Download Evolution, Epidemiology and Etiology of Temporomandibular Joint

JIAOMR
10.5005/jp-journals-10011-1061
REVIEW ARTICLE
Evolution, Epidemiology and Etiology of Temporomandibular Joint Disorders
Evolution, Epidemiology and Etiology of
Temporomandibular Joint Disorders
Sujata M Byahatti
Reader, Department of Oral Medicine and Radiology, Maratha Mandals NG Halgekar College of Dental Sciences and Research
Center, Belgaum, Karnataka, India
Correspondence: Sujata M Byahatti, Reader, Department of Oral Medicine and Radiology, Maratha Mandals NG Halgekar
College of Dental Sciences and Research Center, Plot No. 49, Sector No. 9, Malamaruthi Extension, Belgaum-590016, Karnataka
India, e-mail: [email protected]
ABSTRACT
The temporomandibular joint (TMJ) is unique to mammals, but among different mammalian groups, its morphology and function vary enormously. It
is likely that various species show less loading of jaw joints during chewing than humans do. It took approximately 130 million years for the
evolutionary process to stabilize this composite, basic vertebrate head skeleton to the jaws. Very little documentations are noted on anthropology of
TMJ. When it is concerned with epidemiology, temporomandibular disorders (TMDs) have a number of consistent findings and various causative
factors that can contribute to TMDs. The aim of the following article is to provide detailed information regarding its evolution, epidemiology and
various causative factors leading to TMDs.
Key Message: The masticatory system is extremely complex.
Keywords: Temporomandibular joint, TMDs, Epidemiology, Biomechanics, Animal, Mastication.
INTRODUCTION
TMJ is a unique joint in which translatory as well as rotational
movements are possible, and where both the ends of bone articulate
in the same plane with that of other bone. It is also called as
ginglymodiarthroidal type of joint wherein it has sliding movement
between bony surfaces, in addition to hinge movement, common
to diarthroidal joint.1
Jaws and jaw joints hold a particular importance in the history
of vertebrates. Comparative studies of many different species have
also documented to understand the idea of perpetual change over
time. Complicating features of jaws and their joints leading to
those of mammals have derived by selective playing with adaptive
modifications of several original elements.2 The following article
provides detailed information regarding its evolution along with
the epidemiology and etiology of TMDs.
DISCUSSION
The masticatory system is extremely complex. It is primarily made
of bones, muscles, ligaments and teeth. Movement of mandible
needs coordination between them to maximize function and
minimize the damage to surrounding structures. This movement
occurs as a complex series of interrelated three-dimensional
rotational and translational activities, which is determined by
combined activities of both TMJs. This complex biomechanics of
TMJ makes it difficult to understand the insight of temporomandibular joint.3
Temporomandibular joint (TMJ) is a cardinal feature that
separates mammals from other vertebrates. As befits its late
evolutionary origin, the TMJ also makes a tardy developmental
appearance.4
The TMJ is interesting because of its constituent bones,
mandible and squamous temporal, which are intramembranous in
origin. Thus, the tissue that covers each articulating surface is a
secondary cartilage with a fibrous skin derived from the periosteum.
Another nearly constant feature is the intra-articular disk. The disk,
even when incomplete, is associated with the lateral pterygoid
muscle,5 which has led some authors to speculate that it arose as a
tendon, which later formed the new joint.6
Origin of the Vertebrate Head
A complete vertebrate is a species not only with backbone but
also with biting jaws. The first vertebrates had no biting apparatus
but the process of cephalization also produced the singular
structures called the jaws. Furthermore, complete mammals have
long been distinguished from all other vertebrates and from
animals2 very nearly mammalian largely on the basis of their jaw
ear structure. However, there is an even greater significance to
jaw joints in vertebrate evolution. The true diarthrodial joint was
first formed in fishes, and its basic structure remained essentially
unchanged when it was appropriated by the limbs of land animals.
Diarthrognathus7and Probainognathus8 have contact between
two bones, squamosal and dentary, which form the jaw joint in
mammals.
Diarthroses are the most complex joints with a wide single
articular cavity surrounded by a specialized sleeve lined with a
synovial membrane.2 Schizarthrosis are joints made more mobile
by several small separated splits or joint spaces interrupting their
bonding tissues. The simplest joints are synarthroses in which the
parts are made slightly movable by a binding of cartilage,
fibrocartilage or connective tissue between them.2
Evolutionary Stages
The primary jaws were modified gill arches that were connected
at their caudal ends by a simple hinge joint. There was an obvious
mechanical deficiency in this sort of arrangement because the joint
was left hanging-free, protruding slightly on each side like
Journal of Indian Academy of Oral Medicine and Radiology, October-December 2010;22(4):S13-18
S13
Sujata M Byahatti
bowlegged elbows of a primitive reptile within the body wall. The
jaws were further strengthened, stiffened and protected by the
armor of numerous dermal bony plates plastered to their outer
surface. Some of their bones at the edge of the mouth also
developed teeth. These outer tooth bearing plates braced by
adjacent dermal bones are known as secondary jaws. However,
the primary jaws still formed the single joint on each side for the
entire jaw complex.2
Despite its status as a mammalian identifier, the TMJ shows
remarkable morphological and functional variation in different
species, reflecting not only the great mammalian adaptive radiation
in feeding mechanisms, but also freedom from constraints, such
as bearing body weight. The most extreme evolutionary variants
include: (1) loss of the synovial cavity in some baleen whales;
(2) loss (or possibly primitive absence) of the disk in monotremes,
some marsupials, and some edentates (anteaters and sloths);5,9
(3) variations in the orientation of the joint cavity from parasagittal
(many rodents) to transverse (many carnivorans); and (4) reversal
of the usual convex/concave relationship so that the mandibular
condyle becomes the female element.10 In addition, the relative
size of the joint is exceedingly variable. Soft tissue details, such
as capsular ligaments11and collagen orientation in the disk12 are
also highly species specific. The striking anatomical differences
in TMJs are clearly tied to biomechanics. The features mentioned
above are either correlates of loading (e.g., size of articular
surfaces) or movement (e.g., orientation of the joint) or both.
Loading of the TMJ is a reaction force arising from the
contraction of jaw muscles; its magnitude depends strongly on
the position of the bite point relative to the muscle action line.
The evolution of the TMJ is thought to have coincided with a
period of low reaction loads with higher loading having evolved
repeatedly in different lineages,13 including our own. Rodents fall
in the category of minimal TMJ loading, especially during chewing.
In contrast, carnivorans such as dogs probably sustain TMJ loads
that are higher than those in primates.14 Complex movement in
three planes of space is also a primitive characteristic of TMJ, at
least if embryology is any indication6 but there is no uniformity in
how movements are accomplished. Opening of the jaw usually
involves a combination of forward sliding and rotation around a
transverse axis, but some carnivorans have lost the ability to slide
and some specialized anteaters instead use a rotation around the
long axis of the curved mandible.9 Similarly, transverse movement
is usually accomplished by moving one condyle forward and the
other one backward, but carnivorans use a combination of lateral
sliding and rotation around the long axis of the mandible.15
Amphibia
The single joint for the double jaws (Figs 1A to C). The jaws of
these creatures were used only for protection. The skull became
kinetic, new movable joints appeared within the cranium. This
ingenious device was a shuttling pterygopalatine component
coordinated with joints between the frontal and nasal bones.
Proliferation of loose, movable parts imparts the architectural
stability of the skull. This kinesis has disappeared in the crania of
reptiles, such as turtles and crocodiles those feed in water.2
In the carnivorous Pelycosauria, with which we are more
directly concerned since they include the ancestors of all the later
S14
A
B
C
Figs 1A to C: Reptilian jaw (A) Agnathia (B) Gnathostome
(C) Osteichthyes
mammal-like reptiles and so of the mammals, the teeth are all of a
simple blade-like form. They have distal and mesial cutting edges,
often serrated like a bread saw. This demonstrates that the
sharpening of the teeth by direct tooth-to-tooth contact,16 which
is so important in there in mammals, did not take place in these
mammal-like reptiles.17
The skull of a primitive amphibia tends to be long, wide and
remarkably flat. The first notable change from the amphibian
structure was the disappearance of the otic notch that supported
the tympanum of the primitive ear. The teeth began to lose their
continuity of repetition that is different segments along the dental
line developed teeth of different sizes and incipient functions.2
Reptilia
Reptiles cannot chew.2 In general, they use their teeth only to seize
their prey, and if this cannot be swallowed whole, it is torn apart
by a number of animals or by a single animal ‘worrying’ it. The
JAYPEE
Evolution, Epidemiology and Etiology of Temporomandibular Joint Disorders
group of reptiles which later gave rise to mammals - the ‘mammallike reptiles diverged at an early stage from the main reptilian stem,
and by the Permian, some 250 million years ago, were widespread
and might reasonably be regarded as the ‘Lords of Creation’. Later
their place has been taken by the dinosaurs, which remained the
dominant group until the latest Cretaceous. The mammal like
reptiles did not, however, quite disappear. Small members of the
group survived, perhaps in areas where there was insufficient food
for the large dinosaurs, or by eating items of food too trivial for
their notice. In this group of tiny mammal-like reptiles, a number
of changes took place, all probably associated with the acquisition
of the ability to maintain a body temperature above that of their
surroundings. This increased their activity and their ability to avoid
their enemies, but it carried the penalty that it vastly increased the
food requirement.17
Reptilia2 have loss of bony parts (Figs 2A to D). In the
Pelycosauria, the lower jaw is of an essentially reptilian form. The
A
B
tooth bearing bone or dentary has a strictly limited extension distal
to the tooth row; the other bones of the jaw are well-developed
and comprise the posterior third of the jaw. The quadrate—the
skull bone which forms with the articular in the lower jaw, the
jaw hinge, is a large bone with a considerable dorsoventral
extension.17
Mammalian Architectural Theme
The viscerocranium provides roofs and walls to the upper food
way, the neurocranium houses the brain whereas the mandible is
a long, straight, level bar with its fulcrum, the jaw joint at the
backend. The mandible walls the upper food way, which is roofed
above by the palate and floored below by a muscular hammock
hung between the bony bodies of both sides. This is the basic
characteristic of mammalian skull, from it, two adaptive feeding
modifications labeled carnivores as opposed to herbivores exist.2
The early American forms are grouped as the Pelycosauria,
comprising carnivorous, piscivorous and herbivorous forms. The
herbivores are of interest as they were the first group of vertebrates
to exploit plant life directly as food. The specialization of the teeth
and masticatory apparatus is such in herbivorous forms that their
capacity for further evolution is limited, so that major evolutionary
changes are always initiated by carnivorous or insectivorous
forms.17
Austrolopithecus africanus skull (Fig. 3) is the least differentiated. The jaws protrude sharply housing a short cheek teeth. The
upper jaw has outstanding canine buttresses whereas the lower
jaw is fairly shallow. The zygomatic arches are quite slender. The
teeth are broad, spatulate, bulky and long rooted as they project
from their sturdy buttresses.2 Austrolopithecus boisei skull
(Fig. 4) is considerably differentiated. The skull dorsum is deeply
vaulted in a short asymmetrical arch, the supraorbital ridges are
bulky, jaws are severely retruded, no canine buttresses, and massive
zygomatic buttresses give the face a “dished” in frontal plane.
The teeth are smaller and occlusal surfaces are more than three
times greater than in modern man.2
Masticatory Action in Primitive Man
Animals, such as pig, bear, and humans can masticate a variety of
foods to a satisfactory degree. It is readily accepted that muscle
C
D
Figs 2A to D: Amphibian Jaw (A) Amphibian (B) Reptile
(C) Mammals like reptile (D) Mammal
Fig. 3: Australopithecus Africanus skull
Journal of Indian Academy of Oral Medicine and Radiology, October-December 2010;22(4):S13-18
S15
Sujata M Byahatti
A
Fig. 4: Australopithecus boisei skull
attachments in the humans depend upon the functional activity of
the individual for their development and that muscle development
can reflect the exercise and activity that each muscle experiences.2
Modifications of the muscular elements (Figs 5A to C) of the
apparatus were evident in the specialization of lateral pterygoid
muscle and a decrease in the bulk of temporalis muscle. Bilateral
contraction of the lateral pterygoid muscles permitted a
modification of condylar movement within the glenoid fossa to
include a protrusive excursion. It has been suggested that primitive
man’s protrusive movement has merely been a bilateral sequel to
the individual forward movement of each blanching condyle during
lateral excursions of the mandible.3
It must, of course, be remembered that nature has evolved
satisfactory modifications over countless periods of time and that
adequate adaptation may not be possible in a single lifetime.
Indeed, with observation of a wide range of functional activities
that have been satisfactorily accommodated by modification of
this joint in the animal kingdom, one is drawn to the belief that
the lack of time to respond is responsible for masticatory
dysfunction in the most cases.2
Changes in the masticatory apparatus of primitive man were
not only the result of his omnivorous diet, but also of the adaptation
of the upright posture that necessitated a change in the position of
the head relative to the spine. The inclusion of a protrusive mandibular movement and modification of the associated musculature
are characteristics of the hominoid masticatory apparatus.2
Epidemiology of TMDs
It is evident from the numerous epidemiologic studies on the
occurrence of TMDs in the general population where there are a
number of consistent findings. Firstly, signs of TMD appear in
about 60 to 70% of the general population and yet only about one
in four people with signs are actually aware of or report any
symptoms.18 Furthermore, only about 5% of the population will
have symptoms severe enough for them to seek treatment.
Another consistent finding is that of those who seek treatment
for TMD, by far the greatest majority is females outnumbering
males by atleast four to one. It is suspected that TMD affects both
males and females in almost equal numbers in general population
although females are possibly more likely to seek treatment.
S16
B
C
Figs 5A to C: Different groups of muscle attachments in
mandible
Although, TMD may occur at any age, the most common time of
presentation is early adulthood.19
The prevalence of TMD signs and symptoms20 in a large elderly
sample was composed of medicare recipients, where the sample
size was 429 subjects derived from an eligible sample of 866
subjects. The mean age of the sample was 74.4 years and 42%
were males overall, 12% of the subjects reported a history of TMD
and 6.5% reported pain with jaw function. Joint noise was
documented in 35.2% of the sample, joint tenderness in 8.4%,
muscle tenderness in 12.8% and limitation of jaw motion in 22.4%.
In pediatric populations,20 it has been reported that on a sample of
11 and 15 years subjects, who had been examined for signs and
symptoms, the sample was composed of 119 subjects where the
point prevalence of subjects reporting one or more symptoms of
JAYPEE
Evolution, Epidemiology and Etiology of Temporomandibular Joint Disorders
TMD increased with age (35% at age 7, 61% at age 11, and 66%
at age 15), 60% of the sample reported one or more TMD
symptoms, 66% reported one or more symptoms at age 15.
somatization, anxiety, and low self esteem. Combination therapy
(education, pharmacotherapy, trigger point therapy, physiotherapy
and intraoral appliances and relaxation therapy) may be helpful in
providing a better outcome.
Etiology
The causes of TMD range from traumatic injury to immunemediated systemic disease to neoplastic growths to incompletely
understood neurobiologic mechanisms.21,22 Less common but
better recognized causes of TMD are (1) a wide range of direct
injuries, such as fractures of the mandibular condyle (2) systemic
diseases, such as immune-mediated arthritis (3) growth
disturbances and (4) tumors. Some nonfunctional movements of
the mandible (bruxing) and tooth clenching habits are clinically
associated with a variety of jaw muscle symptoms and associated
less clearly with internal joint disk derangements.23 Chronic
parafunctional clenching is suspected of association with chronic
TMD and has been shown experimentally to cause acute TMD in
human beings.24 However, these behaviors are not established as
causes of TMD and may be propagating factors only.
Malocclusion is not established as an important factor in
TMD.25-27 There is no compelling evidence that orthodontic
treatment increases or decreases the chances of developing TMD
nor is there any evidence of increased risk for TMD related to
any particular type of orthodontic mechanics or to orthodontic
treatments with tooth extractions.28,29 TMD is also caused by health
care manipulations, e.g. holding mouth open wide, prolonging wide
opening of mouth, stretching or forcing the mouth open, forcing
the jaws shut, relate to routine dental examination, oral
endotracheal intubation for general anesthesia, and the entire range
of dental services from restorative and orthodontic treatments to
tooth extraction to orthognathic surgery. There is no scientific
evidence that common or routine dental or medical procedures
cause TMD. Orthognathic surgery, orthodontic treatment,
prosthodontic rehabilitation and mandibular fracture repairs have
been associated with morphologic TMJ changes and worsening
of pre-existing TMD.30-33
Diagnosis of TMDs
The gold standard of diagnosis in TMDs consists of (1) patient
history (2) physical evaluation, and in the most chronic cases,
(3) behavioral or psychologic assessment.23,34-39 This evaluation
should include a detailed pain and jaw function history as well as
objective measurements of such jaw functions as interincisal
opening, opening pattern, and a range of eccentric jaw motions.
TMJ sounds should be described and related to symptoms.
CONCLUSION
The different evolutionary stages have made this TMJ as complex
structure.
Clinical manifestation may not be completely contributory in
the diagnosis of TMDs. They need to correlate with standard
diagnostic modalities for the confirmation of origin of particular
problem. Various etiological factors have made the management
of TMDs challenging. Treatments of TMDs are behavioral,
psychologic and psychosocial factors rather than physical or
structural factors. Poor outcome could be related to depression,
REFERENCES
1. Anil Govindrao Ghom (Ed). A textbook of Oral Medicine, (1st ed).
Jaypee Brothers Medical Publishers (P) Ltd. 2005:530.
2. Sarnat, Laskin. ‘The TMJ-A biological basis for clinical practice’ (4th
ed).
3. Okeson JP. ‘Management of temporomandibular disorders and
occlusion’ (4th ed). Mosby Elsevier publisher Linda McKinley, 1998.
4. Smith KK. The evolution of mammalian development. Bull Mus Comp
Zool 2001;156:119-35.
5. Sprinz R. A note on the mandibular intra-articular disc in the joints of
Marsupialia and Monotremata. Proc Zool Soc London 1965;144:32738.
6. Du Brul EL. Evolution of the temporomandibular joint. In: Sarnat BG
(Ed). The Temporomandibular Joint. Charles C Thomas, Springfield,
IL; 1964;3-27.
7. Crompton AW. Proceedings of the Zoological Society of London
1958;130:183.
8. Romer AS, Price LI. Special Papers of the Geological Society of America
1940;28:1.
9. Naples VL. Morphology, evolution and function of feeding in the giant
anteater (Myrmecophaga tridactyla). J Zool 1999;249:19-41.
10. Bermejo A, González O, González JM. The pig as an animal model for
experimentation on the temporomandibular articular complex. Oral Surg
Oral Med Oral Pathol 1993;75:18-23.
11. Herring SW, Decker JD, Liu ZJ, Ma T. The temporomandibular joint
in miniature pigs: Anatomy, cell replication, and relation to loading.
Anat Rec 2002;266:152-66.
12. Gillbe GV. A comparison of the disc in the craniomandibular joint of
three mammals. Acta Anat 1973;86:394-409.
13. Crompton AW, Parker P. Evolution of the mammalian masticatory
apparatus. Am Sci 1978;66:192-201.
14. Herring SW. Animal models of temporomandibular disorders: How to
choose. In: Sessle BJ, Bryant PS, Dionne RA (Eds). Temporomandibular
Disorders and Related Pain Conditions. IASP Press, Seattle; 1995;
323-28.
15. Scapino RP. The third joint of the canine jaw. J Morphol 1965;116:2350.
16. Every RG, Kohne WG. Journal of the Linnean Society (Zoology)
1971;50(Suppl):23.
17. Kermack KA. Evolution of Mammalian Dental Structures (University
College, London, Gower Street, London WCJ). Section of odontology
389-92.
18. George Dimitroulis, M Franklin Dolwick, Henry. A Gremillion
‘Temporomandibular disorders. Clinical evaluation’. ADJ1995;
40(0):301-05.
19. Welden Bell. ‘Clinical management of temporomandibular joint
disorders’, Chicago, 1982, year Book medical publishers.
20. Fonseca RJ. ‘A textbook of oral and maxillofacial sugery’ (1st ed), 4th
volume p 39-46.
21. Milam SB, Schmitz JP. Molecular biology of temporomandibular joint
disorders: Proposed mechanisms of disease. J Oral Maxillofac Surg
1998;56:89-191.
22. Kopp S. The influence of neuropeptides, serotonin, and interleukin 10
on temporomandibular joint pain and inflammation. J Oral Maxillofac
Surg 1998;56:189-91.
23. Okeson JP. Orofacial pain: Guidelines for assessment, diagnosis, and
management. Chicago: Quintessence Publishing Co; 1996.
24. Glaros AG, Tabacchi KN, Glass EG. Effect of parafunctional clenching
on TMD pain. J Orofac Pain 1998;12:145-52.
Journal of Indian Academy of Oral Medicine and Radiology, October-December 2010;22(4):S13-18
S17
Sujata M Byahatti
25. Seligman DA, Pullinger AG. The role of intercuspal occlusal
relationships in temporomandibular disorders: A review. J
Craniomandib Disord Facial Oral Pain 1991;5:96-106.
26. Seligman DA, Pullinger AG. The role of functional occlusal relationships
in temporomandibular disorders: A review. J Craniomandib Disord
Facial Oral Pain 1991;5:265-79.
27. Bales JM, Epstein JB. The role of malocclusion and orthodontics in
temporomandibular disorders. J Can Dent Assoc 1994;60:899-905.
28. McNamara JA, Turp JC. Orthodontic treatment and temporomandibular
disorders: Is there a relationship?, Clinical studies. J Orofac Orthop
1997;58:74-89.
29. Turp JC, McNamara JA. Orthodontic treatment and temporomandibular
disorders: Is there a relationship?, Clinical implications. J Orofac Orthop
1997;58:136-43.
30. Tucker MR, Thomas PM. Temporomandibular disorders and dentofacial
skeletal deformities: Selected readings in oral and maxillofacial surgery.
Dallas: University of Texas Southwestern Medical Center at Dallas;
1996;4(5).
31. Hoppenreijs TJM, Freihofer HPM, Stoelinga PJW, Tuinzing DB,
van’t Hof MA. Condylar remodeling and resorption after Le Fort I
and bimaxillary osteotomies in patients with anterior open bite: A
S18
32.
33.
34.
35.
36.
37.
38.
39.
clinical and radiological study. Int J Oral Maxillofac Surg 1998;
27:81-91.
Arnett GW, Milam SB, Gottesman L. Progressive mandibular retrusionidiopathic condylar resorption, 1. Am J Orthod Dentofac Orthop
1996;110:8-15.
Arnett GW, Milam SB, Gottesman L. Progressive mandibular retrusionidiopathic condylar resorption, Am J Orthod Dentofac Orthop
1996;110:117-27.
Truelove EL, Sommers EE, LeResche L, Dworkin SF,Von Korff M.
Clinical diagnostic criteria for TMD. J Am Dent Assoc 1992;143:47-54.
Okeson JP. Current terminology and diagnostic classification schemes.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;83:61-66.
Dworkin SF, LeResche L. Research diagnostic criteria for temporomandibular disorders: Review, criteria, examinations and specifications,
critique. J Craniomandib Disord Facial Oral Pain 1992;6:302-06.
Fricton J, Schiffman E. Reliability of a craniomandibular index. J Dent
Res 1986;65:1359-64.
Fricton JR, Schiffman EL. The craniomandibular index: Validity.
J Prosthet Dent 1987;58:222-28.
LeResche L, Von Korff MR (Eds). Research diagnostic criteria. J
Craniomandib Disord Facial Oral Pain 1992;6:327-34.
JAYPEE