJ disorders,and 151 control women without TMJ disordersselected from adult female dental hygiene pa-tients.93,94 They found a strong association be-

tween TMJ disorders and severe mandibular ret-rognathia in adult women (odds ratio, 6.3).They suggested that in some women this re-sulted from TMJ disorders influencing mandib-ular development over time. However, among asubset of women the data support the reversehypothesis that severe mandibular retrognathiamight influence the development of TMJ disor-ders.93,94 We would suggest that because of theprevalence of DD in asymptomatic children and young adults (34%)27 and the prevalence of DDin children and young adults (45%)29 present-ing for orthodontic treatment, the environment

for “less” growth might be present at a youngage.

This review is not about rheumatoid arthritis,but there are similar findings.95,96 Rheumatoidarthritis patients when compared with controlsdemonstrate a smaller mandible with an alteredmorphology and position. The mandible be-comes more retruded by rotating posteriorly around the molar region and was characterizedby appositional growth in the gonion area, ver-tical growth in the anterior part, and proclina-tion of the low er incisors.

Hwang et al97

evaluated 111 patients (56 ex-perimental and 55 control) on the basis of apositive response to at least one clinical test (joint sounds, pain, and/or limitation of jaw movement). Experimental subjects with a TMJdisorder (n 56 pain patients) had a morehyperdivergent facial profile, more lingual tilt-ing of the maxillary incisors, and a steeper in-clined occlusal plane compared with subjects without TMJ disorders (n 55 control subjects).

There was a significant correlation between thestructure of the lo wer face and having a TMD.

Flores-Mir et al98 followed 40 subjects (21girls, 19 boys) who had undergone orthodontictreatment between initial records (T1) and final

records (T2). Mean follow-up time between T1and T2 was 43.68 months. They suggested that TMJ disk abnormality was associated with re-duced forward growth of the maxillary and man-dibular bodies, and disk abnormality was associ-ated with reduced downward growth of themandibular ramus.

Ferrario et al67 examined pretreatment lat-eral cephalograms of 41 skeletal Class I femalepatients aged 11-15. They were divided accord-ing to MP-SN angle: lower than 28° degrees(hypodivergent, 10 girls), between 31° and 34°

(normodivergent, 18 girls), or larger than 37°(hyperdivergent, 13 girls). There were smallermandibles in the hyperdivergent girls. Onecould hypothesize that this effect (hyperdiver-gence of the face) might be related to the pres-ence of DD, which has decreased potentialgrowth even though they do not have TMDsymptoms.

Nebbe et al99 compared bilateral DD patients with controls and found that the craniofacialpattern in individuals with bilateral DDN is char-acterized by a reduction in posterior vertical faceheight. The palatal and mandibular planes show

a more marked convergence toward the poste-rior region of the face in individuals with DDNcompared with the group with bilateral normaldisk position.

Bosio et al13 studied differences in skeletalfeatures among 3 study groups: (1) asymptom-atic volunteers with no TMJ DD, (2) symptomaticpatients with no TMJ DD, and (3) symptomaticpatients with bilateral TMJ DD. The degree of retrognathism was found to be significantly greater in females as compared with males in allgroups. Symptomatic patients with bilateral DD

had a retropositioned mandible as compared with asymptomatic volunteers and symptomaticpatients with no DD.

Summary

We have presented a possible relationship be-tween cranial facial morphology and internalderangement. This condition seems to be re-lated to DD and the arthritic process that “some”

24 Tallents et al



joints go through. This is validated by the fact that the same proinflammatory cytokines, matrixdegrading enzymes, and neurogenic processesfound in other joints (knee) and similar eventshave been documented in animal models. This

might or might not be associated with pain inhumans. From some of the cited studies thereare patients with no pain before a dental proce-dure and pain symptoms after treatment. How do we as clinicians deal with this in practice? Do we warn all patients they might have pain afterorthodontics and/or orthognathic surgery, oreven restorative dentistry? The Kaiser Perma-nente study found a strong association betweenTMDs and severe mandibular retrognathia inadult women.93,94 This high prevalence of ret-rognathia in patients with TMDs should make us

cautious when treating a patient seeking care to“improve their bite.” We must assign “risk” tothis and inform patients that there might be riskin seeking treatment.

This review generated the following conclu-sions, cautions, and recommendations:

1. Does DD represent a risk factor, with or with-out pain, that could affect facial growthand/or the development of TMD?

First, animal studies previously presentedstrongly suggest that the surgical creation of DDcan affect the growth and development of sev-

eral craniofacial structures including the cranialbase, midface, and mandible.30-34

Second, the literature reviewed in relation toDD in growing children suggests that they are at risk to have at least altered mandibular growth with possible development of a retrognathic fa-cial appearance and increased lower facialheight.9,13,88-90 Recent studies93-94 suggested astrong relationship between TMDs and severeretrognathia.

2. Are there clinical and radiographic findingsthat might assist in recognizing risk? We sug-gest using clinical and radiographic featuresto assign risk:

Clinical findings:

a. Female5-8,13,26-28,58

b. Family history of TMD16,26

c. Previous history of trauma26

d. Limitation of jaw opening26

e. Joint noise26-28

f. Other joint problems/systemic illness26,100-104

Radiographic findings:

a. Horizontal overlap (overjet)15,16,26,70,88-90

b. Increased mandibular planeangle9,13,28,66-68,74-77,88-92

c. Retrognathic mandible9,12,13,66,67,73-77,88-92

d. Tilted palatal plane9,99

e. Tipped back condyles9,70,74

f. Increased gonial angle9,10-14,74

g. Condyle flattening, osteophyte formation,and/or vertical ramus asymmetry on a Pan-orex radiograph58,59,68,75,91

3. What are the potential outcomes for patientspresenting with pain initially and what is a

patient’s risk for continued pain in conjunc-tion with treatment?Macfarlane et al105 conducted a comprehen-sive 20-year prospective longitudinal study of children ages 11-12 who were followed to ages30-31 and evaluated overall TMD prevalence.Subjects were eventually grouped as to whether they received orthodontic treatment or not. Results showed that the prevalence of TMD was higher in female subjects at all fol-low-up time points except at baseline. Theresults also showed that prevalence and per-

sistence of TMD in subjects who receivedorthodontic treatment did not differ fromthose who did not receive orthodontic treat-ment. An earlier study also suggested that having had orthodontic treatment does not increase the risk of TMD.26 This still does not define when a patient might have symptoms with or without treatment.Patients having orthognathic surgery present-ing with TMD signs and symptoms before theinitiation of treatment have about 67%-90%chance of seeing improvement in their symp-toms, 11%-33% chance of either showing noimprovement or having their signs and symp-toms worsening, and about 3%-12% chanceof developing de novo TMD signs and symp-toms when none were present initially.72,78-80

4. Should a clinician be more concerned about patients who present with a complaint of TMJpain and concurrently have a large open biteor increased overjet?




We believe that this is a risk factor, and theclinician should communicate this to theirpatients/parents.

5. Do patients who present with symptoms suchas TMJ pain have evidence of catabolic tissue

changes within their TMJs?There is sufficient literature from lavage stud-ies48-57 that there are both catabolic and an-abolic processes taking place in painful joints.

6. Do extremes of hyperdivergent facial formrepresent a risk of DJD?The hyperdivergent facial profile seems to beassociated with DJD (OA).9,12,13,28,68,74-77,88-92

Therefore, the clinician should investigatethe history for signs and symptoms if irrevers-ible treatment is going to be performed. Thepresence of a small or flattened condyle is

sufficient to encourage suspicion.7. Are jaw joint problems associated with other

systemic illnesses?

Several studies suggest that TMJ disorders coex-ist (comorbid conditions) with other conditionssuch as chronic fatigue syndrome, fibromyalgia,irritable bowel syndrome, multiple chemical sen-sitivity, TMD, tension headache, interstitial cys-titis, and postconcussion syndrome.100-104 Thesemight represent an individual who is not healthy 104 and might continue to have general-ized somatic pains, regardless of what we might

consider appropriate treatment.

References

1. Okesson JP: Orofacial Pain: Guidelines for Assessment,

Diagnosis and Management. Carol Stream, IL, Quintes-sence Publishing Co Inc, 1996, p 116

2. Katzberg RW, Westesson PL, Tallents RH, et al: Ortho-

dontics and temporomandibular joint disorders. Am J

Orthod Dentofacial Orthop 109:515-520, 19963. Wilkes CH: Internal derangement of the temporoman-

dibular joint: Pathologic variations. Arch Otolaryngol

Head Neck Surg 115:469-477, 1989

4. Schellhas KP: Internal derangement of the temporo-mandibular joint: Radiologic staging with clinical, sur-

gical and pathologic correlation. Magn Reson Imaging

7:495-515, 1989

5. Toller PA: Osteoarthrosis of the mandibular condyle.Br Dent J 134:223-231, 1973

6. Oberg T, Carlsson GE, Fajers CM: The temporoman-

dibular joint: A morphometric study on a human au-

topsy material. Acta Odontol Scand 29:349-384, 19717. Blackwood HJJ: Arthritis of the mandibular joint. Br

Dent J 115:317-326, 1963

8. Kopp S: Subjective symptoms in temporomandibular joint osteoarthrosis. Acta Odontol Scand 35:207-215,1977

9. Gidarakou IK, Tallents RH, Kyrkanides S, et al: Com-parison of skeletal and dental morphology in asymp-tomatic volunteers and symptomatic patients with bilat-

eral degenerative joint disease. Angle Orthod 73:71-78,2003

10. Stringert H, Worms F: Variations in skeletal and dentalpatterns in patients with structural and functional al-terations of the temporomandibular joint: A prelimi-nary report. Am J Orthod Dentofacial Orthop 89:285-297, 1986

11. Brand JW, Nielson KJ, Tallents RH, et al: Lateral ceph-alometric analysis of skeletal patterns in patients withand without internal derangement of the temporoman-dibular joint. Am J Orthod Dentofacial Orthop 107:121-128, 1995

12. Dibbets JM, van der Weele LT: Signs and symptoms of temporomandibular disorder (TMD) and craniofac-ial form. Am J Orthod Dentofacial Orthop 110:73-78,

199613. Bósio JA, Burch JG, Tallents RH, et al: Lateral cepha-

lometric analysis of asymptomatic volunteers and symp-tomatic patients with and without bilateral joint diskdisplacement. Am J Orthod Dentofacial Orthop 114:248-255, 1998

14. Dibbets JMH: Temporomandibular joint dysfunctionand craniofacial growth, in Carlsson D, McNamara JA,Ribbens KA (eds): Developmental Aspects of TMJ Dis-orders. Ann Arbor, MI, Craniofacial Growth Series,1985, pp 151-182

15. Pullinger A, Seligman D, Gornbein J: A multiple logis-tic regression analysis of the risk and relative odds of temporomandibular disorders as a function of com-mon occlusal features. J Dent Res 729:68-79, 1993

16. Kahn J, Tallents RH, Katzberg RW, et al: Associationbetween dental occlusal variables and intraarticulartemporomandibular joint disorders: Horizontal and vertical overlap. J Prosthet Dent 79:658- 662, 1998

17. Kircos LT, Ortendahl DA, Mark AS, et al: Magneticresonance imaging of the TMJ disk in asymptomatic volunteers. J Oral Maxillofac Surg 45:852-854, 1987

18. Kaplan PA, Tu HK, Sleder PR, et al: Inferior joint spacearthrography of normal temporomandibular joints: Re-assessment of diagnostic criteria. Radiology 159:585-589, 1986

19. Westesson PL, Eriksson L, Kurita K: Reliability of anegative clinical temporomandibular joint examina-tion: Prevalence of disk displacement in asymptomatic

temporomandibular joints. Oral Surg Oral Med OralPathol 68:551-554, 198920. Negendank WG, Fernandez-Madrid FR, Heilbrun LK, et

al: Magnetic resonance imaging of meniscal degenerationin asymptomatic knees. J Orthop Res 8:311-320, 1990

21. Kornick J, Trefelner E, McCarthy S, et al: Meniscalabnormalities in the asymptomatic population at MR imaging. Radiology 177:463-465, 1990

22. Boden SD, Davis DO, Dina TS, et al: A prospective andblinded investigation of magnetic resonance imagingof the knee: Abnormal findings in asymptomatic subjects. Clin Orthop Relat Res 282:177-185, 1992

26 Tallents et al



23. Shellock FG, Morris E, Deutsch AL, et al: Hematopoi-

etic bone marrow hyperplasia: High prevalence on MR

images of the knee in asymptomatic marathon runners.

AJR Am J Roentgenol 158:335-338, 1992

24. Boden SD, McCowin PR, Davis DO, et al: Abnormal

magnetic-resonance scans of the cervical spine in

asymptomatic subjects: A prospective investigation.Bone Joint Surg 72:1178-1184, 1990

25. Boden SD, Davis DO, Dina TS, et al: Abnormal mag-

netic-resonance scans of the lumbar spine in asymp-

tomatic subjects: A prospective investigation. J Bone

Joint Surg 72:403-408, 1990

26. Tallents RH, Katzberg RW, Murphy WC, et al: Magnetic

resonance imaging findings in asymptomatic volun-

teers and symptomatic TMD patients. J Prosthet Dent

75:529-533, 1996

27. Ribeiro RF, Tallents RH, Katzberg RW, et al: The prev-

alence of disc displacement in symptomatic and asymp-

tomatic volunteers from 6 to 25 years. J Orofac Pain

11:37-47, 1997

28. Nebbe B, Major PW: Prevalence of TMJ disc displace-ment in a pre-orthodontic adolescent sample. Angle

Orthod 70:454-463, 2000

29. Kamelchuk L, Nebbe B, Baker C, et al: Adolescent TMJ

tomography and magnetic resonance imaging: A com-

parative analysis. J Orofac Pain 11:321-327, 1997

30. Tallents RH, Macher DJ, Rivoli P, et al: An animal

model for meniscus displacement in the rabbit. J Cran-

iomandib Disord Facial Oral Pain 4:233-240, 1990

31. Arigo J: Morphometric Evaluation of the Bony Condyle

and Ramus in TMD. Senior thesis, Division of Ortho-

dontics, Eastman, Dental Center, Rochester, NY, 1998

32. Hatala MP, Macher DJ, Tallents RH, et al: Effect of a

surgically created disk displacement on mandibular

symmetry in the growing rabbit. Oral Surg Oral Med

Oral Pathol Oral Radiol Endod 82:625-633, 1996

33. Qadan S, Macher DJ, Tallents RH, et al: The effect of

surgically induced anterior disc displacement of the

temporomandibular joint on the midface and cranial

base. Clin Orthod Res 2:124-132, 1999

34. Bryndahl F, Eriksson L, Legrell PE, et al: Bilateral TMJ

disk displacement induces mandibular retrognathia. J

Dent Res 85:1118-1123, 2006

35. McDevitt C, Gilbertson E, Muir H: An experimental

model of osteoarthritis: Early morphological and bio-

chemical changes. J Bone Joint Surg 59:24-35, 1977

36. Radin EL, Ehrlich MG, Chernack R, et al: Effect of

repetitive impulsive loading on the knee joints of rab-

bits. Clin Orthop 131:288-293, 1978

37. Pelletier JP, Martel-Palletier J, Altman RD, et al: Collag-enolytic activity and collagen matric breakdown of the

articular cartilage in de Pond-Nuki dog model of osteo-

arthritis. Arthritis Rheum 26:866-874, 1983

38. Bank RA, Soudry M, Maroudas A, et al: The increased

swelling and instantaneous deformation of osteoar-

thritic cartilage is highly correlated with collagen deg-

radation. Arthritis Rheum 43:2202-2210, 2000

39. Chen MH, Broom N: On the ultrastructure of softened

cartilage: A possible model for structural transforma-

tion. J Anat 192:329-341, 1998

40. Lark MW, Bayne EK, Flanagan J, et al: Inhibition of

cartilage degradation and changes in physical proper-

ties induced by IL-1beta and retinoic acid using matrix

metalloproteinase inhibitors. Arch Biochem Biophys

344:404-412, 1997

41. Guilak F, Ratcliffe A, Lane N, et al: Mechanical and

biochemical changes in the superficial zone of articularcartilage in canine experimental osteoarthritis. J Or-

thop Res 12:474-484, 1994

42. Puzas JE, Landeau JM, Tallents R, et al: Degradative

pathways in tissues of the temporomandibular joint:

Use of in vitro and in vivo models to characterize

matrix metalloproteinase and cytokine activity. Cells

Tissues Organs 169:248-256, 2001

43. Lai YC, Shaftel SS, Miller JN, et al: Intraarticular induc-

tion of interleukin-1beta expression in the adult

mouse, with resultant temporomandibular joint patho-

logic changes, dysfunction, and pain. Arthritis Rheum

54:1184-1197, 2006

44. Bonnet CS, Walsh DA: Osteoarthritis, angiogenesis and

inflammation. Rheumatology (Oxford) 44:7-16, 200545. Niissalo S, Hukkanen M, Imai S, et al: Neuropeptides in

experimental and degenerative arthritis. Ann N Y Acad

Sci 966:384-399, 2002

46. Conrozier T, Chappuis-Cellier C, Richard M, et al:

Increased serum C-reactive protein levels by immunon-

ephelometry in patients with rapidly destructive hip

osteoarthritis. Rev Rhum Engl Ed 65:759-765, 1998

47. Spector TD, Hart DJ, Nandra D, et al: Low-level in-

creases in serum C-reactive protein are present in early

osteoarthritis of the knee and predict progressive dis-

ease. Arthritis Rheum 40:723-727, 1997

48. Smith RJ, Justen JM, Ulrich RG, et al: Induction of

neutral proteinase and prostanoid production in bo-

vine nasal chondrocytes by interleukin-1 and tumor

necrosis factor alpha: Modulation of these cellular re-

sponses by interleukin-6 and platelet derived growth

factor. Clin Immunol Immunopathol 64:135-144, 1992

49. Sandy JD: Proteolytic degradation of normal and osteo-

arthritic cartilage matrix, in Brandt KD, Doherty M,

Lohmander LS (eds): Osteoarthritis. New York, Oxford

University Press, 2003, pp 82-91

50. Goldring SR, Goldring MB: The role of cytokines in

cartilage matrix degeneration in osteoarthritis. Clin

Orthop Relat Res 427:S27-S36, 2004 (suppl)

51. Smith MD, Triantafillou S, Parker A, et al: Synovial

membrane inflammation and cytokine production in

patients with early osteoarthritis. J Rheumatol 24:365-

371, 1997

52. Mizui T, Ishimaru J, Miyamoto K, et al: Matrix metal-loproteinase in synovial lavage fluid of patients with

disorders of the temporomandibular joint. Br J Oral

Maxillofac Surg 39:310-314, 2001

53. Segami N, Suzuki T, Sato J, et al: Does joint effusion

on T2 magnetic resonance images reflect synovitis?

Part 3—Comparison of histologic findings of ar-

throscopically obtained synovium in internal de-

rangements of the temporomandibular joint. Oral

Surg Oral Med Oral Patholo Oral Radiol Endod

95:761-766, 2003




54. Ijima Y, Kobayashi M, Kubota E: Role of interleukin-1 ininduction of matrix metalloproteinases synthesized by

rat temporomandibular joint chondrocytes and disc

cells. Eur J Oral Sci 109:50-59, 200155. Ishimaru JI, Oguma Y, Goss AN: Matrix metalloprotei-

nase and tissue inhibitor of metalloproteinase in serum

and lavage synovial fluid of patients with temporoman-dibular joint disorders. Br J Oral Maxillofac Surg 38:

354-359, 2000

56. Kubota E, Kubota T, Matsumoto J, et al: Synovial fluidcytokines and proteinases as markers of temporoman-

dibular joint disease. J Oral Maxillofac Surg 56:192-198,1998

57. Lohmander LS, Hoermer LA, Lark MW: Metalloprotei-

nase, tissue inhibitor, and proteoglycan fragments inknee synovial fluid in human osteoarthritis. Arthritis

Rheum 36:181-189, 1993

58. Papadaki ME, Tayebaty F, Kaban LB, et al: Condylarresorption. Oral Maxillofac Surg Clin North Am 19:

223-234, 200759. Arnett GW, Milam SB, Gottesman L: Progressive man-

dibular retrusion-idiopathic condylar resorption: Part I.

Am J Orthod Dentofacial Orthop 110:8-15, 199660. Gunson MJ, Arnett GW, Formby B, et al: Oral contra-

ceptive pill use and abnormal menstrual cycles in

women with severe condylar resorption: A case for low serum 17b-estradiol as a major factor in progressive

condylar resorption. Am J Orthod Dentofacial Orthop136:772-779, 2009

61. Gidarakou IK, Tallents RH, Kyrkanides S, et al: Com-

parison of skeletal and dental morphology in asymp-tomatic volunteers and symptomatic patients with bilat-

eral disk displacement with reduction. Angle Orthod

72:541-546, 200262. Gidarakou IK, Tallents RH, Kyrkanides S, et al: Com-

parison of skeletal and dental morphology in asymp-tomatic volunteers and symptomatic patients with nor-

mal temporomandibular joints. Angle Orthod 73:116-

120, 200363. Gidarakou IK, Tallents RH, Kyrkanides S, et al: Com-

parison of skeletal and dental morphology in asymp-

tomatic volunteers and symptomatic patients with uni-lateral disk displacement without reduction. Angle

Orthod 3:121-127, 200364. Gidarakou IK, Tallents RH, Stein S, et al: Comparison

of skeletal and dental morphology in asymptomatic

volunteers and symptomatic patients with unilateraldisk displacement with reduction. Angle Orthod 74:

212-219, 2004

65. Gidarakou IK, Tallents RH, Kyrkanides S, et al: Com-parison of skeletal and dental morphology in asymp-

tomatic volunteers and symptomatic patients with bilat-eral disk displacement without reduction. Angle

Orthod 2004:684-690, 200466. Ferrario VF, Sforza C, De Franco DJ: Mandibular shape

and skeletal divergency. Eur J Orthod 21:145-153, 199967. Ferrario VF, Sforza C, de Franco DJ: Mandibular shape

and skeletal divergency. Eur J Orthod 21:145-153, 1999

68. Nebbe B, Major PW, Prasad NG, et al: TMJ internalderangement and adolescent craniofacial morphology:

A pilot study. Angle Orthod 67:407-414, 1997

69. Kurita H, Ohtsuka A, Kobayashi H, et al: Resorption of the lateral pole of the mandibular condyle in temporo-mandibular disc displacement. Dentomaxillofac Radiol30:88-91, 2001

70. Kurita H, Ohtsuka A, Kobayashi H, et al: Relationshipbetween increased horizontal condylar angle and re-

sorption of the posterosuperior region of the lateralpole of the mandibular condyle in temporomandibular joint internal derangement. Dentomaxillofac Radiol32:26-29, 2003

71. Oberg T, Carlsson GE, Fajers CM: The temporoman-dibular joint: A morphologic study on a human autopsy material. Acta Odontol Scand 29:349-384, 1971

72. Kerstens HT, Tuinzing DB, van der Kwast WA: Tem-poromandibular joint symptoms in orthognathic sur-gery. J Craniomaxillofac Surg 17:215-218, 1989

73. Stein S, Tallents RH, Hatala MA, et al: The effect of TMJ internal derangement on craniofacial morphol-ogy. Presented at the Annual Winter Meeting of theRochester Section of the AADR, 1996

74. Dibbets JM, Van Der Weele LT, Uildriks AKJ: Symp-

toms of TMJ dysfunction: Indicators of growth pat-terns? J Pedodontics 9:265-284, 1985

75. Link JL, Nickerson JW: Temporomandibular joint in-ternal derangements in an orthognathic surgery popu-lation. Int J Adult Orthodon Orthognath Surg 7:161-169, 1992

76. Schellhas KP, Keck RJ: Disorders of skeletal occlusionand temporomandibular joint disease. NW Dent 68:35-39, 1989

77. Schellhas KP, Pollei SR, Wilkes CH: Pediatric internalderangements of the temporomandibular joint: Effect on facial development. Am J Orthod Dentofac Orthop104:51-59, 1993

78. White CS, Dolwick MF: Prevalence and variance of temporomandibular dysfunction in orthognathic sur-

gery patients. Int J Adult Orthodon Orthognath Surg7:1-14, 1992

79. Upton LG, Scott RF, Hayward JR: Major maxilloman-dibular malrelations and temporomandibular joint pain-dysfunction. J Prosthet Dent 51:686-690, 1984

80. Karabouta I, Martis C: The TMJ dysfunction syndromebefore and after sagittal split osteotomy of the rami. JMaxillofac Surg 13:185-188, 1985

81. Stringert HG, Worms FW: Variations in skeletal anddental patterns in patients with structural and func-tional alterations of the temporomandibular joint: A preliminary report. Am J Orthod 89:285-297, 1986

82. Kerstens HC, Tuinzing DB, Golding RP, et al: Condylaratrophy and osteoarthrosis after bimaxillary surgery.

Oral Surg Oral Med Oral Pathol 69:274-280, 199083. Schellhas KP, Piper MA, Bessette RW, et al: Mandibularretrusion, temporomandibular joint derangement andorthognathic surgery planning. Plast Reconstr Surg 90:218-232, 1992

84. Link JL, Nickerson JW Jr: Temporomandibular joint internal derangements in an orthognathic surgery pop-ulation. Int J Adult Orthodon Orthognath Surg 7:161-169, 1992

85. Kahnberg KE: TMJ complications associated with supe-rior repositioning of the maxilla. J Craniomandib Prac6:312-315, 1988

28 Tallents et al



86. Wolford LM, Reiche-Fischel O, Mehra P: Changes in

temporomandibular joint dysfunction after orthog-

nathic surgery. J Oral Maxillofac Surg 61:655-660, 2003

87. Wolford LM, Karras S, Mehra P: Concomitant temporo-

mandibular joint and orthognathic surgery: A prelimi-

nary report. J Oral Maxillofac Surg 60:356-362, 2002

88. Boering G: Arthrosis deformans van het kaakgewricht.Leiden, Stafleu & Tholen, 1966

89. Björk A, Skieller V: Normal and abnormal growth of

the mandible: A synthesis of longitudinal cephalomet-

ric implant studies over a period of 25 years. Eur J Or-

thod 5:1-46, 1983

90. Schellhas KP, Piper MA, Omlie MR: Facial skeleton

remodeling due to temporomandibular joint degener-

ation: An imaging study of 100 patients. AJR Am J

Roentgenol 155:373-383, 1990

91. Nickerson JW Jr, Moystad A: Observations on individu-

als with radiographic bilateral condylar remodeling. J

Craniomandib Prac 1:20-37, 1983

92. Schellhas KP, Pollei SR, Wilkes CH: Pediatric internal

derangements of the temporomandibular joint: Effect

on facial development. Am J Orthod Dentofac Orthop

104:51-59, 1993

93. Miller JR, Burgess JA, Critchlow CW: Association be-

tween mandibular retrognathia and TMJ disorders in

adult females. J Public Health Dent 64:157-163, 2004

94. Miller JR, Manci L, Critchlow C: Severe retrognathia as

a risk factor for recent onset painful TMJ disorders

among adult females. J Orthod 32:249-256, 2005

95. Stabrun AE: Impaired mandibular growth and microg-

nathic development in children with juvenile rheuma-

toid arthritis. Eur J Orthod 13:423-434, 1991

96. Larheim TA, Haanaes HR, Ruud AF: Mandibular

growth, temporomandibular joint changes and den-

tal occlusion in juvenile rheumatoid arthritis: A 17-

year follow-up study. Scand J Rheumatol 10:225-233,1981

97. Hwang CJ, Sung SJ, Kim SJ: Lateral cephalometric char-acteristics of malocclusion patients with temporoman-dibular joint disorder symptoms. Am J Orthod Dento-facial Orthop 129:497-503, 2006

98. Flores-Mir C, Nebbe B, Heo G, et al: Longitudinal study of temporomandibular joint disc status and craniofacial

growth. Am J Orthod Dentofacial Orthop 130:324-330,2006

99. Nebbe B, Major PW, Prasad NGN: Adolescent femalecraniofacial morphology associated with advanced bi-lateral TMJ disc displacement. Angle Orthod 20:701-712, 1998

100. Buchwald D, Garrity D: Comparison of patients withchronic fatigue syndrome, fibromyalgia, and multiplechemical sensitivities. Arch Intern Med 154:2049-2053,1994

101. Aaron LA, Burke MM, Buchwald D: Overlapping con-ditions among patients with chronic fatigue syndrome,fibromyalgia, and temporomandibular disorder. ArchIntern Med 160:221-227, 2000

102. Eriksson PO, Lindman R, Stål P, et al: Symptoms and

signs of mandibular dysfunction in primary fibromyal-gia syndrome (PSF) patients. Swed Dent J 12:141-149,1988

103. Korszun A, Papadopoulos E, Demitrack M, et al: Therelationship between temporomandibular disordersand stress-associated syndromes. Oral Surg Oral MedOral Pathol Oral Radiol Endod 86:416-420, 1998

104. Hedenberg-Magnusson B, Ernberg M, Kopp S: Symp-toms and signs of temporomandibular disorders in pa-tients with fibromyalgia and local myalgia of the tem-poromandibular system: A comparative study. ActaOdontol Scand 55:344-349, 1997

105. Macfarlane TV, Kenealy P, Kingdon HA, et al: Twenty- year cohort study of health gain from orthodontic treat-ment: Temporomandibular disorders. Am J Orthod

Dentofacial Orthop 135:e1-e8, 2009, discussion 692-3.97.108


predisposing and precipitating.pdf

Documents