2. CONTENTS
1. Introduction
2. Terminology
3. History of TMDs
4. Epidemiology of TMDs
5. Theories of Etiology
6. Development of functional disturbances in the masticatory
system
3. 7. Etiologic Considerations Of Temporomandibular
Disorders
Occlusal Factors
Trauma
Emotional stress
Deep Pain input
Parafunctional habits
8. Food for thought
9. Conclusion
10. References
5. TERMINOLOGY
1934 James Costen....Costen Syndrome
1959 Shore coined temporomandibular joint disturbances
temporomandibular joint dysfunction syndrome
Ramfjord and Ash- functional temporomandibular joint
disturbances
Bell suggested the term temporomadibular disorders
(TMDs)
Jeffrey P Okeson. Management of temporomandibular disorder and occlusion. 4th editionc
6. HISTORY OF TMDS
In 1934 Dr James Costen, an otolaryngologist
In 1930s and 1940s ...raise the bite as suggested by
Costen.
Late 1940s and 1950s...role of occlusal interferences.
Importance was given to masticatoy muscle disorders
In 1960s and into 1970s occlusion and later emotional
stress
In 1970s disorders arising from intracapsular sources
Jeffrey P Okeson. Management of temporomandibular disorder and occlusion. 4th edition
7. EPIDEMIOLOGY OF TMDS1
1. 41% at least one symptom
2. 56% at least one clinical sign
3. Only 10% symptoms that were severe enough to make
the patient seek treatment.
4. The greatest factor for seeking treatment is the degree
of pain experienced.
5. Most symptoms are seen in 20-40 year age group.
8. THEORIES OF ETIOLOGY OF TMDS
Biomedical model comprising
• The mechanical displacement theory2
• The trauma theory3
• The biomedical theory4
• The osteoarthritic theory5
• The muscle theory6
The Neuromuscular Theory7
The Psychophysiological Theory8-10
The Multifactorial Theory1,11,12
The biopsychosocial Model13
9. THE MECHANICAL DISPLACEMENT THEORY
Etiology oftemporomandibular disorders:the journey so far . INTERNATIONAL DENTISTRY
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10. THE TRAUMA THEORY
Zarb and Speck
Micro-/Macrotrauma as the principal factor.
no critical appraisal for the multitude of factors
involved
Etiology oftemporomandibular disorders:the journey so far . INTERNATIONAL DENTISTRY
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11. THE BIOMEDICAL THEORY
Reade
Supported the role of trauma in the initiation of the
disorder.
The condition will either resolve or in presence of certain
factors like disrupted occlusion, parafunctional habits and
occupational activities, will progress further.
Psychological elements were recognized as important
maintaining influences.
Etiology oftemporomandibular disorders:the journey so far . INTERNATIONAL DENTISTRY
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12. THE OSTEOARTHRITIC THEORY
Stegenga
Osteoarthrosis as the causative factor for TMD.
Muscular symptoms and internal derangement
were secondary to joint pathology.
Can explain some subcategories of TMD but
fails to explain the rest.
Eitiology of Temporomandibular disorders: the journey so far . INTERNATIONAL
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13. THE MUSCLE THEORY
Travell and Rinzler
Primary etiologic factor was in the masticatory
muscles themselves.
The myalgia in the facial region is caused by chronic
myospasm which is secondary to parafunctional
habits.
Denied any influence of the occlusion.
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14. THE NEUROMUSCULAR THEORY
Ramjford.
Occlusal interferences were the causative factor for
the disorder.
Occlusal interferences caused an altered
proprioceptive feedback, leading to incoordination
and spasm of some of the masticatory muscles.
Etiology oftemporomandibular disorders:the journey so far . INTERNATIONAL DENTISTRY
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15. THE PSYCHOPHYSIOLOGICAL THEORY
Schwartz and Laskin.
Suggested that the psychological factors are more
important than the occlusal disturbances in
initiating the disorder.
It is the interaction between physiological
predisposition, and psychological stress which
causes TMD.
The effect on the individual depended on their
ability to cope with stressEtiology oftemporomandibular disorders:the journey so far . INTERNATIONAL DENTISTRY
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16. THE PSYCHOLOGICAL THEORY
Emotional disturbances initiating centrally,
induced muscular hyperactivity which led to
parafunctional habits and so indirectly to occlusal
abnormalities.
In TMD patient the behavioural aspect of the
patient needs to be studied.
It is still not clear whether they are the cause or the
consequence of pain.
Etiology of temporomandibular disorders: the journey so far . INTERNATIONAL
DENTISTRY SA VOL. 12, NO. 4
17. THE MULTIFACTORIAL THEORY
The etiology is multifactorial for
TMD even though finding the
primary etiologic factor can be
difficult for the individual patient.
The etiology will be different in
young and in older patients.
Factors influencing the disorder
have been categorized by Bell into
the predisposing, initiating and
perpetuating factors.
Etiology oftemporomandibular disorders:the journey so far . INTERNATIONAL DENTISTRY SA VOL. 12, NO.
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18. THE BIOPSYCHOSOCIAL MODEL - 1992,
DWORKIN
integrates both the
physical disorder factors,
i.e., biological factors
and the illness impact
factors, i.e.,
psychological and social
factors.
20. disturbances in the masticatory
system1
• Normal + An event Physiologic TMD
function tolerance
symptoms
21. Normal Function
complex neuromuscular control system.
The brainstem (specifically the central pattern generator)
regulates muscle action by the way of muscle engrams
When sudden, unexpected sensory input is received,
protective reflex mechanism is activated, creating a decrease
in muscle activity in the area of the input.
22. Events During normal function of the masticatory system events
can occur that may influence function. The events can be
of local or systemic origin.
Local Events
1. Placement of an improperly occluding crown.
2. Secondary to trauma involving local tissues, such as the
postinjection response following local anesthesia.
3. Trauma can also arise from opening the mouth too wide
4. Unaccustomed use ---- bruxism
5. Constant deep pain input.
6. unknown cause (idiopathic pain)
23. Systemic Events
The entire body and/or the Central Nervous System
may be involved as an event.
One of the most common types of systemic
alterations is the increased level of emotional stress.
24. Physiologic Tolerance
All individuals do not respond in the same manner to the
same event.
After how long or after what severity is the event perceived as
unpleasant describes the physiologic tolerance.
Physiologic tolerance can be influenced by both local and
systemic factors.
25. Local Factors
How the masticatory system responds to local factors
is influenced by its orthopaedic stability.
Orthopaedic instability related to the occlusion, the
joints or both.
1. genetic, developemental or iatrogenic causes.
2. alterations in the normal anatomic form, such as a
disc displacement or an arthritic condition.
3. disharmony between the ICP and the MS position
of the joints.
26. Systemic Factors
Influenced by diet, gender and genetics.
Presence of acute or chronic diseases.
Effectiveness of the pain modulation system
27. Temporomandibular symptoms
•When functional change
exceeds a critical level,
alterations in the tissues
begin, this level is known
as the structural
tolerance.
•If the structural
tolerance of any
component is exceeded
breakdown will occur.
initial breakdown --- the lowest structural tolerance
28.
29. Etiologic Considerations Of
Temporomandibular Disorders1,14
• Predisposing factor – factors that increase the risk of TMD or
orofacial pain.
• Initiating factors – factors that cause the onset of disorder.
• Perpetuating factors – factors that interfere with healing and
complicate management.
• Contributing factors –factors that initiate, perpetuate or result in a
disorder.
30. Predisposing factors
Systemic factor – Medical conditions such as rheumatic
infections, nutritional and metabolic disorders
Psychologic factors – Personality, behaviour
Structural factors – All types of occlusal discrepancies,
improper dental treatment, postural abnormalities,
skeletal deformation, past-injuries etc.
Genetic factors
31. Initiating factors:-
Trauma – Micro or macro trauma
Overloading of joint structures – Parafunctional
habits etc.
Perpetuating factors:-
Mechanical and muscular stress
Metabolic problems
33. Occlusal Condition
Earlier : Main causative factor
Now: Little or no role
Divided the fraternity into Occlusionists and non-
occlusionists.
34. Reasons for the controversy
The evaluation of the relationship of occlusion and
TMDs should be done in both static and dynamic
conditions.
Faulty study design?
Occlusion and Temporomandibular
Disorders (TMD): Still Unsolved
Question? - Alanen15
35. Pullinger et al16 used a blinded multifactorial analysis of
each factor in combination with the other factors.
They concluded that no single occlusal factor was able to
differentiate patients from healthy subjects. 4 occlusal
features however occurred mainly in TMD patients
1. presence of skeletal anterior open bite
2. retruded contact position and intercuspal position slides
of greater than 2 mm.
3. overjets of greater than 4mm
4. five or more missing and unreplaced posterior teeth.
36. They concluded that although the relative odds for
disease were elevated with several occlusal variables,
clear definition of disease groups was evident only in
selective extreme ranges, thus occlusion cannot be
considered as the most important factor in the definition
of TMDs.
37. Dynamic functional relationship between
occlusion and TMD
When considering the dynamic relation, the occlusal
condition can affect some TMDs in 2 ways
1. effect of occlusal factors on orthopaedic stability
2. effect of acute changes in the occlusal condition and
TMD
38. 1. Effect of occlusal factors on orthopaedic
stability
39. 2 factors determine whether an intracapsular
disorder will develop
1. the degree of orthopaedic instability: a
discrepancy of 1-2mm....
shifts greater than 3mm present as significant
risk factors.
2. the amount of loading: bruxism patients with
orthopaedic instability.
Patients with unilateral chewing patterns.
40. 2. Effect of acute changes in the occlusal
condition and TMD
activities of the masticatory system can be
divided into 2 basic types:
1) Functional which includes chewing, speaking
and swallowing; and
2) Parafunctional which includes clenching or
grinding of the teeth.
41. Functional Muscle Activities :
Controlled activities
Protective reflexes are constantly present,
guarding against potential damaging contacts.
Interfering tooth contacts during function have
inhibitory effects on functional muscle activity.
Functional activities are directly influenced by
the occlusal condition.
42. Parafunctional activities
Totally different controlling mechanism.
Instead of being inhibited by tooth contacts, earlier
concepts suggested that parafunctional activities are
actually provoked by certain tooth contacts.
However these concepts for the most parts have been
disapproved.
43. How do occlusal interferences affect muscle symptoms?
An acute change will precipitate protective co-
contraction. and at the same time has an inhibitory
effect on the parafunctional activity.
As the occlusal interferences become chronic the
muscle response is altered in 2 ways:
1. alter the muscle engram so as to avoid the potentially
damaging contact.
2. tooth movement to accommodate for the heavy
loading
44. Trauma
• Ample evidence supports the fact that trauma can
lead to TMDs.
• Greater impact on intracapsular disorders than
muscular disorders.
Trauma can be divided into 2 basic types
Macrotrauma
Microtrauma
45. Macrotrauma17
most common structural alterations affecting the
TMJ are elongation of the discal ligaments.
Can be further divided into Direct
INDIRECT
46. Direct trauma - a blow to the chin, can instantly
create an intracapsular disorder.
The open mouth trauma can lead to discal
displacement and/or dislocation.
Closed mouth trauma is less injurious to the
condyle disc complex as the intercuspation of the
teeth maintains the jaw position.
Iatrogenic trauma: intubation procedures during
general anesthesia, third molar extraction
procedures.
47. Indirect trauma
injury that may occur to the TMJ secondary to a
sudden force that does not directly impact or contact
the mandible.
The most common type is associated with cervical
flexion-extension (whiplash) injuries seen in road
traffic high speed accidents.
48. Microtrauma
Any small force that is repeatedly applied to the joint
structures over a long period of time.
Mechanism of Microtrauma:
loading exceeds the functional limit of the tissues,
collagen fibrils become fragmented
decrease in the stiffness of the collagen network.
proteoglycan water gel swells and flow out into the joint
space,
49. Softening of the articular surface called chondromalacia.
Early stage of chondromalacia is reversible if the
excessive loading is reduced.
Loading continues to exceed the capacity of the articular
tissues, irreversible changes can occur.
50. Clenching or bruxism leads to posterior border
thinning of the disc, which causes elongation of the
inferior retrodiscal ligaments which eventually leads
to disc displacement.
Disharmony between ICP and MS positions.
51. Emotional Stress
The hypothalamus, the reticular system, and particularly
the limbic system are primarily responsible for the
emotional state of the individual.
Mechanism of Action
Stress activates the hypothalamus
prepares the body to respond by the autonomic system
increases the activity of the gamma efferents
52. intrafusal fibers of the muscle spindle contract.
sensitizes the spindle so that any slight stretching of the
muscle will cause a reflex contracture.
The overall effect is an increase in tonicity of the muscle.
53. Stress is released by two mechanisms:
1. External: released by shouting, cursing, hitting. A more
positive way to release stress is by engaging in physical
exercises.
2. Internal: stress manifests as irritable bowel syndrome,
Hypertension, cardiac arythmias, increased activity of head
and neck muscles.
Emotional stress also leads to decreased physiologic tolerance
due to increased sympathetic tone.
54. Deep Pain Input
Deep pain input can centrally excite the brainstem,
producing protective co-contracture
Patient suffering from toothache will have a limited
mouth opening.
sinus pain , ear pain , pain sources remote to the face
like cervical pain input.
55. Parafunctional Activities
This includes bruxism, clenching and certain oral
habits.
Parafunctional activities can b divided into 2 basic
categories
1. Diurnal: occuring through the day.
2. Noctural: occurring through the night.
56. Diurnal activity: parafunctional activity during the day
clenching and grinding
tongue or cheek biting
finger and thumb sucking
unusual postural habits
occupation realted activities
sub-conscious level therefore merely questioning the
patient is not a reliable way to assess the presence or
absence of these activities.
58. Bruxism: the subconscious, non-functional
grinding of teeth
Associated with a change from deeper to lighter
sleep.
Bruxism may be closely associated with the
arousal phases of sleep.
59. Sleep
REM sleep : 80%
Non-REM sleep: 20%
REM sleep: restoring function of the cortex and
brainstem activity. Psychic Rest
Non-REM sleep: restoring function of the system.
Increased synthesis of protein and RNA. Physical
Rest
60. Deprived of
REM sleep: greater anxiety and irritability
Non-REM sleep: musculoskeletal tenderness, aching
and tenderness.
Duration of Bruxing Event: Average bruxing event
lasts for 9 secs.
Total bruxing time -40 secs per hour.
Bruxism occurs only 5 times during entire sleep with
an average of 8 secs per event.
61. Intensity of Bruxing Events: average bruxing event
involves 60% of the maximum clenching power before
the patient went to sleep.
Sleep Position and Bruxing:
Earlier :persons sleeping on the sides experience more
bruxing activity
Now: research has clarified that bruxing events are moe
when the person is sleeping on his/her back.
62. Bruxing Events and Masticatory Symptoms: Ware
and Rugh studied a group of bruxism patients
without pain and a group with pain.
Concluded that the latter group had a significantly
higher number of bruxing events during REM sleep
than did the former.
Both groups however bruxed more than a control
group
63. Food for thought…
Symptom based treatment????
Greene18 concluded from his review that not only are the old
mechanistic etiologic concepts incorrect, but also that 2 of the
most popular current concepts (biopsychosocial and
multifactorial) are seriously flawed.
Even in the absence of a perfect understanding of etiology,
we still can provide good conservative care, and we should
avoid aggressive and irreversible treatments,
64. Conclusion
To manage TMD effectively the clinician must be able to
determine its etiology.
TMDs are dependant on a variety of factors which have a
complex interplay between them.
Occlusion is not the sole factor responsible for TMDs and
the clinician should recognize that as the Clinician who
only evaluates the occlusion is likely missing as much as
the clinician who never evaluates the occlusion.
65. References
1. Jeffrey P Okeson. Management of temporomandibular disorder and
occlusion. 4th edition: Mosby year book inc. Missouri
2. Molin C. From Bite to mind: A personal and literature review. Int J
Prosthodont. 1999: 12 :279-288
3. Zarb GA, Speck JE. The treatment of mandibular dysfunction. In: Zarb
GA, Carlsson GE, editors. Temporomandipular joint function and
dysfunction. Copenhagen: Munksgaard; 1979.
4. Reade PC. An approach to the management of temporomandibular
joint pain-dysfunction syndrome. J Prosthet Dent 1984;51:91–6.
5. Stegenga B, de Bont LGM, Boering G. Osteoarthrosis as the cause of
craniomandibular pain and dysfunction. A unifying concept. J Oral
Maxillofac Surg 1989;47:249–56.
66. 6. Laskin. Etiology of the pain dysfunction syndrome. J Am Dent
Assoc.1979:79:147
7. Ash and Ramjford. Occlusion:: 4th edition: 1995: W B
Saunders company: Philadelphia
8. Greene CS. Etiology of temporomandibular disorders. Sem Orthod
1995;1:222–8.
9. McNeill C. Management of temporomandibular disorders:
concepts and controversies. J Prosthet Dent 1997;77:510–22.
10. Turner JA, Dworkin SF. Recent developments in psychological
diagnostic procedures: screening for psychological risk factors
forpoor outcomes. JADA 2004;135:1119–25.
11. Pertes and Gross clinical management of temporomandibular
disorders and orofacial pain: 1995: quintessence publishing co inc:
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67. 12. Goldstein. TMD : A review of current understanding. J Prosthet
Dent 1999;88:56-67
13. Dworkin. Perspectives on the interaction of biological,
psychological and social factors in TMD. J Am Dent Assoc.
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14. Bell WE. Temporomandibular disorders. Classification,
diagnosis, management. 3rd ed.. Chicago: Year Book; 1990.
15. Pentti Alanen .Occlusion and Temporomandibular Disorders
(TMD): Still Unsolved Question? J Dent Res 81(8):518-519,
2002
16. Pullinger AG, Seligman DA: A multiple logistic regression
analysis of the risk and relative odds of TMDs as a function of
common occlusal features, J Dent Res72:968-79,1993
17. Sonia Bhat. Etiology of temporomandibular disorders: the
journey so far. international dentistry sa vol. 12, no. 4.88-98
18. Charles S. Greene,.The Etiology of Temporomandibular
Disorders: Implications for Treatment. J OROFAC PAIN
2001;15:93–105.
68. We must do the right as we see the right
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