Several very specific features distinguish the temporomandibular joints and the mandible from joints on other bones; however, it is important to keep in mind that in almost every other respect, they are still synovial joints and have to work under the same rules as any other synovial joints.
1. The mandible is the only major bone with the same functional anatomic joint on both ends. For example, the femur has a hip joint on one end and a knee joint on the other end.
2. Both joints function as a single bilateral anatomic unit which is often referred to as the craniomandibular articulation.
3. The mandible, as a bone, and therefore a mesodermal structure, is unique in that it has teeth, which are ectodermal derivatives, incorporated into it's overall structure. The maxilla also has ectodermal derivatives, again teeth, incorporated into it's structure. That, too, makes the maxilla equally unique in comparison to other bones; however, the maxilla is immobile in function.
4. During normal functional movements the mandibular portion of the craniomandibular articulation comes to a unyielding end point of closure, the dentition of the maxillary arch.
5. The articular surfaces of the total temporomandibular joint articulation, mandibular and cranial, are covered with fibrocartilage while other synovial joints are covered by hyaline cartilage.
6. The temporomandibular joint capsule does not completely surround the joint, but is incomplete in the anterior aspect to allow for condylar motion in an anterior direction during wider opening movements and excursive motion.
7. Within the bilateral articular capsules, a peripherally contiguous fibrocartilage articular disc separates the actual joint into two separate compartments with differing functions. The superior joint compartment performs a primarily sliding-type function (arthrodial, translatory motion) while the inferior joint compartment functions as a hinge (ginglymus) in motion.
8. The temporomandibular joints are classified as ginglymoarthrodial joints, or both hinge and sliding joints.
As noted above, although the temporomandibular joints have some unique features they are still diarthrodial joints and must follow the same general rules of function as any other diarthrodial joint in the body. In general, diarthrodial joints have bones separated by a joint cavity, have joint surfaces lined with hyaline cartilage, have synovial membranes lining the surfaces of the joint cavity that are not directly in apposition, and contain synovial fluid. The purpose of a joint of any description is movement. The mechanical motion of any joint is also responsible for circulation of synovial fluids to all cartilagenous articular surfaces within the joint. Diarthrodial joints have other features in common with other joints in that they are made up of connective tissues containing cells, connective tissue fibers, and ground substance.
1. Cells directly associated with diarthrodial joints are chondrocytes, fibroblasts, osteocytes, and synovial cells. Cells are essentially responsible for the formation of and maintainence of the total extracellular matrix.
a. Chondrocytes - are cartilage forming cells.
b. Fibroblasts - form various connective tissue fibers, collagen, reticular, and elastic.
c. Osteocytes - form bone.
d. Synovial cells - phagocytize, secrete synovial fluids, hyaluronurate, chondroitin sulfate, keratan sulfate, and other proteins
2. Connective tissue fibers found in diarthrodial joints are collagen, reticular, and elastic.
a. Collagen fibers-provide the major structural fiber of the joint. Eleven types of collagen are recognized at this time. Collagens occur in all eukaryotic animal phyla except protozoans. Type 1 collagen consists of heavier type of fiber that is found in bone and in the fibrocartilage of the temporomandibular joints. Type II collagen is a thinner type of fiber and is produced by the chondrocytes within hyaline cartilage. Type IV collagen is found in basement membranes where it forms a fibrous structure similar to "chicken wire" in appearance. All collagen molecules are composed of three polypeptide chains, each one containing considerable lengths of Gly-X-Y tripeptide sequence which structurally allows a molecular triple helix formation. Once secreted into the extracellular space by the cells as pro-collagen molecules, carboxyl and amino terminal extension peptides are cleaved off by pro-collagen peptidases resulting in the formation of insoluble, cross-linked, extracellular aggragates which function primarily as supporting elements within tissues. Collagen fibers are commonly formed into heavy sheets and bundles of parallel oriented fibers, this regular orientation of fibers accounting for the white, glistening surface sheen associated with ligament and tendons.
b. Reticular fibers are small diameter branching fibers that are found surrounding larger collagenous fibers. The reticular fibrocytes resemble embryonic connective tissues and mesenchymal cells and are likely responsible for repairing tissue damage after being activated by an inflammatory process.
c. Elastic fibers are intermediate size fibers that are highly elastic. The structural component is a protein called elastin which is extensively cross-linked and randomly coiled allowing the fibers to stretch and recoil. Elastic fibers are concentrated in the superior lamina of the retrodiscal tissues and medial peripheral attachments of the articular disc to the petrotympanic fissure. The elastic properties of these tissues allow the articular disc to move in association with the mandibular condyle. Elastic fiber formation is closely associated to the secreting cell surface and is thought to be a mechanism by which the fibroblast cell closely controls fiber orientation. Elastin may be chemically similar to a Type VI collagen.
3. Ground substance refers to the rather amorphous material in which the chondrocyte cells and fibers are embedded. Chemically, ground substance is made up of dissaccharide molecules called glycosaminoglycans. A high negative charge on these polysaccharide molecules imparted by the presence of numerous sulfate and carboyxl groups makes them chemically bind large amounts of water and cations. Other macromolecular components called proteoglycans are also found in the extracellular matrix. These consist of linear backbone molecules of hyaluronic acid attached to protein cores. Hyaluronic acid is usually considered an 'honorary' proteoglycan, because the polysaccharide chain is not covalently bound to a protein core as described above. Additionally, hyaluronic acid is not thought to be synthesized in the Golgi apparatus of the chondrocytes as are the other glycosaminoglycans. It is also found as a coating closely surrounding cell surfaces and as a free polysaccharide in synovial fluid and the vitreous humor of the eye.
In the vitreous body of the eye, and in synovial fluid of joints, the high concentration of hyaluronic acid produces a highly viscous gel which functions to retard water movement and migration of cells, or other particles, into the light path of the eye, or away from the load bearing cartilage surfaces of joints. Keratan sulfate and chondroitin sulfate molecules are formed by the Golgi apparatus of the chondrocytes. These proteoglycan complexes are directly synthesized on a protein core. The completed proteoglycans attach to the protein cores giving the whole macromolecular structure an appearance similar to the bristles on a bottle brush. The high negative charge density of the glycosaminoglycan chains thus formed allows them to repel each other and bind large quantities of water giving them a highly desirable physical structure in functions where they must act as cushions for repetitive, variable, compressive loads (joint cartilage, aorta, and tendons). Compressive forces applied to the cartilage surfaces gradually displace water from the molecular structure, but when the load is removed, the proteoglycan molecules imbibe water and re-expand rapidly. Proteoglycans are responsible for the structural properties of cartilage giving it elasticity, resistance to compression, and osmotic properties that give rise to expansion and contraction in volume.
Neither fibrocartilage, nor hyaline cartilage forming the lining cartilage of diarthrodial joints has any inherent blood supply incorporated into the cartilage layer itself. The chondrocytes depend on diffusion of nutrient molecules from the synovial fluid into and throughout the ground substance. The process of diffusion is assisted by the action of hydrostatic forces produced at the cartilage surface by joint motion. Thus, active joint motion, and active fluid exchange brought about by this movement, is necessary for normal nutrition and physiologic maintainence of the cartilage layers of a joint.
The articular cartilage lining the opposing surfaces of diarthrodial joints consist of chondrocytes embedded in a matrix of collagen fibers and osmotically active ground substances, or proteoglycans. Fibrocartilage and hyaline cartilage layers in joints are completely avascular, are devoid of nerve endings, and have no lymphatic drainage.
While the fibrous content of hyaline cartilage surfaces is smaller diameter and less obvious Type II collagen, fibrocartilage surfaces have heavier Type I collagen bundles that account for the white, glistening appearance of the tissue. In fibrocartilage surfaces the collagen fibers bundles are found to generally run parallel to the joint surface, but they also decend through the ground substance matrix to anchor firmly in the subchondral bone. A surface layer of hyaluronodate, or hyaluronic acid gel forms the actual highly lubricated load bearing surface of the articular cartilages. Thus lubricated by synovial fluids, the hyaline and/or fibrocartilage layers of joint surfaces provide a remarkably low friction and self lubricating load bearing surface. Cartilage surfaces bathed in synovial fluids are also quite active osmotically during normal function and the unrestricted flow of synovial fluid over all joint surfaces is essential for the cartilage surface resiliency and lack of friction.
The osmotically active nature of the joint cartilage is attibuted to the presence of the proteoglycan ground substances within which the action of compressive forces results in the release of water molecules from the cartilage surface into the synovial fluid. As a result of compressive loading and egress of water molecules from the surface, the cartilagenous surface can be diminished in thickness. Releasing compressive forces generally results in the return of water molecules from synovial fluids to the cartilage surfaces restoring original volume to the tissue. Normal function thus would consist of periods of time where the joint surfaces are being compressibly loaded and decreased in volume, and periods of time where the joint surfaces are unloaded, allowing an increase in volume. The collagen fibers embedded within the ground substance of hyaline, or fibrocartilage layers, reinforce the structural integrity of the cartilage layer and also function to resist osmotic expansion of the cartilage layer beyond what is essentially the normal thickness, or volume of the cartilage layers. The physical characteristics resulting from this structural combination of fibers, matrix, and osmotic activity are essentially those of tissue resiliency and resistance to permanent deformation under loading.
In day-to-day function, many diarthrodial joints spend extended periods of time under compressive loading, while others may spend the greatest proportion of time in a state of extension, or traction. Either state is physiologically tolerable as long as a certain amount of what would be termed "normal motion" occurs and synovial fluid circulation over and into the lining cartilages is allowed to occur without interuption.
The synovial membranes line all of the surfaces of diarthrodial joints, excepting the articular surfaces, and the articular discs, or meniscal structures within the joints.
The synovial membrane is made up of an intimal layer of synovial cells from one to four cells in depth that rest over a loosely organized subintimal connective tissue layer that has an extensive plexus of small vessels and numerous fibroblasts, mast cells, and macrophages. In contrast to other secretory cell layers, the synovial layer lacks a distinct basement membrane separating it from the underlying connective tissues. This enables a rapid diffusion of substances into and out of the joint cavities and back into the circulatory or lymphatic systems. Synovial fluid is considered to be a dialysate of plasma.
Two types of synovial cells are recognized: Type A cells are responsible for the synthesis and transport of hyaluronodate and are involved in active phagocytosis of any particulate debris transported to them by synovial fluid circulation. They have prominant golgi apparatus when viewed by electron microscopy. Type B cells are responsible for synthesis and transport of proteins into the synovial fluid. They have a prominant endoplasmic reticulum when viewed by electron microscopy.
Functionally, the synovial membrane produces the synovial fluids which serve to (1) lubricate the joints surfaces during all joint movement,(2) provide essential nutrients for the chondrocytes within the cartilage matrix, (3) aid in the phagocytosis of, and elimination of particulate and dissolved substances within the closed joint cavities, and (4) provide the necessary vehicle for transport and diffusion of substances into and out of the joint cavities and joint tissues. Lymphatic drainage occurs outside of the synovial layer.
Intracapsular inflammatory changes affecting the synovial membrane are associated with elevated protein level in the synovial fluid. The sodium hyaluronodate content of synovial fluid is not dispersed throughout the fluid, but is concentrated on the actual articular surfaces where it forms the lubricating and sliding surface of the joint. Hyaluronodate also seems to form a barrier layer that prevents migration of cartilage proteoglycan molecules into the actual joint space and also restricts inflow of synovial fluid enzymes into the cartilage layer.
In the abscence of normal circulation of synovial fluid problems seem to occur. In the early sixties, and interestingly enough, when I had my first clinical experience with a so-called "TMJ patient" (incidently, a patient who also happened to be a eminent medical librarian) I was directed to an article by Toller, who hypothesized that alteration in synovial fluid viscosity and a possible failure in normal joint lubrication may result in joint clicking and subsequent internal derangement of the temporomandibular joint. Koop, et al, tried to correlate levels of plasma proteins in synovial fluids collected from the temporomandibular joints with inflammatory changes and joint pain, but only about 25% (7 of 29) of samples demonstrated elevated protein levels. Some years later, Quinn and Bazan performed more sophisticated synovial fluid analyses on specimens of synovial fluid collected during TMJ arthroscopies and reported elevated levels of prostaglandin E2 and leukotriene B4 from joints that demonstrated synovitis to visual inspection.
Quinn expanded on Toller's orginal hypothesis and reported the necessity of a balance between normal synthesis and degradation of the collagen and proteoglycans of articular cartilage extracellular matrix in sustaining normal cartilage in the temporomandibular joints. Any factor that overwhelmed the normal physiologic capacity of the joint could lead to conditions where cartilage matrix degradation exceeded synthesis and would ultimately be associated with cartilage breakdown (softening, fibrillation (roughness), and surface erosion), alteration in synovial fluid viscosity, impaired lubricity and sliding capacity, and impairment in the normal movement of the articular disc. Of course, the ongoing result of these initial processes could eventually lead to erosion of the joint surfaces, and development of fibrous, or even bony ankylosis. Further research supporting this view was reported by Israel et al, who found increased levels of keratan sulfate in synovial fluid specimens sampled, and increased evidence of early osteoarthritis in patients undergoing arthroscopy that was not initially detected by clinical examination alone. Increased levels of keratan sulfate in synovial fluid samples thus served to indicate accelerated proteoglycan degeneration in temporomandibular joints with osteoarthritis.
In 1970, Salter coined a phrase "continuous passive motion", which was based on his observations that extended immobilization of any joint had deletorious effects on subsequent joint health. He noted that during a period of immobilization as short as three weeks, that synovial membranes became adherent to the associated joint surfaces much like adhesive tape sticks to skin surfaces. For all practical purposes, this adhesive phenomenon eliminated the actual joint and synovial fluid space between lining cartilage and synovial membranes and blocked normal synovial fluid interchange in the affected area. Nutritional flow between the synovial fluids and the underlying cartilagenous surfaces ceases. Thus, as a direct result of the lack of normal bathing of the joint surfaces with synovial fluid, the ensuing result was formation of a necrotic, or otherwise irreparable lesion that Salter referred to as "obliterative degeneration" of the articular cartilage.
The very action of joint movement appears to be necessary for the normal physiology of a joint. Motion is essential for the nutrition and lubrication of a joint, and the lack of what would be termed "normal motion" of a joint would appear to have potentially harmful effects on joint biochemistry. By extension of the previous line of reasoning, it would appear that any external factor that alters the basic homeostatic physiologic mechanism of the temporomandibular joint could become a significant factor in development of what everybody seems fond of calling "TMJ Problems". In essence, the physical mechanisms that could have significant importance on temporomandibular joint "health" (indeed, any diarthrodial joint by extension) may be as simple, or complex as:
1. Overloading a joint by any excessive applied force, external direct trauma.
2. Chewing hard objects, especially in unilateral function.
3. Chewing in a abnormal joint, or jaw position, gnawing.
4. Biting fingernails - with mandible thrusting.
5. Prolonged jaw clenching, possibly stress related.
6. Bruxing, which, it must be understood, rarely occurs in a dainty, and minimally excursive manner.
7. Occlusal disharmony, microtrauma.
8. Biochemical changes, systemic disease (Juvenile Rheumatoid Arthritis)
9. TIME ! That period of duration an insulting, or overloaded condition remains in effect.
10. Repetition rate.
11. Lack of normal joint movement, for any reason.
Therefore, it would appear that a process of initiation of damage comes down to basics: joint positional relationship (possibly abnormal) during force application, level of applied abnormal force, the duration of applied abnormal force, and any limitation of normal joint movement. There may also be external biochemical factors involved in the process that are not immediately evident, e.g., systemic diseases, physiologic effects of stress, bad genes, etc.
Joint positional relationship - assumes that a normal joint, in a normal, unstrained anatomic relationship, can probably physiologically sustain a significant degree of overload without any physiologic damage at all. What constitutes a physiologically tolerable degree of overload is an individual variable that depends on, for one thing, the degree of "normal loading" the joint usually experiences on a day-to-day, week-to-week, month-to-month basis. "Conditioning", might be a more understandable concept in this case. If a joint, any joint, is wholly adapted to a certain physiologic loading, and that loading has never been exceeded for any reason, sudden, or sustained application of excessive loading may produce unphysiologic response in that joint, most often manifested by an initial report of joint pain and stiffness some time after the initial insult. As a nation of weekend worriers, weekend diggers, and weekend lifters, we should all know the feeling well. The duration in this case is probably best qualified as being "occasional". Joints, all over the body, report back their general dissatisfaction with what we did to them, and being normal, well adjusted people, we recognize that we "overdid it" and we get under our desks, and bedcovers, and suck our thumbs and analgesics while lying back waiting for that feeling to go away. Usually, within a couple of days, we tend to forget the message reported by our own homeostatic mechanisms, and we begin to feel like we could do it all over again, or forget that we did what we did and swore we would never do again.
In a military boot camp, and with a basic body that is also operating at a prime period of life from a physiologic point of view, a sustained regime of insults interspersed with periods of rest and optimized nutrition gradually results in a body wide set of joints, or other myofascial structures, that successfully adapt to the demands of the drill instructors. It may even surprise most to realize that even the most miserable recruit has been placed in that seemingly exposed position fully expecting the worst, and fully working within the designs of legions of exercise physiologists employed by the government to produce a "well conditioned" individual at the end of the process.
It would appear that some individuals are predisposed to development of temporomandibular joint dysfunction. Just by rote, most clinician would agree that the majority of all patients with complaints in this area are female. Does this mean that femaleness is a significant predisposing factor to development of joint problems bodywide? The answer may be a resounding yes! to first glance, but, then again, may really only reflect the fact that females generally seek medical treatment more often than males. However, there may also be a set of predisposing factors beyond what are usually called pathophysiologic factors by many experts, that are also involved in the overall picture and that have not yet been fully recognized for their contribution as predisposing factors.
What could these factors be? The usual pathophysiologic factors associated with TMD problems are metabolic, neurologic, vascular, hormonal, nutritional, rheumatologic, degenerative, neoplastic, and infectious processes. Any single one, or any combination of this list of factors can be involved in an individual patient's problem, and all of them are well known to have great variability between individuals. Additionally, any one of these factors can also function as predisposing, initiating, or perpetuating mechanisms in craniomandibular disorders. Their individual importance, again, varies with every particular patient, but they are ignored at the clinician's peril. Together, or individually, they exercise significant influence on the clinical outcome of any case. To this previous list we can also add behavioral, psychosocial, physical factors, and even economic factors, for in the ideal world where such lists are often drawn, every patient with any significant health problem would receive "proper" treatment without regard to their socio-economic status.
Behavioral, pyschosocial, and psychologic factors are generally thought to include emotional state, personality traits, and individual self perception, or attitude. Physical factors are numerous, beginning with what is inherited to begin with, modified by environmental and developmental factors, or altered by iatrogenic stewardship and patient indifference and ignorance. This latter group would include occlusal disharmonies, malrelations of the jaws, and structural changes brought about by loss of teeth and subsequent failure to properly restore function.
While there is some controversy about whether malocclusion is an initiator, non-affector, or resultant of TMD, the debate is really nothing more than a rehash of the "which came first, chicken or egg" dilema. It is probably safe to assume that every individual clinician has his own pet opinion about the connection between malocclusion and development of TMD symptoms. An item in the "News" section of a recent ADA Journal noted that researchers at the University of Connecticut have been studying the synovial fluid of TMD patients and found tumor necrosis factor-alpha, a cytokine, or a protein associated with immune responses, including inflammation, and found that there is a positive correlation between the level of tumor necrosis factor-alpha and the pain reported by the patients in the study. Others will continually debate whether TMD pain/dysfunction is a disease, or simply a psychosomatic disorder; one side insisting that a chronic pain syndrome requires an underlying disease process, while the other maintains a position that there may be observable pathophysiologic changes within the temporomandibular joints that can be detected with sophisticated laboratory testing. That undeniable pathopysiologic changes are occurring within the synovial tissues of some temporomandibular joints, and affecting some patients is amply demonstrated by the U.C. study and an earlier report of the Arthritis Foundation(16) regarding proliferation of excessive synovial tissue and increased synovial fluid production in juvenile rheumatoid arthritis cases
The debate will never be settled in favor of one opinion or another due to the nature of the problem, and the magnitude of influencing factors that can come into play in development and maturation of a temporomandibular joint dysfunction problem.
1. Hasselbacher, P. Normal structure and function, in Kelly, W. N. (Ed.) Textbook of Internal Medicine, Philadelphia, PA, Lippincott, 1989, pp.968-971.
2. Jimenez, S. A. The connective tissues: Structure, function and metabolism, in Schumacher, H. R. (Ed.): Primer on the Rheumatic Diseases. Atlanta, GA, Arthritis Foundation, 1988, pp 6-14.
3. Howell, D. S. and Manicourt, D. H. Complex polysaccharides, in Schumacher, H. R. (Ed.): Primer on the Rheumatic Diseases. Atlanta, GA, Arthritis Foundation, 1988, pp 15-18.
4. Cohen, A. S., Brandt, K D., and Krey, P. R. Synovial fluid, in Cohen, A. S.(ed): Laboratory Diagnostic Procedures in the Rheumatic Diseases. Boston, MA, Little, Brown, 1975, pp 1-62.
5. Radin, E. R., Rose, M. R., Blaha, J. D., et al. Practical Biomechanics for the Orthopedic Surgeon (ed 2). New York, NY, Churchill Livingstone, 1992, pp 152 - 158.
6. Weiss, C. Basic structure of diarthrodial joints, in Parisien, J. S. (ed); Arthroscopic Surgery. New York, NY, McGraw-Hill, 1988, pp 3 - 18.
7. Toller, P. A. The synovial apparatus and temporomandibular joint function. Brit Dent J, 111:355, 1961.8Koop, S., Wenneberg, B., and Clemensson, E. Clinical, microscopical and biochemical investigation of synovial fluid from temporomandibular joints. Scan J Dent Res, 91:33, 1983.
9. Quinn, J. H. and Bazan, M. D. Identification of prostaglandin E2 and leuktriene b4 in the synovial fluid of painful, dysfunctional temporomandibular joints. J Oral Maxillofac Surg, 48: 968, 1970.
10. Quinn, J. H. Pathogenesis of temporomandibular joint chondromalacia and arthralgia, in Merrill, R. G. (ed): Oral and Maxillofacial Surgery Clinics of North America, Disorders of the TMJ I: Diagnosis and Arthroscopy, vol I. Philadelphia, PA, Saunders, 1989, pp 47 - 57.
11. Israel, H. I., Saed-Nejad, F., and Ratcliffe, A. Early diagnosis of osteoarthritis of the temporomandibular joint: Correlation between arthroscopic diagnosis and keratan sulfate levels in the synovial fluid. J Oral Maxillofac Surg 49:708, 1991.
12. Salter, R. CPM, Williams & Wilkins, Baltimore, MD, 1993.13 McNeill, C., Danzig, W. M., Farrar, W. B., et al. Craniomandibular (TMJ) - The state of the art. Position Paper of the American Academy of Craniomandibular Disorders. J Pros Dent 1980; 44:434-437.
14. News, JADA 126:24 1995.15 Exchange of letters, Dworkin, S.F., and Lerner, T. R, and Schlagel, E. Letters, JADA 126:16-18, 1995.
16. Arthritis in children. Atlanta: The Arthritis Foundation; 1994.
Copyright İR. E. Brossman, 1995
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