Download The etiologic factor in pain for temporal tendonitis

SECTIONEDITOR
Photomicrographic
etiologic
factor
evidence of insertion
tendonosis:
in pain for temporal
tendonitis
The
Edwin A. Eirnest, III, D.M.D., Mario E. Martinez, D.M.D., M.S.,
David B. Rydzewski,
M.D., and E. George Salter, Ph.D.
Montgomery, Ala.
A patient with the classic signs and symptoms of temporal tendonitis was treated
with excisional surgery of the temporal tendon and its respective mandibular
coronoid process. The excised tissue was submitted to pathology for microscopic
analysis, and the results were confirmed by two pathologists.
Degenerative
signs of
focal atrophy and tissue necrosis were evident and served to describe the focal
nature of the painful condition of temporal tendonitis. The description for the pain
pattern is given, along with the recommended method for diagnostic testing. The
current method of surgical management using radiofrequency
thermal ablation is
described, which replaces the more tissue-destructive,
excisional approach. (J
PROSTHET DIENT 1991;65:127-31.)
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either vertical elongation of the coronoid process or lateral
flaring of the coronoid process with subsequent pain. The
pain experienced was attributed to physical impingement
of the coronoid process and temporal tendon on the maxillary process tuberosity or zygomatic arch. Farrar and
McCarty’ also reported “hypertrophy of the entire temporal muscle, zygoma, and coronoid,” and believed this to be
another etiology of temporal tendon pain.
The frequent regeneration of the coronoid process after
coronoidectomy and reattachment of the temporal tendon
has been observed by various cliniciansz4 Our experience
has not revealed “hypertrophy” or “physical impingement” of the coronoid process and temporal tendon to be
a common finding. Clinical studies indicate that this is a
Fig. 1. Lateral view of temporal muscle and lateral head
temporal tendon attachment at coronoid process.
a = Temporal muscle; b = temporal tendon lateral head
inserting into coronoid process. (From Ernest EA. Temporal tendinitis-migraine
mimic. Montgomery, Ala: Ernest
Publications, 1986, with permission.)
Fig. 2. Anterior view of base of mandibular ramus with
metal probe pressed against medial head tendon insertion.
a, Ramus; b, metal probe; c, medial tendon insertion; d,
buccinator muscle. (From Ernest EA. Temporal tendinitis-migraine mimic. Montgomery, Ala: Ernest Publications, 1986, with permission.)
hronic pain of the temporal tendon has been recognized for a number of years by a relatively small number
of clinicians. However, much of the prescribed therapy has
only been anecdotal because the etiologic evidence for
temporal tendonitis has been lacking. This article presents
physical evidence that helps to explain the reason for the
pain that is experienced by patients with temporal tendonitis.
Pain of the mandibular coronoid process and the temporal tendon attachment was described in 1980 and named
“coronoid impingement.“’ The condition was described as
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rare etiology in pain of the temporal tendon. We found that
most patients who s,uffer pain of the temporal tendons have
an insertion tendonosis of the tendon fibers at or near the
coronoid process tip on the anterior border.
This article describes a patient history with degenerative
changes common ‘to patients who exhibit insertion tendonosis and who suffer the painful condition of temporal
tendonitis.
Farrar and McCarty’s’ report of the “pain behind the eye
extending into the dorsum of the neck” as representative
of the “hypertrophy of the entire temporalis muscle, zygoma, and coronoid,” is also part of the typical pain pattern
of temporal tendonitis in the large number of patients that
we have seen.
ANATOMY
The temporal m.uscle has its origin on the lateral aspect
of the temporal bane of the cranium. The temporal muscle
is fan-shaped with the broadest aspect at the superior border of the temporal bone. The “handle” of the “fan” is the
temporal tendon, which extends inferiorly and passes medial to the zygomatic arch and attaches to the tip of the
mandibular coronoid process. The temporal muscle is usually divided into ELsuperficial and a deep belly.5y6 The su-
perficial belly gives rise to the lateral head temporal
tendon, which attaches to the mandibular coronoid process
(Fig. 1). The deep belly of the temporal muscle gives rise
to a medial head temporal tendon, which is not often recognized by either anatomists or clinicians. This insertion is
on the medial aspect of the mandibular ramus at its base
(Fig. 2).
INJURY
An injury to the lateral head temporal tendon that
inserts on the mandibular coronoid process may be caused
by trauma or prolonged contraction of the temporal muscle caused by either emotional distress or temporomandibular joint disk displacement.5 An injury to the medial head
temporal tendon may also produce a pain pattern identical to the lateral head condition.5 The nerve supply to the
temporal tendons is provided by the anterior and posterior
deep temporal nerves, which are sensory branches of the
third division of the trigeminal cranial nerve.
PATIENT
HISTORY
REPORT
On May 21,1986, a well-nourished white woman, 24 years
of age, was evaluated for bilateral complaints of 5 months’
duration including (1) headaches, facial pain, (2) jaws ach-
Fig. 3. Digital palpation of lateral head temporal tendon and coronoid process. (From
Ernest EA. Temporal tendinitis-migraine
mimic. Montgomery, Ala: Ernest Publications,
11986,with permission.)
Fig. 4. Pain pattern of temporal tendinitis. (From Ernest EA. Temporal tendinitis-migraine mimic. Montgomery, Ala: Ernest Publications, 1986, with permission.)
:Fig. 5. Local anesthetic injection of lateral head temporal tendon, intraoral approach.
(From Ernest EA. Temporal tendinitis-migraine
mimic. Montgomery, Ala: Ernest Publications, 1986, with permission.)
Fig. 6. Low power photomicrograph of anterior border of coronoid process tip of mandible. a, Bony tip; b, insertion zone of temporal tendon; c, degenerated tendon fibers; d, degenerated muscle fibers. C and d show both homogenous appearance and loss of fiber cellular detail. (From Ernest EA. Temporal tendinitis-migraine
mimic. Montgomery, Ala:
Ernest Publications, 1986, with permission.)
Fig. 7. Medium power photomicrograph of anterior border of coronoid process tip of
mandible. a, Bony surface; b, insertion zone; c, degenerated tendon fiber; d, degenerated
muscle fiber. (From Ernest EA. Temporal tendinitis-migraine
mimic. Montgomery, Ala:
Ernest Publications, 1986, with permission.)
Fig. 8. High power photomicrograph of degenerated tendon and muscle fibers. All cellular details of tendon and muscle fibers are lost due to degeneration. c, Degenerated tendon
fibers; d, degenerated muscle fibers. (From Ernest EA. Temporal tendinitis-migraine
mimic. Montgomery, Ala: Ernest Publications, 1986, with permission,)
Fig. 9. Diagrammatic representation of disintegration of tendon fibers. (From Ernest EA.
Temporal tendinitis-migraine
mimic. Montgomery, Ala: Ernest Publications, 1986, with
permission.)
Fig. 10. Drawing depicts intraoral position of radio-frequency probe directed by fluoroscopic monitoring. (From Ernest EA. Temporal tendinitis-migraine
mimic. Montgomery,
Ala: Ernest Publications, 1986, with permission.)
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ing and popping, and (3) shoulder, back, and neck pain.
The onset of her painful condition was directly related to
an accidental fall onto concrete. The accident was precipitated by a grand ma1 seizure. The patient’s pain pattern
conformed to the reported descriptions of temporal
tendonitis.7 The pain pattern was initially determined by
digital palpation of the mandibular coronoid process on
each side (Fig. 3). The digital pressure exacerbated the
clinical pain pattern (Fig. 4).
Pain pattern of temporal tendonitis
head, medial head, or both)
(lateral
1. Jaw joint hurts and aches; jaw opening may be
restricted due to painful tendon not stretching freely.
2. Ear pain and pressure is often present.
3. Upper or upper and lower posterior teeth may ache
and throb or feel sensitive.
5. Pain radiates from cheek to eye.
6. Temple aches and hurts (temple headache) with pain
radiation over the ear to the back of the head and into the
neck.
7. Aching pain at the attachment of the tendon is noted
when it is palpated by the index finger.
Initial therapy for this patient consisted of oral, anti-inflammatory medications, an acrylic resin bite plane, and
local anesthetic injections (Fig. 5), which were applied repeatedly but unsuccessfully over a a-month period. The
patient was then referred to an oral and maxillofacial surgeon for evaluation for possible bilateral coronoidectomy
and temporal tendon resection. The surgeon concurred
with the diagnosis of refractory temporal tendonitis (lateral head) and scheduled the patient for surgery on June 19,
1986. The temporal tendons were resected bilaterally and
the coronoid processes were removed bilaterally as well.
The patient had an uneventful recovery from surgery and
at the time of this report’s preparation, was still free of the
original pain disorder of temporal tendonitis.
Microscopic
by swelling and then shriveling of the insertion fibers with
disintegration of the fine structure (Fig. 9). This process is
followed by fatty degeneration, formation of foci of necrosis, appearance of hyalin, and deposition of calcium. The
nerve-end organs within the tendon insertion become irritated by the increased tissue pressure, necrotic foci, and
pathologic deposits. Initially, the tendon hurts only when
in active function, but as the condition worsens, there is a
persistent sensation of pain, even at rest. There is also
noted a reflex restriction of movement when the patient
may try to open the mouth. The restriction may also cause
a loading pressure at the jaw joint and either initiate or aggrevate clicking or locking of the TMJ articular disk.5 The
signs and symptoms at the jaw joint may confuse the diagnosis and falsely suggest a primary TMJ problem instead
of the true nature of the problem, temporal tendonitis.
CONCLUSION
This patient history describes the degenerative changes
that may occur in a patient as a result of trauma and the
predisposing factors of the aging process. As the connective
tissues age and progressively lose elasticity, any chronic
strain, emotional distress, or traumatic insult has the potential to initiate degenerative changes or “wear lesions”
that may ultimately become irreversible. The degenerative
progression often produces pain on movement in the early
phase and as the condition “matures,” the pain then
becomes a constant feature.
Many of the chronic pain disorders of the head and neck
are in the category just described (connective tissue aging
plus strain or trauma). The degenerative tissue area of
temporal tendonitis is actually small and is now successfully treated by radiofrequency generator thermoneurolysis5 (Fig. 10). This approach obviates the need for
an ablative resection approach to treat a focal soft tissue
pain disorder.
examination
The excised coronoid processes were submitted to the
pathology department at Humana Hospital, East Montgomery, Ala., for microscopic study. The specimens were
later sent to the University of Alabama Medical Center in
Birmingham, Department of Oral Pathology, for additional
studies. The conclusion of both pathologists was “Evidence
of degenerative tendon and muscle tissue with loss of cellular outline and homogeneous appearance of tendon fiber
and muscle fiber” (Figs. 6 through 8). This finding supports
the work of other author$-l1 in relation to the unique degenerative changes associated with soft tissue insertions in
the narrow bony processes.The combination of (1) aging of
connective tissue and (2) degeneration change that takes
place due to stress or trauma produces a precipitate
formation. This precipitate formation is first characterized
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REFERENCES
1. Farrar WB, McCarty WL Jr. A clinical outline of temporomandibular
joint diagnosis and treatment. 6th ed. Montgomery, Ala: Normandie
Publications, 1980;5, 7-8.
2. Farrar WB, McCarty WL Jr. Clinical outline of temporomandibular
joint diagnosis and treatment. 7th ed. Montgomery, Ala: Normandie
Publications, 1983;7-8.
3. Chierici G, Miller AJ. Experimental study of muscle reattachment following surgical detachment. J Oral Maxillofac Surg 1984;42:485-90.
4. Boyd TG, Castelli WA, Huelke DF. Removal of the temporalis muscle
from its origin: effects on the size and shape of the coronoid process. J
Dent Res 1967;46:997-1001.
5. Ernest EA. Temporal tendinitis: a painful disorder that mimics migraine headache. J Nemo1 Orthopaed Med Surg 1987;8:159-67.
6. Harn SD, Shackelford LS. Further evaluations of the superficial and
deep tendons of the human temporalis muscle. Anat Ret 1982;202:53748.
7. Ernest EA. Temporal tendinitis-the
migraine mimic. Montgomery,
Ala: Ernest Publications, 1986.
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DR. EDWIN A. ERNEST,III
1523 CLUBPL.
DULUTH,GA 30136-5018
8. Steinmann EP. Styloid syndrome in absence of an elongated process.
Acta Otolaryngol 1968;66:347-56.
9. Belart W. Uber die zapophysis der vertebralen querfortsatz. Schweiz
Med Wochenschr 195’7;87:540.
10. Fahlgren H, Jansa 13, Lofstedt S. Retrofaryngeal tendinit. Svensk
Lakartidn 1966:63:3779.
11. Glatthaar E. Uber tendinosen. Deutsch 2 Chir 1944;258:393.
Contributing
author
H. Ray Evans, D.M.D., Montgomery,
An epidemiologic
evaluation
of two diagnostic
schemes for temporomandibular
disorders
Linda LeResche,
Sc.D.,* Samuel F. Dworkin,
Earl E. Sommers,
D.D.S., M.S.D.,***
and
Edmond L. Truelove,
D.D.S., M.S.D.****
University
of Washington,
School of Dentistry,
D.D.S.,
Ala.
classification
Ph.D.,**
Seattle, Wash.
Few diagnostic classification
schemes for temporomandibular
disorders (TMD)
have been applied systematically
to examine the prevalence of various subtypes of
TMD in clinic or community populations. In this study, computer algorithms
were
developed for classifying
subjects according to the scheme of Eversole and
Machado (1985) and a classi5cation
scheme recently developed in our own
research at the University
of Washington. The diagnostic algorithms
were applied
to clinical esamination
data for (1) persons without TMD pain (community controls) and (2) persons reporting TMD pain in the prior 6 months (community
subjects with pain), identified in a random sample survey of a health maintenance
organization
(HMO) population, as well as (3) clinic patients seeking treatment for
TMD through the same HMO. Prevalence rates for myofascial pain dysfunction in
clinic patients were much higher under the University
of Washington approach,
whereas rates of internal derangement
(type I) and degenerative
joint disease
were similar under the two schemes. These similar prevalence rates were not,
however, accompanied by high concordance between the two schemes. These
results highlight the complexities
of differential
diagnosis of TMD in 5eld research,
and suggest that further evaluation
of alternative
diagnostic schemes is warranted.
(J PRosTHE’r DENT 1991;65:131-7.)
I
n 1969, La.skin wrote, “There are two aspects to the
successful management of any disease process: one is the
establishment of an accurate diagnosis; the other is an understanding of its etiology so that a rational treatment plan
can be formulated. Unfortunately, in the management of
many problems involving the temporomandibular joint, we
This investigation was supported by United States Public Health
Service research grants No. 1 ROl DE07197 and lPO1 DE08773
from the National Institute of Dental Research, National
tutes of Health, Bethesda, Md.
Insti-
*Research Associate Professor, Department of Oral Medicine.
**Professor,
Psychiatry
Department
of Oral Medicine and Department
and Elehavioral Sciences, School of Medicine.
of
***Lecturer, Department of Oral Medicine.
****Associate Professor and Chairperson, Department of Oral
Medicine.
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have not been highly successful in either of these areas.“l
Since Laskin’s statement, consensus has emerged that
temporomandibular disorders (TMD) represent a group of
distinct entities, probably with different etiologies, natural
histories,
and prognoses.2
A number
of authors
have
presented approaches to the classification of one or more of
these disorders, including myofascial pain-dysfunction
(MPD),lp 3various internal derangements of the contents of
the joint space (ID),4-6 and degenerative joint disease
(DJD).7~8 A few more comprehensive schemes have been
presented as well. 2*g-11On superficial examination, these
diagnostic approaches may appear similar, or at least compatible. However, on closer view they are found to differ,
sometimes in their fundamental concepts and often in detail. As a result, consensus has not yet been achieved as to
which signs and symptoms are pathognomonic of each of
the disorders.
While this situation is regrettable, it should not be sur-
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