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11.6:
Teeth, jaws and related structures
Maxillary
and Mandibular Bone Cavities
Long
neglected as a clinical entity, sinus headache has become a common
complaint of patients with facial pain. Although pain is associated with
some sinus disease, most experts feel that the magnitude and instances
of sinus headache have been exaggerated by the public (Schor, 1993).
Most physicians dealing with headache feel that acute or chronic
headache processes are not a result of overt paranasal sinus disease.
The subject is well-review by Schor (1993). A major advance in
elucidating the cause of pain in a substantial proportion of these
patients has been made by Roberts and Person (1979) and by Ratner et al
(1979). These investigators found radiologically undetectable infected
maxillary or mandibular bone cavities at previous tooth extraction sites
in two large series of patients with atypical facial pain. They used an
injection of local anesthetic into a tooth extraction site as a
diagnostic test; if facial pain repeatedly disappeared following such an
injection, curettage of the jaw bone and antibiotic treatment were then
carried out. Twenty-three patients were treated in the uncontrolled
series of Ratner et al (1979), and 14 were pain-free or nearly pain-free
after treatment and evaluated for 9 months to over 4 years. Further
experience has affirmed these favorable results (Roberts et al, 1984;
Ratner et al, 1986). Microscopic examination of the bone removed by
curettage showed a highly vascular abnormal healing response of bone and
low-grade inflammation. A complex mix of aerobic and anaerobic flora was
cultured in virtually all cases. Jaw bone curettage is an outpatient
procedure that is usually completed within an hour.
Among
patients with nondescript facial pain referred to Raskin, about 10
percent have suspicious tooth extraction sites prior to onset of the
pain and have positive responses to local infiltration of a local
anesthetic. Nineteen patients have undergone curettage and have been
evaluated for 2 to 4 years; 15 of them are pain-free or nearly
pain-free; 3 are 50 percent improved; and only 1 is not improved. An
aggressive oral surgical evaluation is obviously an important element in
the evaluation of patients with facial pain, including trigeminal
neuralgia. Two patients among 67, seen by Raskin, with trigeminal
neuralgia were completely cured by curettage and often involved a tooth
extraction site (Raskin, 1988).
With
appropriate stimulation of healthy diseased teeth, it is possible to
analyze a variety of face and head pains that stem from the teeth. Use
of locally acting anesthetics to interfere with toothache-induced
headache allows one to assume that the painful experience was caused by
afferent impulses arising from the stimulated tooth.
The
cracked tooth syndrome (incomplete tooth fracture) may produce pain
radiating to the head following mastication. Appropriate therapy will
help resolve the matter.
Toothaches
can produce severe headache. Noxious stimulation of the tooth may
produce sensations of fullness, numbness, and stiffness five minutes
after the stimulation of a particular tooth. The entire subject of pain
from the teeth and jaws as a source of headache and facial pain is
well-reviewed by Howell (1993).
11.7:
Temporomandibular joint disease
Temporomandibular
joint syndrome
The
temporomandibular joint syndrome or TMJ is probably overdiagnosed.
Actual incidence is much less than what is actually diagnosed.
Degenerative disease of the temporomandibular joint may produce a
characteristic pain syndrome described by Costen (1936). It often occurs
in middle or later life in individuals in whom malocclusion, usually
from loss of teeth, has led to mechanical injury of the joint surfaces,
although it may also occur in young individuals, particularly women (Reik
and Hale, 1981). Pain is caused by erosion of the bone of the glenoid
fossa, with impaction of the condyles against the thin bone separating
them from the dura and its rich nerve supply, irritation of the
auriculotemporal nerve by uncontrolled medial and backward movement of
the condyles, and irritation of the chorda tympani nerve by the condyle
where it emerges from the tympanic plate at the medial edge of the
glenoid fossa.
According
to Guralnick et al. (1978), most patients with the temporomandibular
syndrome fall into two categories: those with organic joint
abnormalities, including ankylosis, neoplasia, trauma, and arthritis;
and those with facial pain, noise in the temporomandibular joint, and
restricted motion without organic joint disease. Patients with organic
disease probably make up only a small percentage of all patients with
disorders of the temporomandibular joint.
In this
syndrome, the pain that is described is of moderate to severe intensity
and is distributed over the vertex, occiput, supraorbital region, and
about the ears. Pain intensity commonly increases as the day progresses.
In some patients, it is accompanied by a burning sensation of the
throat, tongue, and side of the nose. Other patients complain of dryness
of the mouth. Symptoms attributable to pressure of the condyle upon the
Eustachian tube include impairment of hearing and a congested sensation
in the ears. Palpation of the joint capsule to demonstrate looseness of
the condyles may support the diagnosis. In some patients, a flat object
interposed between the jaws provides diagnostic relief of pain, and
correction of the underlying malocclusion is usually curative (Costen,
1936). Guralnick et al. (1978) have also recommended counseling, local
heat therapy, muscle relaxants and analgesics, and midline opening jaw
exercise to restore abnormal muscle function, while Reik and Hale (1981)
believe that the majority of patients with temporomandibular joint pain
will respond to physical measures combined with a soft diet, salicylates,
and tricyclic antidepressants.
Controversy
abounds regarding all aspects of the pain syndrome that may result from
disorders of the temporomandibular joint; the criteria for diagnosis are
in dispute, epidemiologic and demographic data are of dubious value. The
one point of agreement regarding this disorder is that masticatory
muscle spasm and fatigue is the cause of pain (Dubner et al, 1978).
TMJ is
apparently more common among women of a wide age range, unilateral ear
or preauricular pain that radiates to the temple, jaw, or neck is the
usual major complaint. Pain is deep, dull, and continuous, worse in the
morning (especially if bruxism is a factor), and worsened by chewing.
Many patients describe prior subluxation or "locking" of the
jaw with some manipulation required to correct it. There is limitation
of jaw motion and deviation of the jaw upon opening. On examination,
tenderness of the masticatory muscles and clicking of the joint are
usually found. The four cardinal signs and symptoms are pain,
tenderness, clicking, and limitation of movement of the jaw (Guralnick
et al, 1978). There is usually no radiologic evidence of
temporomandibular joint disease.
Temporomandibular
joint dysfunction has yet to be clearly defined. There is little
question that the syndrome exists and Raskin believes it to be a
biologic problem, not a psychological one. Raskin has seen many patients
with pain about the ear caused by migraine or cluster headache with much
secondary muscle contraction involving the masticatory muscle
ipsilaterally, resulting in asymmetrical jaw opening. Raskin has never
seen headache as the primary symptom of temporomandibular joint
dysfunction (Raskin, 1988).
The
syndrome is no longer believed to be caused by condylar displacement (Cawson,
1986) but rather by masticatory muscle spasm and fatigue resulting from
malocclusion, bruxism, or teeth clenching. A widely held view,
popularized by Laskin (1969), is that the syndrome is
psychophysiological in mechanism; simply stated, masticatory spasm is
held to be a tension-relieving mechanism. Sparse evidence supports this
view: the analogy of this proposed mechanism to that of
"muscle-contraction headache," a thoroughly discredited
mechanism, is ironic.
Physical
disorders of the temporomandibular joint are rarely a source of
significant symptoms. Rheumatoid arthritis frequently involves the
joint, yet joint pain is no more common in such patients than in a
control population (Chalmers and Blair, 1973). Fracture of the condylar
neck subsequent to falling on one’s chin is relatively common and
often causes severe malocclusion but does not usually give rise to
preauricular pain (Cawson, 1986). Moreover, rigorous measurements of jaw
motion and of electrical activity of masticatory muscles show that 80
percent of asymptomatic subjects have imbalanced masticatory muscle
activity and occlusion (Cooper and Rabuzzi, 1984).
The
widely held view that emotional stress is a primary cause of
temporomandibular joint dysfunction has led to the widespread use of
behavioral-relaxation therapies with what appear to be good results in
uncontrolled studies; however, attenuation of pain has not correlated
well with lower masseter muscle tension (Scott and Gregg, 1980).
Others
have advocated local heat, a soft diet, elimination of gross occlusal
discrepancies with a bite guard, nonsteroidal anti-inflammatory drugs,
and midline-opening jaw exercises (Guralnick et al, 1978). The large
majority of patients improve regardless of the type of treatment, but no
long-term control group has been studied to establish the natural
history of this disorder.
A
number of surgical procedures have also been performed, with
inconsistent results (House et al, 1984).
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