Implications of temporomandibulardisorders for facial growth and orthodontic treatment

Implications of Temporomandibular Disorders for Facial Growth and Orthodontic Treatment jos M.H. Dibbets and David S. Carlson The purpose of this article is to review the literature concerning the possible associations between temporomandibular disorders (TMD), orthodontic therapy, mandibular growth, and facial form. Consideration of the association between TMD and orthodontic treatment leads to one conclusion: there is no evidence that orthodontic treatment generally increases or decreases the chances of developing TMD later in life. Still, our understanding of TMD is not final, and the expanding diagnostic knowledge continues to call for new longitudinal studies focusing on the developmental basis of temporomandibular disorders. Little is known about the potential effect of TMD on facial development. However, information relating to the normal development, growth, and adaptation of the temporomandibular joint all tend to emphasize the significant ontogenetic plasticity of the growth-related secondary cartilage associated with the TMJ, within the bounds of normal function and histophysiology. With the exception of such diseases as juvenile rheumatoid arthritis and osteoarthritis, little is known about the influence of TM pathology or myofascial disorders on facial growth. Also, little is known about the possible influence of disc interferences on facial growth. However, the condyle is known to play a prominent role in normal mandibular growth and, consequently, facial development. Thus, categories of TMD that involve dysplasia of the condylar cartilage could be associated with aberrant facial growth and form. (Semin Orthod 1995;1:258-272.) Copyright © 1995 by W.B. Saunders Company

hree conceptual problems are most ap-

T p a r e n t when considering the orthodontic implications o f t e m p o r o m a n d i b u l a r disorders (TMD). One is contained in the statement of the problem itself; ie, it is not possible at this time to actually test the statement that orthodontic t r e a t m e n t causes TMD. Even the most c o m p r e h e n s i v e studies in this area at present do not generate cause-and-effect answers. At most, such studies can show or reject associations b e t w e e n o r t h o d o n t i c t r e a t m e n t a n d From the Department of Orthodontics, Philipps University, Marburg, Germany; and the Department of Biomedical Sciences, Center for Craniofacial Research, Baylor College of Dentist~, Dallas, TX. Supported in part by NIH-NIDR DE 08824 to DSC. Address correspondence to David S. Carlson, PhD, Department of Biomedical Sciences, Baylor College of Dentistry, PO Box 660677, Dallas, TX 75266-06677. Copyright © 1995 by W.B. Saunders Company 1073-8746/95/0107-000755.00/0 258

TMD. T h e r e f o r e , the problem to be addressed in this article must be f o r m u l a t e d with care. A second concern is the o f t e n - h e a r d notion that T M D is a "multifactoriaI disorder." This p r o p o s i t i o n clearly e m p h a s i z e s two r e l a t e d points. First is the implicit assumption within such a statement that T M D is a single, wellcharacterized clinical problem; second, is the m o r e explicit assumption that T M D has a potentially wide variety o f efficient causes. Unfortunately, the concept o f T M D as a multifactorial disorder has d o n e little to enrich o u r thinking, and may even have constrained or inhibited p r o p e r u n d e r s t a n d i n g o f the causes and implications of T M disorders. C o n s i d e r e d broadly, signs and symptoms o f disorders o f the t e m p o r o m a n d i b u l a r joint (TMJ), such as pain, limitation o f jaw o p e n i n g and excursion, inflammation, and d e g e n e r a t i o n , u n d o u b t e d l y have many potential and discrete causes. However, this partial list o f characteristics illustrates

Seminars in Orthodontics, Vol 1, No 4 (December), 1995: pp 258-272

TM1), Facial Growth, and Orthodontic Treatment

the fact that it is u n w a r r a n t e d to c o n s i d e r T M D as a single disorder, with a discrete a n d well-defined progression. Although recent studies have i n t r o d u c e d a variety o f new diagnostic p r o c e d u r e s with p r o m i s i n g sensitivity and specificity, t h e r e exists no consensus as to which signs a n d s y m p t o m s facilitate selective differential diagnosis within the b r o a d category T M D . T h e notion that T M D is a single d i s o r d e r precipitated by a wide variety of specific causes is especially u n f r u i t f u l as it concerns the possible effects o f existing T M disorders on subsequent growth and orthodontic/orthopedic t r e a t m e n t . For e x a m p l e , myofascial pain, internal dis(: d e r a n g e i n e n t , and osteoarthrosis each fit the b r o a d classification o f TM1); yet each is very d i f f e r e n t in t e r m s o f the target tissues that may be affected. T h e r e f o r e , it must be c o n s i d e r e d that each will most likely have d i f f e r e n t specific effects and implications [0r facial g r o w t h a n d f o r possible o r t h o d o n t i c treatment. A third p r o b l e m relates to the age-related expression o f T M D in the general population, and in the specific clinical o r t h o d o n t i c population. Most c o m m o n l y , it is t h o u g h t that TM1) is a d i s o r d e r e x p r e s s e d u n i q u e l y in y o u n g to m i d d l e - a g e d adults, t Iowever, signs and symptoms of T M D do occur in children a n d adolescents. I :~ Like all diseases and disorders, especially those associated with a b n o r m a l structure c a u s e d by g r o w t h a n d r e m o d e l i n g , certain manifestations o f T M I ) m u s t have a developm e n t a l basis. *'5 Essential issues that e m e r g e f r o m this a s s u m p t i o n c o n c e r n the specific factors p r e d i s p o s i n g to or leading u p to TM1) in subaduhs, the impact of T M D on facial growth and f o r m , and the implications of this |k)r orthodontic t r e a t m e n t . Potential confusion at)out the scope, causes, and characteristics o f TM1), as well as its natural p r o g r e s s i o n , gives rise to t h r e e caveats thal are essential to consider with respect to the implications o f T M D for facial growth prohlems a n d f o r o r t h o d o n t i c t r e a t m e n t . First, T M D is not a single disorder, but r a t h e r is a b r o a d classification of a n u m b e r o f disorders that may affect differentially a n u m b e r o f relatively i n d e p e n d e n t tissues within the T M J and associated structures. Second, within the b r o a d classification of T M D , there exists no

259

consensus as to which signs a n d s y m p t o m s facilitate selective differential diagnosis. T h i s of_ ten leads to confusion a n d a p p a r e n t disagreem e n t c o n c e r n i n g the etiology o f the disorder, as well as the n a t u r e o f the affected tissues. Finally, T M D should be c o n s i d e r e d within the b r o a d e r context o f growth a n d a d a p t i v e responses by cells a n d tissues c o m p r i s i n g the T M J a n d masticatory system. In this article, we take the position that signs and s y m p t o m s as r e p o r t e d in the literature are indicators o f an a r r a y o f p r o b l e m s , collectively r e f e r r e d to as T M D . C o n s i d e r a t i o n o f the imp l i c a t i o n s l h a t T M D m a y h a v e fi)r facial growth a n d o r t h o d o n t i c t r e a t m e n t has t h r e e parts. T h e first reviews the literature relating to the association between signs a n d s y m p t o m s attributed to T M I ) a n d o r t h o d o n t i c t r e a t m e n t . T h e s e c o n d p a r t focuses on T M J g r o w t h . Base(| on the a s s u m p t i o n that T M D m a y be characterized by the p r e s e n c e o f c o m p r o m i s e d tissues a n d dysfunction o f the T M ] , this section will p r o v i d e a context a n d f o u n d a t i o n for the third a n d final section, which explores the potential effect o f specific T M D s on m a n d i b u lar a n d facial growth and f o r m .

T M D and Orthodontic Treatment Initial identification o f a putative causal relationship between occlusal factors a n d pain in the region o f the T M J is generally attributed to Costen in 1934. ~ Since that time, various types o f corrective t h e r a p y involving o r t h o d o n t i c / o r t h o p e d i c a p p r o a c h e s a n d occlusal adjustm e n t have heen p r o p o s e d to correct the malocclusion a n d thereby to alleviate the signs a n d synlptoms o f T M D . 7 :j It was assumed generally that structural or functional malocclusions cause T M D , and that n o r m a l i z a t k m o f the occlusion by m e a n s o f occlusal a d j u s t m e n t a n d o r t h o d o n t i c s should c o r r e c t the d i s o r d e r . 4-~ T h i s c o n c e p t t e n d e d to be e m b r a c e d with s o m e e n t h u s i a s m by m a n y orthodontists. 8't° H o w ever, this presents s o m e t h i n g o f a d i l e m m a . t f f it is a s s u m e d that o r t h o d o n t i c t r e a t m e n t can alleviate T M D via alteration o f the way the teeth fit t o g e t h e r a n d t h e r e b y influencing the position a n d function o f the condyle-disc assembly, t h e n it m u s t also be accepted that orthodontic t r e a t m e n t can cause T M D t h r o u g h the same general process.

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A n o t h e r interesting dichotomy concerning the relationship between T M I ) and o r t h o d o n tic t r e a t m e n t has developed recently. A h h o u g h it is more c o m m o n to r e g a r d malocclusion as a predisposing factor for TMD, recent publications by Schellhas and colleagues *~ have reversed this causal relationship and proposed that T M D , and internal d e r a n g e m e n t of the disc specifically, is a causal factor leading to malocclusion, which then requires orthodontic t r e a t m e n t because o f abnormal facial growth and form. ttowever, the latter twist on the maIo c c l u s i o n - T M D concept, which will be discussed in m o r e detail later, is highly questionable because o f methodological problems. Several specific orthodontically related procedures have been p r o p o s e d to cause TMD. Conventional wisdom led to the assumption 15 years ago that extractions a n d / o r orthodontic t r e a t m e n t p r o c e d u r e s are responsible for the initiation o f TMD. O t h e r putative causes included such d i c h o t o m o u s interventions as distalization of the mandible caused by retraction of tire u p p e r incisors, thereby "trapping" the condyle-disc assembly, and anterior protrusion o f the mandible. All of the information purporting to s u p p o r t this assumption was simply intuitive, a n e c d o t a l and, at best, retrospective. 10 Several years have elapsed between initiation and completion o f well-designed longitudinal studies on the interaction between orthodontic t r e a t m e n t and TMD, which are absolutely necessary to establish the relative validity of this association. Since that time a n u m b e r of publications have e x p l o r e d the possibility o f a significant r e l a t i o n s h i p b e t w e e n T M D and orthodontic t r e a t m e n t using credible methodological a p p r o a c h e s . H o w e v e r , at the same time t h r o u g h significant progress in diagnostic capabilities via such techniques as magnetic resonance imaging o f the joint and e n h a n c e d clinical p r o c e d u r e s , for example, it became clear that T M D should no longer be considered a discrete disorder, t :+Because none o f the original unfavorable claims, as logical as they once seemed to be, can be upheld a n y m o r e today, it seems p r u d e n t not to speculate on associations between orthodontics and T M D before clinical trials have been completed. T w o critical review articles dealing with the evidence c o n c e r n i n g the association between

T M D and o r t h o d o n t i c t r e a t m e n t were published very recently by Sadowsky vt and by McN a m a r a and colleagues. ') Sadowsky 14 reviewed 14 studies totaling 1,300 patients who had previously u n d e r g o n e orthodontic treatment. McN a m a r a and coworkers ') provided an excellent historical overview and reviewed data f r o m more than 150 clinical studies covering several t h o u s a n d subjects. A l t h o u g h d i f f e r e n t in scope, both reviews arrived at very similar overall conclusions based on their extensive consideration of the literature. According to Sadowsky, "the o v e r w h e h n i n g evidence supports the conclusion that o r t h o d o n t i c treatment p e r f o r m e d on children and adolescents is generally not a risk for the d e v e h ) p m e n t o f T M D years later." Similarly, M c N a m a r a and coworkcrs f o u n d no evidence for increased risk o f T M D in orthodontic patients. T h e review by McNarnara and coworkers, 9 also provides a m o r e in-depth analysis o f the data from the literature c o n c e r n i n g T M D as it relates to occlusal status, orthodontics iI1 general, specific types of o r t h o d o n t i c t r e a t m e n t (including extraction/nonextraction) and TMI), and orthodontk: a p p r o a c h e s designed for prevention o f TMD. With respect to the relationship between functional occlusal factors and T M D , M(:Namara a n d colleagues evaluated 20 studies with a total o f m o r e than 7,000 participating individuals f r o m h e a h h y and patient populations. In light o f apparently conflicting conclusions and contentions f r o m these studies, their general conclusion was that it is m o r e i m p o r t a n t to carefully examine the methodology used than the conclusions in each of the individual studies. From the data, McNamara and coworkers concluded further that, except for a fe~ defined occlusal conditions, such as a n t e r i o r o p e n bites, overjets m o r e than 6 ram, RCP-ICP slides over 4 ram, unilateral crossbites, and five or m o r e missing posterior teeth, there is relatively low risk o f occlusal factors being associated with TMI). N o n e o f the studies r e v i e w e d i d e n t i f i e d a cause-effect relationship arid all correlation coefficients were very low (r < 0.3), explaining less than 10% of the total variation. McNamara and colleagues -qalso critically reviewed published data concerning the occurrence of signs and symptoms in studies totaling over 10,000 healthy individuals. T h e y f o u n d

TMD, Facial Growth, and Orthodontic Treatment

that an average of 32% o f this combined population exhibited at least one symptom, and 55% showed at least one sign of TMD. Moreover, they noted lhat the signs and symptoms of T M D occur in healthy individuals, and the n u m b e r o f signs and synlptoms increase with age, particularly d u r i n g adolescence. Because of these findings, they concluded that the occ u r r e n c e o f signs and symptoms d u r i n g orthodontic t r e a t m e n t must be considered within the context o f normal longitudinal changes. Moreover, o r t h o d o n t i c t r e a t m e n t d u r i n g adolescence generally does not increase or decrease the odds of developing T M I ) later in life. Considering the issue o f orthodontic treatm e n t m o r e specifically, M c N a m a r a and colleagues concluded that it is not reasonable to assume that T M disorders that originate or are first r e p o r t e d d u r i n g treatment are necessarily related to the treatment. T h e y noted specifically that there is no scientific evidence to indicate that extraction of teeth as part o f art o r t h o d o n t i c u-eatment plata increases the risk of TMD. Nor is there evidence ti)r clewtted risk fbr TM1) associated with any particular type o f o r t h o d o n t i c mechanics. Although a stable occlusion is a reasonable orthodontic treatment goal, not achieving a specific gnathologic ideal occlusion does not result in T M D signs and symptoms. Finally, McNatnara and coworkers also concluded that there is no evidence to indicate that o r t h o d o n t i c treatment can p r e v e n t TMD, although when m o r e severe T M D signs and symptoms are present, sintple treatments usually (:art alleviate thcnt in ntost patients.

Normal Development

of the TMJ

T h e T M J provides the essential f u n c t i o n a l connection between the cranium and the upper and lower jaw. ttowever, the primary function o f the TMJ in general, and o f the mandibular condyle in particular, is not so simple, and it changes d u r i n g development. Considered specifically, the primary roles o f the mandibular condyle are twofold, and they may be considered within three arbitrary phases o f dev e l o p m e n t . I5 T h e first p r i m a r y role of the m a n d i b u l a r condyle is directed toward growth, which is most evident and i m p o r t a n t prenatally

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and early postnatally (phase I), and diminishes in expression as d e v e l o p m e n t proceeds postnatally t h r o u g h adolescence (phase II). T h e second role o f tile m a n d i b u l a r condyle is dir e c t e d t o w a r d m a n d i b u l a r articulation attd load-bearing capabilities. Beginning in incipient fornt, because the m a n d i b l e may m o v e prenatally, the articular f u n c t i o n gains primacy as the growth function diminishes d u r i n g phase I 1. With a d u h h o o d (phase I I I), condylar growth has essentially ceased, t h o u g h remodeling may continue t h r o u g h o u t life, while articular function continues. Essentially, the earlier growth function and the later articular functiota can be considered as c o m p e t i n g roles within the n t a n d i h u l a r condyle. Unlike typical growth cartilage, such as that f o u n d in synchondroses (ie, epiphyses and cranial base), the condylar cartilage nmst be capable hoth o f active growth and o f withstanding sonte d e g r e e o f loading caused by the forces o f mastication. Unfortunately, the tissues artd i u s t o m o r p h o l o g y o f the T M J are not optimally suited for this purpose because they are derived from a specialization o f periosteuin and are characterized by a special type o f i n t r a m e m b r a n o u s skeletal formation. As a result, v:u-iations in articular function, especially d u r i n g phases I and II o f d e v e l o p m e n t , may have important consequences for d e v e l o p m e n t o f the mandible and, thus, for facial form. Furt h e r m o r c , variations in nlandibular function, trauma, and a history o f disease may play a significant role in c o m p r o m i s e o f the tissues o f the developing T M ] , and thus in disorders o f the T M ] . tlowever, the potential adaptive capabilities o f the T M tissues will u n d o u b t e d l y play a significant role in the aw)idance and alleviation o f T M disorders via normal processes o f developnmnt and growth. N o r m a l events arid conditions e x p e r i e n c e d by the 'FM l during d e v e l o p m e n t and growth can be resolved e[tectively by the process o f adaptation. However, pathology o f the TMJ inay occur if the physiological hounds o f normal adaptation are exceeded, caused by the n a t u r e of the p e r t u r bation, the capabilities of the tissues comprising the TMJ, o r b o t h . 4'16'17 To effectively consider the potential association between TMD and facial growth and form it is necessary to understand the nature of the tissues comprising the TMJ, their rela-

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tionship to the normal growth process, and the manner in which they express themselves during maturation. In the following section, the development and growth of the TMJ will be reviewed briefly, with emphasis on the growthrelated tissues.

Morphogenesis In h u m a n fetuses the condyle originates around 7 to 7.5 weeks of gestation as a condensation of mesenchymaI tissue separate from the developing intramembranous bone of the mandible and squamous portion of the temporal bone. ~s By 16 to 17 weeks a fullv formed joint is present.~9 Interposed between the mandibular condyle and temporal articulation is the articular disc, which is derived from the same mesenchymaI mass as the lateral pterygoid muscle.

Histomorphology (Fig 1) The nature of the various layers of tissue associated with the articular and growth-related skeletal tissues comprising the TMJ, and the specific terms used to define them, have been the subject of considerable discussion (see Carlson ~7 for a more complete review). In general, it is appreciated that the growth-related '

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skeletal tissues comprising both the mandibular condyle and the squamous portion of the temporal bone arise from a specialized skeletogenic membrane (ie, periosteum/perichondrium). Moreover, it is understood that growth of all skeletal tissues associated with the TMJ takes places via osseous replacement of intramembranously formed secondary cartilage, especially within the condyle, but also along the subarticular surface of the squamous temporal bone. Secondary

Cartilage

In part because of its atypical development and cellular structure, the cartilage of the mandibular condyle and articular eminence is designated as a special form of periosteally/perichondrally derived hyaline, cartilage, called secondary cartilage3 °'9~ Although primary cartilage, which gives rise to the cartilaginous template of the limbs and cranial base, forms very early in development, secondary cartilages develop considerably later, arising and being maintained in areas where intramembranous bone is exposed to local intermittent biomechanical stress. Modulation between the chondroblastic and osteoblastic phenotype in response to altered local biomechanical circumstances is caused by the bipotential nature of the undifferentiated cells of the periosteal/ perichondrial membranes. 99-~

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Figure 1. Photomicrographs of parasagittal sections of the left TMJ from a young rhesus monkey (Macaca mulatta) demonstrating the histomorphology of the TMJ. (A) Low power overview of the TMJ. Note the continuous nature of the periosteum (p) along the posterior border of the ramus as it splits to form the joint capsule and articular disc (a), and then splits again to fbrm the outer fibrous articular layers and inner chondrogenic layers of the mandibular condyle and fossa (c). (B) Medium power view of the condylar cartilage, articular disc, and articular eminence. (Modified with permission from Carlson DS. Growth of the temporomandibular joint. In: Zarb et al, editors. Temporomandibular Joint and Masticatory Muscle Disorders. Copenhagen, Denmark, Munksgaard. 1994.)

TMD, Facial Growth, and Orthodontic 7'reatment

Articular Layer At the sites of articulation between the condyle and temporal bone within the TM|, the outer, fibrous layer of the bilaminar perichondrium thickens somewhat, enhancing its protective function. This fibrous connective tissue layer, which is continuous with the fibrous layer of the periosteum along the neck of the mandible and along the temporal bone, becomes known as the articular layer. Although the articular layer is analogous to an articular cartilage, because it provides a similar articular function, the TMJ does not have a true articular cartilage.

Prechondroblastic Layer Immediately deep to the articular layer is the prechondroblastic or proliferative layer, which is an irregular layer of densely packed cells continuous with the osteogenic layer of the periosteum. The prechondroblastic layer is the preponderant site of mitotic activity in the condylar cartilage and squamous temporal region, supplying cells for both the articular layer and underlying cartilage or bone. 2"s-2~

Chondroblastic Layer On its deep surface, the flauened cells of tire deepest parts of the prechondroblastic layer become larger and more ovoid shape, witb a dense nucleus typical of chondrocytes, ~:~ as they come to occupy the chondroblastic zone. ~1 In growing individuals, the chondrocytes in the deepest layers are considerably hypertrophic, with characteristically large lacunae.

Zone of Endochondral Ossification The deepest three to five cell layers are surrounded by a matrix that is mineralized. The last of these is ill direct contact with the front of invading vascular cells and osteoblasts in the zone of endochondral ossification.

Temporal Portion of the TMJ The growth-related tissue overlying the crest and posterior slope of the articular eminence, with which the condyle articulates during the power stroke of mastication and incision, is similar, although less luxuriant, to that covering the condyle. It also is characterized by a perichondrium with a thickened fibrous layer

263

and subadjacent secondary hyaline cartilage that is typically considerably thinner than that observed in the condyle. In contrast, the mandibular t0ssa, which is not heavily loaded during function, is comprised of lamellar bone overlayed by a periosteurn, but there is no cartilage throughout postnatal developmenc

Growth of the TMJ Neonatal-Juvenile Period Most of the maior morphological changes associated with growth of the T M | are completed during the first decade of life. The neonatal mandibular condyle is capped by a relatively thick, highly vascularized, and very mitotically active secondary cartilage. In general, as tile mandible is displaced downward and forward by the growing midface, the condylar cartilage grows actively via perichondrial deposition in a superior and posterosuperior direction Io maintain its articulation with the temporal component of the "FM]. The anterior-inferior region of the condyle, the condylar neck, arid the bony medial and lateral poles of the condyle tend to be resorptive. During tile first year of life the mandibular condyle becomes progressively less vascularized and the entire growth cartilage layer becomes significantly thinner. By 6 months of age, there is up to a two-thirds reduction in the thickness of the cartilage layer (to 0.50 ram) in humans, :m primarily caused by reduction in the zone of hypertrophy. The thickness of the growth cartilage remains constant from infancy through adolescence. Also, by 6 months of age there is a significant reduction in the number and size of vascular canals within the condylar cartilage; those that persist do so in the medial and p o s t e r i o r aspects o f the condyle, where growth is most active. By 3 years of age in humans, vascular canals are no longer present. Growth of the articular surface of the temporal bone is characterized by enlargement of the articular eminence and postglenoid region, which becomes evident by around 8 months of age and continues through development of the mixed dentition. The S-shaped curve that characterizes the temporal component of the TMJ becomes evident during this period. By 6

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or 7 years of age the articular eminence may enlarge to 5 to 6 mm in height. At this point, compact osseous tissue and secondary osteons are present within the articular eminence and postglenoid process. Also during the period of early mixed dentition the articular layer of the condyle becomes thicker and the cartilage laver thins to approximately 0.3 mm in humans. The underlying bone trabeculae, although sparse, become progressively thicker and remain oriented superiorly and posteriorly, toward the direction of condylar growth. This pattern of growth continues through the period of the late mixed dentition, approximately 7 to 12 years of age. The articular disc remains highly vascularized and rich in fibroblasts during the first few years of life. After that time, the central part of the disc becomes avascular and less cellular, and the collagen fibers become oriented perpendicular to each other, anteroposteriorly and mediolaterally. The periphery of the disc and, in particular, its most posterior region, the so-called retrodiscal or bilaminar region, remain highly vascularized as well as being characterized by the presence of nerve endings.

Juvenile-Adolescent Period The second decade of life, especially toward its latter half, is characterized primarily by ~'O" -"~ _- %'-"5,,s-V4m

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c o n t i n u e d but progressive slowing of the growth of the TMJ. By age 10, the mandibular condyle is characterized by a maintenance of the relativelv thick articular tissue layer, progressive reduction in the size of the entire growth cartilage layer, and evidence of increased mineralization in the deeper portion of the hypertrophic zone. After age 13 to 15 years, the cartilage layer decreases further in thickness; however, it is not necessarily lost altogether (Fig 2). The proliferative layer is present through at least the age of 18. 3~ Hypertrophic condylar cartilage, which is an indication of an actively growing condyle, has been observed in autopsy specimens throughout the second decade of life and, in some subjects, through age 30. 3~ By 19 to 27 years of age, only islands of cartilage cells typically remain in the superior and anterior regions of the condyle. :~1'33 The onset of a cortical bone cap coalescing the trabecular bone beneath the condylar cartilage becomes apparent by approximately 10 to 12 years of age, and it becomes essentially complete by 20 years of age. 34 As documented by Lubsen and coworkers 32 and by Pullinger and colleagues, 35 the bone cap increases in thickness from approximately 0.1 mm in immature subjects, to 0.4 mm in young adults, to 0.6 mm in adults. With the formation of the bone cap, the tissue immediately deep to the prechondroblastic layer of the mandibular

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Figure 2. High power view of a parasagittal view of the articular eminence (A) and condylar cartilage (B) of a juvenile rhesus monkey. A, articular layer, comprised of the dense connective tissue specialization of the outer, fibrous layer of periosteum. G, entire growth cartilage, which can be subdivided further into four zones: prechondroblastic or proliferative zone (P); chondroblastic zone (C); zone of hypertrophy (H); and zone of endochondral ossification (E). (Modified with permission from Carlson DS. Growth of the temporomandibular joint. In: Zarb et al, editors. Temporomandibular Joint and Masticatory Muscle Disorders. Copenhagen, Denmark, Munksgaard. 1994.)

265

TMD, Facial Growth, and Orthodontic Treatment .¢

condyle and the articular eminence now hecome fibrocartilage, characterized by less cell n u m b e r , more extracellular matrix, and a nonh y p e r t r o p h i c a p p e a r a n c e typical o f hyaline cartilage that is not actively growing.

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Adulthood T h e cartilage o f the h u m a n I'M] is essentially completely replaced by bone a r o u n d the beginning of the f o u r t h decade of life. T h e articular tissue remains relatively u n c h a n g e d in appearance t h r o u g h o u t a d u l t h o o d , although it may u n d e r g o metaplastic transformation into tibrocartilage, d e p e n d i n g on the biomechanicalloading to which the joint was subjected. Deep to the a r t i c u l a r l a y e r in the n t a n d i b u l a r condyle the tibrocartilage is typk:ally partially mineralized, at which time it is r e f e r r e d to as c h o n d r o i d - t y p e bone (Fig 3). Within the nfineralized, c h o n d r o i d bone layer, islands o f hyaline cartilage may be f o u n d until relatively old age. Once the bony cap is fully present, active growth o f the m a n d i b u l a r condyle has essentially ceased, although progressive and regressive r e m o d e l i n g may continue t h r o u g h o u t life, largely in response to the local biomechanical environ I n e n t . 15.17,36 TMD, Mandibular Facial Form

Growth,

and

As discussed previously, the broad category o f T M D is characterized by a rntmber o f signs and symptoms. Some of these, such as idiopathic joint and muscle pain (eg, myofascial pain) and limitation of jaw m o v e m e n t , might be considered acute conditions o f short-term, transient, or episodic nature. 1~ Even if they occur in y o u n g individuals, there is no reason to assume that such signs and symptoms are necessarily indicative o f an u n d e r l y i n g disorder that would have an adverse long-term e t t e c t on maxillofacial growth and form. Although there is a large a m o u n t o f literature d o c u m e n t ing the association between muscle function and facial form, a7-4° there are no data to indicate a relationship between muscle dysfunction associated with T M D (eg, myofascial pain/ dysfunction) and abnormal facial growth. 4l However, it is possible that some combination o f similar signs and symptoms could indicate the presence of a m o r e p r o f o u n d disorder

Figure 3. Photomicrographs of the crest of the articular eminence (A) and mandibular condyle (B) of a young aduh rhesus monkey (M. mulatta). Note: the pronounced presence of collagenous fibers (9') running between the articular tissue and the underlying bone in the condyle and the extensive bone cap in both the articular eminence and the condyle. (Modified with permission from Carlson DS. Growth of the temporomandibularjomt. In: Zarb et al, editors. 1 emporoman(libular Joint and Masdcatory Muscle Disorders. Copenhagen, Denmark, Munksgaard. 1994.)

that could lead to c o m p r o m i s e and even destruction o f growth-related tissues within the TMJ. 42 Notable in this category o f T M D are inflammatory diseases such as juvenile rheumatoid arthritis (JRA), as well as condylar aplasia or hyperplasia, psoriatic arthritis, ankylosing spondylitis, and neoplasms. Each o f these serious disorders, a h h o u g h they can lead to significant unilateral and bilateral dysplasia o f m a n d i b u l a r and facial growth, are fortunately rare.43, 44 T h e destructive impact o f J R A and some other rare conditions on the mandibular condyle has b e e n well d o c u m e n t e d in the literature. 45-5~ JRA, in particular, has been shown

266

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to have a significant effect on growth o f the mandible and on overall facial f o r m as a result of e x t r e m e c o m p r o m i s e and even destruction o f the cartilage o f the growing m a n d i b u l a r condyle. However, JRA has an estimated prevalence in the general population o f only 1% or less. 4° Moreover, when JRA and o t h e r significant disorders that will affect growth o f the T M J do occur, the systemic manifestations r a t h e r than the dysfunction o f the t e m p o r o m a n d i b u l a r a n d m a n d i b u l a r dysplasia are likely to be the p r e c i p i t a t i n g p r o b l e m s for which the patients seek treatment. 44 T h e r e fore, these disorders will not be discussed further in this article. However, a m o r e c o m m o n d i s o r d e r , o s t e o a r t h r o s i s / o s t e o a r t h r i t i s (OA), that clearly has potential effects on growth o f the TMJ, will be considered. T h e second factor involved in the potential effect of T M D on facial growth and f o r m is the maturational status o f the subject in whom the disorder manifests itself. Obviously, the extent to which facial f o r m could be affected by T M D is d e p e n d e n t on both the duration o f the diso r d e r and the a m o u n t o f growth remaining to be potentially expressed by the individual.

TMD and Growth of the TMJ

Temporal Region Quantitatively, the contribution o f the temporal part o f the T M joint to the d e v e l o p m e n t o f the face is small and not t h o r o u g h l y documented. 52'53 T h e r e are only a few cephalometric reports of horizontal and vertical positional change o f the fossa relative to the maxilla. 54'55 T h e r e is some evidence that the shape o f the glenoid fossa is associated with the growth o f the mandible. 56-~s However, the influence o f T M D on the d e v e l o p m e n t of the articular eminence and its subsequent role on the development of the face is not well known.

Mandibular Condyle In general, the disorder within the realm o f T M D that has the greatest potential affect o n growth o f the m a n d i b u l a r condyle, and consequently on the entire mandible, is OA. T e c h nically, osteoarthrosis is a n o n i n f l a m m a t o r y d e g e n e r a t i v e disease o f movable joints; osteoarthritis is a m o r e severe and symptomatic

inflammatory expression o f this disease. 13 T h e p r e v a l e n c e o f O A in samples r e f e r r e d for T M D problems is estimated to r u n f r o m 8% to 18%. 13 In addition, it has been d o c u m e n t e d that OA affects p r e d o m i n a n t l y adults in the third or f o u r t h decade, with a female to male ratio o f 1 to 5 in the fifth to sixth decade. 13'59 T h e r e are very few reports o n OA and its relationship to facial growth. 1'2'1s'6°-62 In fact, there is very little to be f o u n d on diagnostic criteria pertaining to OA o f the T M J and there is no gold standard for O A . 1'59'63-65 Crepitation, for example, certainly is not an exclusive sign o f O A . 66'67 Only one study has p r o v i d e d estimates o f OA in a y o u n g o r t h o d o n t i c population. 67 In a sample o f 170 children r e f e r r e d for o r t h o d o n tic t r e a t m e n t and followed longitudinally m o r e than 15 years with infracranial radiographs, a diagnosis equivalent to O A was m a d e in 5% o f the individuals, as c o m p a r e d to 8% to 18% in a T M D population, according to Zarb and Carlss o n . 68 In seven o f nine cases the diagnosis was m a d e at age 16 years or younger. T h e documentation for the two o t h e r cases was not sufficient to exclude later development. A l t h o u g h the literature predicts an increase o f OA with age, no new cases o f O A w e r e d i a g n o s e d t h r o u g h the e n d o f the study, at an average age o f 26.5 years. T h u s , it was concluded that OA detected incidentally in the third decade o f life could well be the exacerbation o f an older, l o n g e r existing, o s t e o a r t h r o t i c process. At present, a f u r t h e r 5 year follow-up is available on 90 individuals f r o m this study at an average age o f 31.5 years, and no new cases o f OA have been diagnosed. T h e r e is considerable debate c o n c e r n i n g the relationship between OA and mandibular growth. At the very least, OA within the T M J is typically associated with a b n o r m a l variations in condylar remodeling. OA in a growing child, as indicated by variation in c o n d y l a r f o r m , could be indicative o f a significant variation in the direction o f m a n d i b u l a r growth. O A also is associated with destruction o f articular tissues as well as increased r e m o d e l i n g and thickening o f the subarticular bone. 6'8 As n o t e d previously, the growing T M J lacks a true articular cartilage and is characterized by the presence o f a highly adaptable secondary cartilage located d e e p to the fibrous articular tissue. A1-

TMD, Facial Growth, and Orthodontic Treatment

though the significance of this with respect to the growth and adaptive capabilities of the TMJ is not fully understood, inwflvement of the subarticular cartilage will likely result in a severe compromise or cessation of condylar growth. Although different in terms of etiology, the outcomes of OA and .IRA, as they pertain to the TMJ, are similar. Both JRA and OA, especially in their more severe form, are associated with destruction of the articular tissue and prechondroblastic layer of the mandibular condyle and temporal region. As a result, the mandible exhibits a severely impaired vertical growth at the condyle. When the vertical growth of the condyle is impaired, the vertical cranial development of the entire ramus is blocked, perhaps with the exception of the coronoid process. 6'~'7° Thus, when OA and JRA arise during the period of active facial growth, they may be expected to result in a relatively short ramus, which in turn creates a backward autorotation of the mandible, resulting in an anterior open bite. The facial profiles of patients with OA and .IRA are almost identical and are indeed characterized by backward rotation and a tendency to an open bite.2,49,5 i ,61,71.72 In 1994 it was concluded that there seems to be a typical face for individuals with OA, the distinction being a backward rotated and adapted mandible) ~ Mandibular morphology and position were identical, but somewhat more extreme, in adults relative to juveniles. The diagnosis of OA in juveniles predicted an adapted mandibular morphology and position at adulthood; the diagnosis of OA in adults was already associated with an adapted mandibular morphology and position at adolescence. The latter finding is in agreement with the previous conclusion 67 that OA of the m a n d i b u l a r condyle can take place in early adolescence. Articular Disc

In an excellent review on disc interference disorders, Stohler 73 emphasized the need for a better case definition to delineate the subset of disc-interference disorders, or DID, from other conditions affecting the TMJ. It appears that many subjects without any complaints may exhibit a disc-condyle assembly similar to that observed in DID symptomatic subjects. Also,

967

.joint sounds show tile poorest reliability of all clinically relevant variables. Stohler concluded that advances in modern imaging technology have not enhanced our insights into the etiology of DID and therefore imaging is more likely to result in overemphasis of the mechanical aspects of disc displacement. Specifically, interventions aimed at the repair of the disccondyle complex have not been able to show significant benefit. 7:~ Disc interference disorders, or internal derangements, relate to the disc-condyle assembly and, as such, may be expected to exert little or no influence on mandibular growth. As long as the mesenchymal covering of the condyle remains intact, the growth potential of the condyle will be unaffected. Recently there has been considerable discussion in the clinical literature concerning the potential effect of internal disk derangement (ID) on facial growth and ti~rm. According to Schellhas and coworkers, 12 there is a causal relationship between ID and abnormal growth of the facial skeleton, characterized primarily by mandibular retrognathia, mandibular asymmetry, and occlusat instability. Specifically, they proposed that, "Once a TMJ is internally deranged, adaptive or degenerative osteocartilaginous processes take place in the mandible, temporal bone, and masticatory m u s c l e s . . . In the growing facial skeleton, [this] either retards or arrests condylar growth, which results in decreased vertical dimension in the proximal mandibular segmeut(s) with uhimately mandibular deficiency or asymmetry." In essence, this postulate is an reiteration of Boering's thesis, I which led to the initiation in 1970 of the Groningen prospective longitudinal study on TMD in growing children. 9 According to Schellhas and colleagues,19 the primary factor leading to abnormally deficient mandibular growth in the presence of ID is presumed to be compromise of the blood supply to the mandibular condyle, resulting in osteoarthritis, avascular necrosis (AVN), and regional osteoporosis. Schellhas and coworkers put forward four arguments related to the relationship of ID to m a n d i b u l a r and facial growth. First, it was p r o p o s e d that ID is present in a disproportionately large and previously unrecognized number of young patients (approximately 90%) presenting with

268

Dibbers and Carlson

mandibular deficiency and facial asymmetry. Second, it was postulated that ID is a primary etiologic factor resulting in abnormalities of mandibular growth and facial form. Third, it was proposed that orthodontics and orthognathic surgery cause increased biomechanical loading of the TMJ, which cannot be tolerated by a compromised joint. As a result, fourth, " . . . therapeutic endeavors such as orthodontics and orthognathic surgery may either proyoke or exacerbate mechanical and inflammatory TMJ symptoms . . . " Reaction to the concepts put forward by Schellhas and coworkers concerning the relationship between ID and abnormal growth of the mandible and facial skeleton has generally taken two forms. Those clinicians who consider T M D in general, and ID in particular, to be the dental equivalent of the Black Plague, welcome every a r g u m e n t as a stimulus to finally get the orthodontic specialty to " .. pull its head out of the sand and realize what is h a p p e n i n g in the real world. ''v4 However, others find significant problems with several features of Schellhas' concepts and methodology. For example, it is difficult to accept that one and the same noxious influence, ie, orthodontic treatment, is the principal cause for both provocation and exacerbation of" TMD. This leaves unanswered the question of what provoked the TMD in the first place, later to become exacerbated. It has been stressed previously that mandibular and facial growth will experience relatively little abnormal variation in direction and a m o u n t unless the condylar cartilage, and especially the prechondroblastic layer, is significantly compromised or destroyed. OA, in particular, does have the potential for a significant effect on the condylar tissue that is capable of resulting in alteration of the direction and a m o u n t of condylar growth. Similarly, central to the notion that ID plays a significant causal role in abnormal mandibular and facial growth is the assumption that it results in OA, which in turn leads to AVN and regional osteoporosis. 12 At one time, disc interferences were thought to form the first step in a dangerous cascade of events eventually leading to osteoarthrosis of the bony joint components. 75 This postulate has never been proven and, on the contrary, it seems much more compelling to consider disc

i n t e r f e r e n c e s as an a c c o m p a n y i n g sign o f condylar destruction rather than its cause. 76'68 Simple mechanistic explanations like joint hypermobility also have not stood the scientific test. 77 As long as the mesenchymal covering of the condyle remains undisturbed, no mechanism can be theorized which, as a result of disc interference disorders, induces developmental changes in the normal growth of the mandible. Currently the direct interaction between disc interference disorders and the condition of condvlar tissue is u n k n o w n at best. Although there are at present no postulates that connect disc interference disorders directly with different growth potentials of the face, there is reason to explore the association between disc interference disorders and facial form when signs and symptoms are taken as indicators of growth patterns. ~ T h e association between disc interference disorders and facial morphology traditionally has been assessed by comparing the prevalence of signs and symptoms in a group with characteristic orthodontic anomalies such as deep bite, open bite, or cross bite with that of a reference population. 7s A higher percentage of signs and symptoms in one of these a priori selected groups should be interpreted as an association between T M D and facial morphology. Only a few studies have reversed the question and explored facial m o r p h o l o g y in groups selected on the basis of T M D criteria. Yet, there exists an essential difference between the two approaches. T h e first m e t h o d establishes TMD signs and symptoms in groups selected on the basis of morphological criteria. T h e alternate method seeks morphological characteristics in groups selected on the basis o f T M D criteria. Nesbitt and coworkers, 70 in a retrospective study, concluded that adults with TMJ clicking had significantly deeper bites, greater overjets, and more severe Class I1 occlusal relationships at age 14 to 16 years. Stringert and Worms, s° in a preliminary report, f o u n d a tendency toward an increased horizontal discrepancy in patients with functional alterations of the TMJ. Brand and colleagues sl reported diff e r e n c e s in skeletal p a t t e r n s b e t w e e n 24 women with and 24 women without internal d e r a n g e m e n t c o n f i r m e d by magnetic resonance imaging (MRI). A comprehensive cephalometric analysis made it evident that women

TMD, Facial GrouJth, and Orthodontic Treat~nent

with internal d e r a n g e m e n t had "normal" vertical skeletal relationships, but horizontally significantly smaller m a n d i b l e s and maxillae. This finding must have puzzled the investigators, because they concluded in their last sentence that, "In general, no distinct relationship was f o u n d between the morphological features of the face and the internal d e r a n g e m e n t s of the t e m p o r o m a n d i b u l a r joints." It is difficult to see what mechanism possibly could explain shorter sagittal dimensions in relation to disc interferences, but this difficulty does not justify rejection o f the findings. With a d i f f e r e n t sample, a d i f f e r e n t statistical method, and d i f f e r e n t criteria, ie, palpated clicking and crepitation in contrast to MRIc o n f i r m e d disc i n t e r f e r e n c e disorders, Dibbers and van der Weele s2 f o u n d exactly the same results as B r a n d and coworkers, s1 T h e same set o f horizontal variables in adult patients with a palpated click or crepitation showed a significantly shorter dimension: articular to A point, palate length, articulare to pogonion, and gonion to pogonion. Notably, true vertical facial d i m e n s i o n s n e v e r d i f f e r e d significantly between groups. Because the full d o c u m e n t a t i o n made more than 14 years previously was available, it was possible to d e t e r m i n e the facial dimensions o f these adults at a time when they were still children. It a p p e a r e d that the shorter horizontal d i m e n s i o n s t h a t c h a r a c t e r i z e d adults with clicking joints were already significantly s h o r t e r in their teenage faces, although the majority o f the joints were not yet symptomatic at that age. Faces t e n d e d to be "flat" 14 years before clicking was palpated, thus indicating that characteristic horizontal facial differences p r e c e d e d the e m e r g e n c e o f signs by at least 14 years. This implies that not all T M D signs in adults can be r e g a r d e d as being exclusively the result o f some etiologic factor operating after the teenage period. On the basis o f these studies, signs o f disc i n t e r f e r e n c e disorders are related to horizontal deficits o f the midface. Although the horizontal deficit was already evident at an average age o f 12.5 years, no conclusion can be drawn as to which point in time growth b r o u g h t about this difference. T h e question o f causation or temporal o r d e r o f events cannot be solved bv the present studies.

269

Conclusions Reviewing o f the literature for evidence o f clinical implications o f T M D on facial growth and consequently for o r t h o d o n t i c t r e a t m e n t makes it clear that there still is m u c h work to be done. Many h y p o t h e s e s have b e e n b r o u g h t forward, but over time many have failed scientific clinical evaluation. More studies are in progress. Statistically, an association has not been shown between signs and symptoms assigned to TMD, on the one hand, and quality o r t h o d o n t i c t r e a t m e n t on the other. As o u r understanding o f T M D develops, new studies will have to narrow down the targets o f research. T h e potential adverse effects o f T M D on facial growth have been e x p l o r e d in the literature. In cases o f JRA, osteoarthrosis, a n d o t h e r similar conditions, an adverse effect on m a n d i b u l a r d e v e l o p m e n t has b e e n d o c u mented. It seems that impaired m a n d i b u l a r growth in these patients necessarily results in o r t h o d o n t i c t r e a t m e n t , r a t h e r t h a n the reverse. A n o t h e r controversial issue is the interpretation o f findings of an elevated prevalence o f T M D in individuals selected on the basis o f facial m o r p h o l o g y , eg, o p e n bite. T h i s approach has led to speculation on the etiology o f T M D . We p r o p o s e an a l t e r n a t e r e s e a r c h method, by d e t e r m i n i n g facial m o r p h o l o g y in groups selected on T M D criteria. It appears that disc interferences in adults are associated with a horizontally shorter facial depth. O n e study even f o u n d that these adults were already horizontally shorter many years b e f o r e T M D was d i a g n o s e d . ' T h u s , when studying the implications o f T M D for facial growth and for orthodontic treatment, we have to look at child r e n before the need for t r e a t m e n t is established. T h e etioIogy o f T M D in this perspective antedates o r t h o d o n t i c treatment.

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