JADA Continuing Education
PAINFUL CHEWING AND BLINDNESS: SIGNS AND SYMPTOMS OF TEMPORAL ARTERITIS
DAVID T. ALLEN, D.D.S.,
MARTA C. VOYTOVICH, M.D. and
JAMES C. ALLEN, M.D.
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ABSTRACT
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Background. This case report illustrates the need to consider temporal arteritis in the differential diagnosis of jaw or tooth pain. This disease affects the cranial arteries, more frequently in women and usually in those older than age 60 years, causing jaw pain, visual symptoms, headache, scalp pain and sometimes blindness.
Case Description. A 71-year-old man had jaw pain that increased with chewing and speaking, scalp tenderness and dimming vision. A temporal artery biopsy confirmed the diagnosis of temporal arteritis. Treatment with decreasing amounts of oral steroids over 23 months was successful in relieving his signs and symptoms and in saving his vision.
Clinical Implications. Patients with this disease may seek care from their dentist first. Jaw or tooth pain is the most reliable clinical symptom in the diagnosis of temporal arteritis. Diagnosis and timely referral for treatment with oral steroids can prevent blindness.
Temporal arteritis is also known as cranial arteritis and giant cell arteritis.1 Temporal arteritis may involve any of the arteries of the body, but particularly the cranial arteries. Typically, one or more branches of the carotid artery are involved. The disease develops primarily in patients older than age 60 years and increases in incidence with age. It occurs slightly more frequently in women. The pain is due to ischemia of the muscles of mastication caused by narrowing of the arteries. Clinical manifestations may include pain on chewing, tooth pain, headache, scalp tenderness, visual symptoms, anorexia, anemia and low-grade fever. Involvement of the central retinal artery may cause blindness in one or both eyes. The cause is unknown, but it is thought to involve an autoimmune reaction.
Jaw or tooth pain is the most reliable of all clinical symptoms in the diagnosis of temporal arteritis.2 Hayreh2 described a patient who visited her dentist because of jaw pain and had dental work performed. The next day, she lost her vision as a result of temporal arteritis and blamed her dentist. In another case, a large ulceration on the tongue was caused by temporal arteritis in a 78-year-old woman.3
Temporal arteritis is not as frequently discussed in dental schools and in the dental literature as it is in medical schools and in the medical literature.4–6 Therefore, the practicing dentist needs to be alert to the diagnosis of this disease to prevent blindness.
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CASE REPORT
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In 1989, a 71-year-old white man came to a hospital emergency department with an 11-day history of increasing jaw pain, scalp pain and visual symptoms. The jaw pain increased with chewing and speaking, and it caused the patient to take much longer to eat than he normally did. He complained that his teeth hurt, although he was edentulous. The pain was present on his scalp and under his chin and extended behind his eyes. It was sharp and shooting, resembling the pain he had experienced with shingles (herpes zoster). Visual symptoms included diplopia, pain with eye movement, transient loss of vision and dimming of vision.
The patient’s medical history revealed peptic ulcer disease, hypothyroidism and ocular migraines that occurred about once a month. These migraine headaches were associated with visual symptoms. However, his present pain was different from his usual ocular migraine headaches. Other symptoms included general weakness, difficulty in sleeping, anorexia and a mild fever lasting two days. On physical examination, the palpable temporal arteries were tender to the touch. The patient’s erythrocyte sedimentation rate, or ESR, was elevated at 126 millimeters/hour (normal ESR [Westergren method], 0 to 15 mm/h for men and 0 to 20 mm/h for women). The hematocrit was 37 percent (normal, 42 to 52 percent for men and 37 to 47 percent for women).
The patient was referred to the internal medicine service and then the ophthalmology service, where one of us (J.A.) performed a temporal artery biopsy. The results of the biopsy confirmed the clinical diagnosis of temporal arteritis. A regimen of 80 milligrams of oral prednisone per day was initiated; within a few days, the patient’s symptoms disappeared. The prednisone therapy (80 mg/day) was continued for eight days and then the dosage was decreased to 60 mg/d. The dosage was gradually decreased further as the patient’s ESR returned to normal. Prednisone therapy was discontinued after 23 months. To date, the patient remains asymptomatic, receives no steroid treatment and has 20/25 vision in both eyes.
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DISCUSSION
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The dentist may elicit a history of increased pain on chewing and talking. It is interesting that our patient complained of toothache even though he was edentulous. Other patients may state that they have jaw pain, especially on chewing, but that they do not have a toothache. Intermittent claudication, by definition, is absence of discomfort or pain when a limb is at rest and commencement of pain on exercise. "Jaw claudication" is somewhat of a misnomer but is a term often used in the medical literature to describe pain on chewing. Because of intermittent claudication, some patients eat soft foods that do not require chewing. Other patients complain that they get tired when chewing. Patients who have oral pain symptoms are more likely to have a diagnosis of temporal arteritis confirmed on biopsy than are patients with other clinical symptoms that suggest temporal arteritis.2 The differential diagnosis includes dental pathology, temporo-mandibular joint disorders, migraine headaches and ocular migraine.7
Clinical signs and symptoms vary, depending on which arteries are involved. The onset of temporal arteritis may be acute or gradual. Headache is common and may be unilateral or bilateral in the temporal area. The skin on the jaw and scalp may hurt and the temporal arteries may be nodular and tender to the touch. Narrowing of the lumen of the arteries decreases the supply of blood and oxygen to the muscles of mastication. This lack of blood supply to the visual system will cause visual changes. Visual disturbances may vary and include blurred vision, transient loss of vision, ptosis and diplopia. Central retinal artery involvement with inflammation and ischemia may cause unilateral, bilateral, temporary or permanent visual loss.8 Some patients report that it hurts to comb their hair. Scalp pain is caused by lack of blood supply and can be so severe that it causes scalp necrosis.9 Systemic manifestations may include low-grade fever, anorexia, weight loss, muscle weakness, muscle stiffness and myalgia. Pain and stiffness in the neck and pectoral muscles may be present, along with general malaise. The systemic symptoms are similar to those of polymyalgia rheumatica to which it may be related.10
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EPIDEMIOLOGY
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The cause of temporal arteritis is unknown. Epidemiologic studies have shown an incidence as high as 15 to 30 cases per year per 100,000 people older than age 50 years in some populations.11 Reports of disease presence in first-degree relatives, a predilection for the disease to occur in whites and association with HLA-DR4 (human leukocyte antigen) suggest a genetic predisposition.12 The increasing incidence after age 60 years and predominance in women suggest a relationship with aging and perhaps hormonal changes.13
Temporal arteritis is one of a group of diseases in which vasculitis due to inflammation of the arteries is present.14 This group of diseases with vasculitis includes temporal arteritis, polyarteritis nodosa, erythema nodosum and Takayasu’s arteritis. Temporal arteritis is associated with vasculitis of the carotid arteries of the head. Polyarteritis nodosa affects medium-sized muscular arteries. Erythema nodosa is a skin disease with vasculitis of deep dermal arteries. Takayasu’s arteritis affects the large arteries such as the aorta and its branches. It is thought that all of these diseases are caused by an autoimmune phenomenon.11
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PATHOLOGY
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Temporal arteritis is a granulomatous inflammation affecting arteries that contain elastic tissue. Granulomatous inflammation of the arterial wall, destruction of internal elastic lamina and giant cell formation represent the characteristic pathologic features. The inflammation rarely affects veins. The prominent histologic feature is inflammation, with lymphocyte, epithelioid histiocyte and multi-nucleated inflammatory giant cell infiltration of the intima and media of the arteries, causing disruption of the internal elastic lamina. The inflammation causes luminal narrowing and occlusion of the arteries via intimal proliferation (Figures 1
and 2). The narrowing of the artery lumen is the cause of ischemia and, consequently, pain. The disease may involve one area of an artery and skip another area of the same artery. The disease usually attacks the cranial arteries and occasionally segments of the aorta and its branches, such as the coronary arteries.
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Figure 1. Cross-section of biopsy specimen showing almost complete luminal obliteration by the inflammatory process (four peripheral arrows point to elastica interna, a single arrowhead points to a remaining small narrow lumen) (x100 magnification, hematoxylin-eosin stain).
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Figure 2. Cross-section of biopsy specimen showing transmural inflammation (arrow at elastica interna) (x250 magnification, hematoxylin-eosin stain).
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DIAGNOSIS
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Temporal arteritis is diagnosed by taking a careful medical history and performing a biopsy of one of the temporal arteries.15 If temporal arteritis is suspected, an ESR test should be performed immediately. Laboratory tests can help determine the diagnosis before the biopsy is performed. ESR and C-reactive protein tests are not specific to temporal arteritis, but are helpful in making a diagnosis. An ESR of greater than 100 mm/h is often present in the acute stage of the disease, and is highly suggestive of temporal arteritis.
The odds of a positive biopsy result are 9.1 times greater when patients complain of jaw claudication and 3.4 times greater when neck pain is present.2 The higher the ESR, the more likely that the biopsy results will confirm the presence of temporal arteritis. Some authors16 believe that the C-reactive protein test is equal to, or better than, the ESR test. The odds of a positive biopsy result are 3.2 times greater when a C-reactive protein test result is above 2.45 mg/deciliter (normal findings, 0 to 0.9 mg/dL).2 However, even if the ESR and C-reactive protein rate are not highly elevated, a biopsy should be performed if the patient’s medical history and physical findings suggest temporal arteritis.
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TREATMENT
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When a dentist diagnoses or suspects temporal arteritis, he or she should refer the patient to a physician. The physician should initiate a regimen of oral steroid therapy immediately after obtaining an ESR. A biopsy to confirm the diagnosis should be done within the next few days. Traditionally, biopsies have been performed by ophthalmologists. The biopsy results still will confirm the diagnosis for at least several days after oral steroid therapy has been initiated. Some authors have reported positive biopsy results after months of oral steroid treatment.17–19 (In some cases, a biopsy result may be negative in the presence of disease because the vasculitis may skip some areas of the artery. Therefore, if the biopsy results are negative but the signs and symptoms clearly indicate temporal arteritis, the patient generally is treated with oral steroids.)
Usually, 60 to 80 mg/d of prednisone is administered for about one week. The benefit of higher dosages of steroids is controversial.20 Oral steroid therapy is continued until the symptoms subside and the ESR returns to normal. The patient’s symptoms and ESR are then monitored as the dosage gradually is decreased. This tapering of steroid therapy is done over months and sometimes years. Complications of steroid treatment include hypertension, renal calculi, osteoporosis, decreased resistance to infection, diabetes and psychiatric disturbances. If a complication develops, the patient’s physician might decide to lower the oral steroid dosage.
The prognosis for patients with temporal arteritis usually is good if they are treated promptly; however, the treatment may last for several years. If not treated, the patient is at risk of developing blindness. While oral steroids are beneficial in most cases, a few patients do not respond to them and blindness results, even though they are receiving adequate doses of the drug.21
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CONCLUSION
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Dentists should consider temporal arteritis when an elderly patient, especially a woman, has jaw pain, tooth pain or tongue ulceration unexplained by the dental examination. Pain on chewing is the most reliable of all clinical signs in the diagnosis of temporal arteritis. Failure to diagnose temporal arteritis in a timely fashion may lead to blindness. This disease, which has been called the prime medical emergency in ophthalmology, also should be considered a prime medical emergency for dentists.
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FOOTNOTES
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Dr. Voytovich is an associate professor, Department of Pathology, Medical School, University of Wisconsin, Madison, and Veterans Affairs Hospital, Madison, Wis.
Dr. James. Allen is an associate professor emeritus, Department of Ophthalmology, Medical School, University of Wisconsin, Madison, and Veterans Affairs Hospital, Madison, Wis.
This study was supported in part by Research to Prevent Blindness, New York.
Dr. David Allen is a resident, Department of Dentistry, Mayo Clinic, Rochester, Minn. 55905, e-mail "allen.david{at}mayo.edu". Address reprint requests to Dr. Allen.
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REFERENCES
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- Ghanchi FD, Dutton GN. Current concepts in giant cell (temporal) arteritis. Surv Ophthalmol 1997;42:99–123.[Medline]
- Hayreh SS. Masticatory muscle pain: an important indicator of giant cell arteritis. J Spec Care Dent 1998;18:60–5.
- van der Wal JE, van der Waal I. Oral manifestations of giant cell arteritis. Mund Kiefer Gesichtsch 1997;1:65–7.
- Guttenberg SA, Emery RW, Milobsky SA, Geballa M. Cranial arteritis mimicking odon-togenic pain: report of case. JADA 1989;119:621–3.[Medline]
- Lee AG. Jaw claudication: a sign of giant cell arteritis. JADA 1995;126:1028–9.[Medline]
- Austin D, O’Donnell F, Attanasio R. Temporal arteritis mimics TMJ/myofascial pain syndrome. Ohio Dent J 1992;66:44–7.[Medline]
- Austin DG, Cubillos L. Special considerations in orofacial pain. Dent Clin North Am 1991;35:227–44.[Medline]
- Hayreh SS, Podhajsky PA, Zimmerman B. Ocular manifestations of giant cell arteritis. Am J Ophthalmol 1998;125:509–26.[Medline]
- Rudd JC, Fineman MS, Sergott RC, Eagle RC. Ischemic scalp necrosis preceding loss of visual acuity in giant cell arteritis. Arch Ophthalmol 1998;116:1690–1.[Free Full Text]
- Boesen P, Sorensen SF. Giant cell arteritis, temporal arteritis, and polymyalgia rheumatica in a Danish county: a prospective investigation,1982–1985. Arthritis Rheum 1987;30:294–9.[Medline]
- Machado EB, Michet CJ, Ballard DJ, et al. Trends in incidence and clinical presentation of temporal arteritis in Olmsted County, Minnesota, 1950–1985. Arthritis Rheum 1988;31:745–9.[Medline]
- Hunder GG, Bloch DA, Michel BA, et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum 1990;33:1122–8.[Medline]
- Hunder GG, Michet CJ. Giant cell arteritis and polymyalgia rheumatica. Clin Rheum Dis 1985;11:471–83.[Medline]
- Calabrese LH, Michel BA, Bloch DA, et al. The American College of Rheumatology 1990 criteria for the classification of hypersensitivity vasculitis. Arthritis Rheum 1990;33:1108–13.[Medline]
- Boyev LR, Miller NR, Green WR. Efficacy of unilateral versus bilateral temporal artery biopsies for the diagnosis of giant cell arteritis. Am J Ophthalmol 1999;128:211–5.[Medline]
- Deodhar SD. C-reactive protein: the best laboratory indicator available for monitoring disease activity. Cleve Clin J Med 1989;56:126–30.[Medline]
- Guevara RA, Newman NJ, Grossniklaus HE. Positive temporal artery biopsy 6 months after prednisone treatment. Arch Ophthalmol 1998;116:1252–3.[Free Full Text]
- Papadakis MA, Schwartz ND. Temporal arteritis after normalization of sedimentation rate in polymyalgia rheumatica. Arch Intern Med 1986;146:2283–4.[Medline]
- Achkar AA, Lie JT, Hunder GG, O’Fallon WM, Gabriel SE. How does previous corticosteroid treatment affect the biopsy findings in giant cell (temporal) arteritis? Ann Intern Med 1994;120:987–92.[Abstract/Free Full Text]
- Cornblath WT, Eggenberger ER. Progressive visual loss from giant cell arteritis despite high dose IV methylprednisolone. Ophthalmology 1997;104:854–8.[Medline]
- Hwang JM, Girkin CA, Perry JD, Lai JC, Miller NR, Hellmann DB. Bilateral ocular ischemic syndrome secondary to giant cell arteritis progressing despite corticosteroid treatment. Am J Ophthalmol 1999;127:102–4.[Medline]
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ABSTRACT
CASE REPORT
