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Cranial arteritis mimicking odontogenic pain: report of case
__________ J 'A O A ___________ C L IN IC A L
R E P O R T S
Cranial arteritis mimicking odontogenic pain: report of case Steven A. G uttenberg, DDS Robert W. Emery, DDS Stanley A. M ilobsky, DDS M agdi G eballa, DDS
A 65-year-old p a tien t treated fo r pain of apparent odontogenic origin did not respond to appropriate dental treatment. While the signs and symptoms mimicked a den tal problem , fu rth er d ia g n o stic evaluation determined the “cu lp rit”— cranial arteritis. Proper treatment imme diately after diagnosis is advised as the com plications o f cranial arteritis can include the rapid onset of blindness.
ranial arteritis, frequently related to polymyalgia rheum atica, has also been called tem poral arte ritis, giant-cell arteritis, and “ arteritis of the aged.”12 The term cranial arteritis, however, seems appropriate as the disease symptom complex is primarily a function involving head and neck arteries. F ur therm ore, the presence of g ia n t cells, a lth o u g h typical, is n o t co m p u lso ry ; the temporal artery is not always involved; and the term “aged” is constantly being redefined as the p o p u la tio n becom es older. T he etiologic factors of cranial a rte ritis are u n k n o w n . T h e disease primarily affects those older than 50 years, and there is a female predilection. W ith increased life span of the p o p u la tio n , m ore instan ces of th is disease are expected. T h e onset is fre q u e n tly a b ru p t; is characterized by severe, unilateral, tem poral pain; and the pain may be longlasting and insidious. In addition, the
C
disease may be b ila teral and at tim es can be felt as a sharp or throbbing pain in the o cc ip u t, neck, face, jaw s, or tongue.3 Reports of visual disturbances, ep iso d ic eye p a in , an d m a n d ib u la r claudication are not uncommon.4 6 Intraorally, there may be p ain, b lanching, or necrosis of the tongue because of the involvement of the lingual artery.1'7 The affected vessels (most commonly the superficial temporal, vertebral, o p h th alm ic, or p o ste rio r ciliary arteries) may be tender, thickened, or nodular. Redness and edema of the overlying skin may be seen, or the vessels may be pulseless and nonpalpable. Periorbital an d facial edem a can also occur. On occasion, a fever of unknow n origin may be the only initial symptom. Usually, the temporal arteries are the first to be affected and are eventually involved in nearly all cases.8 In fatal cases, m any of the body’s arteries are involved. Laboratory studies, although nonspe cific, may be useful in arriving at the correct d iag n osis. For exam ple, the erythrocyte se d im en ta tio n rate (ESR) is elevated, and there are fre q u en tly increased numbers of polymorphonuclear leukocytes. A definitive diagnosis can be made by excising a segm ent of the affected vessel, exam ining it histologically, and integrating the inform ation gained with o th e r c lin ic a l fin d in g s.9 M icroscopic fin d in g s, w hile d istin c tiv e, are n o t pathognom onic and they may be observed
in Wegener’s granulomatosis, polyarteritis nodosa, and T akayasu’s disease. T he la tte r vascular diso rd er, also referred to as the aortic arch syndrome or pulseless disease, ap p ea rs id e n tic a l to c ra n ia l a rte ritis except th a t it m ain ly affects y o ung w om en a n d the a o rtic arch branches rather than elderly women and the cranial arteries.10 Early in the disease process, the fibers of the internal elastic m em brane break dow n and becom e su rro u n d e d by a chronic inflammatory response, predom inantly consisting of lymphocytes, mac rophages, and foreign body giant cells.8 Later, the vessel lum en becomes o b lit erated w hen the in tim a th ick en s and the endothelial and subendothelial fibro blasts proliferate. D eterioration of the tu n ic a media vasorum th en occurs as a consequence of extension of the gran ulomatous reaction into the arterial wall. Intravascular thrombosis and subsequent fibrosis may be the final outcome. T rea tm en t of the disease is u su ally favorable; how ever, serious sequelae in c lu d in g blindness, deafness, stroke, or even death can occur. The occurrence of blindness, secondary to obliteration of the central retinal artery or posterior ciliary arteries, is a serious risk in patients with cranial arteritis, and provides the rationale for rapid diagnosis and aggres sive treatm ent.1 A pproxim ately half of the patients w ith cranial arteritis have visual disturbances. Involvement of other vessels m anifests in sym ptom s related to the area w hich the vessels serve JADA, Vol. 119, November 1989 ■ 621
CLINICAL
REPORTS
(occipital symptoms from vertebral artery disease or central nervous system disorders from cerebral artery arteritis). Treatm ent of cranial arteritis requires steroids started in large doses and then tapered to relatively low m aintenance levels when symptoms have disappeared and the ESR has returned to norm al.11 P re d n iso n e is u su a lly the p referred medication, beginning with 40 to 60 mg per day, orally, and tapering slowly for several weeks to a level of 7 to 12 mg, daily. T h e patient may be kept at this dosage for 2 to 5 years, depending on the c lin ic a l response. M o n ito rin g the sedim entation rate may be used as an indicator of progress.
Fig 1 ■ S w elling of left su b m a n d ib u la r area as a result of adenopathy.
Fig 2 ■ Appearance of erythematous skin overlying involved temporal artery, and infraorbital edem a.
Report of case A 65-year-old female patient was referred to an e n d o d o n tist for tre a tm e n t of maxillary left facial pain of 1 to 2 weeks’ duration. T he patient’s medical history included arthritis and a heart m urm ur re q u irin g p ro p h y la x is. She h ad no allergies and took diazepam (V alium , R oche P rod u cts) for anxiety. D u rin g exam ination, a “ persistent” periapical radiolucent area on the mesial root of the maxillary left first m olar was found. It was termed “persistent” as conservative endodontic therapy had been completed. An apicoectomy was performed. After surgery, phenoxym ethylpenicillin (pen ic illin V) an d a c e ta m in o p h en w ith codeine were prescribed. The patient returned the next day with increased p ain . M ild s u b m a n d ib u la r adenopathy was noted, on the left side. T he dosage of penicillin was increased to 500 mg four times per day, and she was seen daily. T he patient’s condition continued to deteriorate and 3 days after the o rig in a l surgery she was referred for o ral an d m a x illo fa c ia l su rg ical evaluation with a presumptive diagnosis of deep space infection. At th is p o in t, the p a tie n t re p o rte d general m alaise, fever, b lurred vision, and increased anxiety. She stated that her scalp hurt so m uch that she could not brush her hair. Slight trismus was noted, but there were no indications of d ysphag ia. H er oral tem p eratu re was 100.2 F. Physical exam ination revealed bilateral temporal erythema and edema, bilateral infraorbital edema, and severe subm andibular adenopathy on the left side (Fig 1). T he term inal portions of the temporal arteries appeared prom inent and were firm and tender to palpation (Fig 2). F unduscopic an d otoscopic 622 ■ JADA, Vol. 119, November 1989
Fig 3 ■ P h o to m icro g rap h of biopsied tem poral
F ig 4 ■ P h o to m ic r o g ra p h of g ia n t c ells, fr e
artery sh o w in g acute and c h ro n ic in flam m ato ry
q u e n tly seen in c ra n ia l a rte ritis (H & E stain ,
in filtra te w ith in the vessel w all (H & E sta in ,
orig m ag
x
100).
o rig m ag x 100).
examinations were normal. T h e d ifferential diagnosis in clu d ed c ra n ia l a rte ritis, p a n s in u s itis w ith a tem p o ral space infectio n , and a n g io neurotic edema. W ater’s view and p an oram ic radiographs did not show any air-fluid levels. L aboratory values ob tained were: hem atocrit, 43.7%; hem o g lo b in , 14.4 g /d L ; w hite blood cells, 17,500/m L3; platelets 358,000/mm3; nor mal differential, Westergren method for erythrocyte sedimentation rate 33.0 m m / h (0-30), C-reactive p ro te in 13.5 m g / dL (0-5). T he clinical exam ination and lab o rato ry studies strongly suggested a diagnosis of cranial arteritis. Therefore, biopsy of the left tem poral artery was perfo rm ed the fo llo w in g day in the hospital. T h e term in al p o rtio n of the left su p e rfic ia l tem poral artery was approached by a 6-cm incision in the hairline, p aralleling the course of the vessel. After sharp and blunt dissection, the artery was easily identified and noted to be grossly occluded and firm . T he vessel was ap p ro p ria te ly lig ated , and a 5-cm section was excised. Histological exam ination revealed acute and chronic inflam m atory cell infiltrate w ithin the w alls of the artery ex ten d in g beyond the walls into the surrounding adventitia
(Fig 3). The cellular com ponent consisted of lymphocytes, plasma cells, and neu trophils; and occasional giant cells were id en tified (Fig 4). D estru ctio n of the elastic lam in a an d th ic k e n in g of the arterial wall with narrow ing of the lumen were seen (Fig 5). The patient’s physician was consulted and prednisone 60 mg per day was started with a dosage schedule that diminished by 10 mg every 6 days. W ithin 8 days, the patient was asym ptom atic and her sedim entation rate had dim inished to 10 m m /hr.
Discussion W hen a 65-year-old patient treated for pain of odontogenic origin did not heal in the expected time, other diagnostic “ avenues” were explored. In patients with cranial arteritis, these actions must be promptly accomplished or irreversible blindness can occur. T his was recently reiterated by Lamey and coworkers4 in their report of four patients with cranial a rte ritis w hich first ap p eared to be o ro facial co n d itio n s to th e ir dental practitioners. In a study that was cited by Freedman and G old,10 the risk of visual impairm ent was related to the presence or absence
CLINICAL
of giant cell arteritis on temporal artery biopsy. When arteritis was not present, there was a 15% chance of visual im pair m ent; how ever, w ith a rte ritis , v isu al disturbances developed in 53% of patients. Temporal artery biopsy also allows the practitioner to make a definitive diagnosis before co m m ittin g a p a tie n t to lo n g term steroid th erap y . T h is w o u ld be especially im p o rtan t in those patients w ith a h ig h likelihood of steroid side effects (patien ts w ith m o rb id obesity, diabetes m ellitus, hypertension, peptic ulcers, osteoporosis, an d w om en and the elderly). Many physicians believe, however, that as soon as a diagnosis of cranial arteritis is considered clinically, they are obligated to start steroid therapy im m ediately to avoid blindness. However, the surgical procedure is relatively sim ple and can be performed using local anesthesia for cachectic patients as described previously in th is case rep o rt. M cD onnell and coworkers12 reported that in a series of 265 temporal artery biopsies performed, there were no complications. Lesions of the vessel may be in te r mittent, and areas of healthy tissue may be interspersed w ith diseased tissue.13-14 It is, therefore, imperative that a sufficient specim en be o b tain ed by the surgeon and m ultiple serial sections be examined by the path o lo g ist. M inim um lengths of 2.5 to 4.0 cm have been suggested.1315 In patients for whom there is high clinical su sp ic io n , an d the frozen section is negative, it is suggested that biopsy of the c o n tra la te ra l tem p o ral artery be p e rfo rm e d .16 It is also im p o rta n t to recognize that previous unilateral biopsies have m issed u p to 14% of a rte ritis diagnoses w hich were later iden tified by bilateral procedures.17 T he two laboratory tests that can be useful a d ju n c ts in the d ia g n o sis an d treatment of cranial arteritis are the ESR and the detection of C-reactive protein in the serum . T h e ESR is a relatively nonspecific examination, useful in detect ing occult disease, confirm ing a diagnosis or differential diagnosis, or follow ing the course of certain diseases. There are two m ain m ethods of p erfo rm in g the test, the Westergren and the W introbe. T he form er is m ore accurate, an d the latter is considered more convenient.18 As in this case report, the ESR rises in cranial arteritis, and as the disease is appropriately treated, the ESR slows.
REPORTS
T h e a u th o r s th a n k N ic h o la s C acciab ev e, M D, c h ie f, d e p a r tm e n t o f p a th o lo g y , C a p ito l H ill H o s p ita l, W a s h in g to n , D C , fo r h is a ss is ta n c e in the p re p a ra tio n of this m anuscript.
Fig 5 ■ P h o to m icro g ra p h of th ick en in g arterial w all w ith n arro w in g lum en (H & E stain, o rig m ag x 40).
It is, therefore, useful during both the diagnostic and treatment phases of this disease. C-reactive protein (CRP) is normally detected in very small am ounts in the serum or not at all. In acute inflammation or necrosis, the CRP increase will occur before the rise in the ESR, and in recovery it tends to disappear before the return of the ESR to normal. A significant rise in serum C R P was seen in the case discussed in this clinical report.
Summary When a patient in pain comes to a dental office or is referred from one dentist to a dental specialist, it is reasonable to assum e th at the p ain is tooth-related. However, this phenom enon would also ap p ly to the o p h th a lm o lo g ist or otorhinolaryngologist who would explore every possible eye, ear, nose, or throat cause of pain before considering a dental origin. Because of its severe m orbidity and possible mortality, a possible diagnosis of cranial arteritis m ust be considered when supposed odontogenic pain does n o t decrease after a p p ro p ria te dental intervention. A case of this disorder has been presented and the disease process and diagnostic and treatment modalities have been described. T he diagnosis of c ra n ia l a rte ritis was d eterm ined by distilling information gathered from the medical history, physical exam ination, tem poral artery biopsy, and laboratory studies. P ro m p t in itia tio n of steroid medication is the preferred treatment.
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D r. G u tte n b e r g is s e n io r a tte n d in g s u rg e o n , W a s h in g to n H o s p i ta l C e n te r; c h ie f, O ra l a n d M a x illo f a c ia l S u r g e r y , C a p ito l H ill H o s p ita l, W ash in g to n ; a n d is p riv a te p ra c titio n e r in W ash in g to n . Dr. E m ery is staff, W a s h in g to n H o s p ita l Center; staff, C ap ito l H ill H ospital; an d is p rivate o ra l a n d m a x illo f a c ia l s u rg e ry p r a c titio n e r in W a s h in g to n . D r. M ilo b sk y is sta ff, W a s h in g to n H o s p i ta l C e n te r; s ta ff, P r o v id e n c e H o s p i ta l in W a s h in g to n ; a n d is p r iv a te o ra l s u rg e ry a n d e n dodontic p ra c titio n e r in W ashington. Dr. G eballa is p riv a te e n d o d o n tic p r a c titio n e r , W a s h in g to n . A ddress re q u e sts fo r re p r in ts to D r. G u tte n b e rg , 916 19th St, N W , Suite 728, W ashington, DC, 20006.
1. Siemssen SE. O n the occurrence of n e crotising lesions in arteritis tem poralis: review of the literature w ith a n o te o n the p o te n tia l risk of a biopsy. Br J P last S urg 1987;40:73-82. 2. P a u lle y JW , H u g h e s J P . G ia n t cell a rte ritis , or arteritis of the aged. Br M ed J 1960;2:1562-7. 3. B eeson PB , M c D e rm o tt W , W y n g a a rd e n JB . T e xtbook of m edicine. P h ilad e lp h ia : WB Saunders, 1979:216-8. 4. L am ey P -J, T a y lo r JA , D evine J. G ia n t cell arteritis. A forgotten diagnosis? Br D ent J 1988; 164:4850. 5. J o n a s so n F, C u lle n JF , E lto n RA. T e m p o ra l a rte ritis . A 14 year e p id e m io lo g ic a l, c lin ic a l a n d prognostic study. Scott M ed J 1979;24:111-7. 6. H o rto n BT. H eadaches an d in te rm itten t c la u d i c atio n of the ja w in te m p o ra l a rte ritis. H e ad a c h e 1962;2:29-40. 7. R osem an BB, G ra n ite E. Massive tongue necrosis secondary to te m p o ra l a rte ritis. J O ral M axillofac Surg 1984;42:682-4. 8. R o b b in s SL. T e x tb o o k of p a th o lo g y . P h il a d elp h ia: WB Saunders, 1962:452-3. 9. P o n g e T , B a rrie r J H , G ro lle a u J-Y , P o n g e A, V lasak AM, C o ttin S. T h e efficacy of selective u n ila te ra l te m p o ra l a rte ry b io p sy versus b ila te ra l b io p s ie s fo r d ia g n o s is o f g ia n t c e ll a r te r itis . J R h eu m ato l 1988;15:997-1000. 10. Freedm an SO, G old P. C linical im m unology. H agerstow n, MD: H a rp e r 8c R ow , 1976:274-7. 11. F re ita g J J , M ille r LW . M a n u a l o f m e d ic a l therapeutics. B oston: L ittle, B row n, 1980:391-2. 12. M c D o n n e ll P J , M o o re G W , M ille r N R , H u tc h in s G M , G re e n W R. T e m p o r a l a rte ritis . A clin ic o p ath o lo g ic study. O p h th a lm o lo g y 1986;93:51830. 13. K lein R G , C am pbell R J, H u n d e r G G , Carney JA . S kip lesions in te m p o ra l a rte ritis. M ayo C lin P roc 1976;51:504-10. 14. A lbert DM, R u c h m a n MC, K eltner JL . S kip a re a s in te m p o ra l a r te r itis . A rc h O p h th a lm o l 1976;94:2072-7. 15. C ohen DN, S m ith T R . Skip areas in tem poral a rte ritis : m y th versus fact. T r a n s A m A cad O p h th a lm o l O tolaryngol 1974;78:772-83. 16. N a d ea u SE. T e m p o r a l a rte ritis : a d e cisio n a n aly tic a p p ro a c h to te m p o ra l artery biopsy. Acta N eurol Scand 1988;78:90-100. 17. H a ll S, H u n d e r G G . Is tem poral artery biopsy prudent? M ayo C lin Proc 1984;59:793-6. 18. W allach J. In te rp re ta tio n of d ia g n o stic tests. B oston: L ittle, B row n, 1978:105-7.
G uttenberg-O thers : CRANIAL ARTERITIS MIMICKING O DO NTOGENIC PAIN ■ 623
R E P O R T S
Cranial arteritis mimicking odontogenic pain: report of case Steven A. G uttenberg, DDS Robert W. Emery, DDS Stanley A. M ilobsky, DDS M agdi G eballa, DDS
A 65-year-old p a tien t treated fo r pain of apparent odontogenic origin did not respond to appropriate dental treatment. While the signs and symptoms mimicked a den tal problem , fu rth er d ia g n o stic evaluation determined the “cu lp rit”— cranial arteritis. Proper treatment imme diately after diagnosis is advised as the com plications o f cranial arteritis can include the rapid onset of blindness.
ranial arteritis, frequently related to polymyalgia rheum atica, has also been called tem poral arte ritis, giant-cell arteritis, and “ arteritis of the aged.”12 The term cranial arteritis, however, seems appropriate as the disease symptom complex is primarily a function involving head and neck arteries. F ur therm ore, the presence of g ia n t cells, a lth o u g h typical, is n o t co m p u lso ry ; the temporal artery is not always involved; and the term “aged” is constantly being redefined as the p o p u la tio n becom es older. T he etiologic factors of cranial a rte ritis are u n k n o w n . T h e disease primarily affects those older than 50 years, and there is a female predilection. W ith increased life span of the p o p u la tio n , m ore instan ces of th is disease are expected. T h e onset is fre q u e n tly a b ru p t; is characterized by severe, unilateral, tem poral pain; and the pain may be longlasting and insidious. In addition, the
C
disease may be b ila teral and at tim es can be felt as a sharp or throbbing pain in the o cc ip u t, neck, face, jaw s, or tongue.3 Reports of visual disturbances, ep iso d ic eye p a in , an d m a n d ib u la r claudication are not uncommon.4 6 Intraorally, there may be p ain, b lanching, or necrosis of the tongue because of the involvement of the lingual artery.1'7 The affected vessels (most commonly the superficial temporal, vertebral, o p h th alm ic, or p o ste rio r ciliary arteries) may be tender, thickened, or nodular. Redness and edema of the overlying skin may be seen, or the vessels may be pulseless and nonpalpable. Periorbital an d facial edem a can also occur. On occasion, a fever of unknow n origin may be the only initial symptom. Usually, the temporal arteries are the first to be affected and are eventually involved in nearly all cases.8 In fatal cases, m any of the body’s arteries are involved. Laboratory studies, although nonspe cific, may be useful in arriving at the correct d iag n osis. For exam ple, the erythrocyte se d im en ta tio n rate (ESR) is elevated, and there are fre q u en tly increased numbers of polymorphonuclear leukocytes. A definitive diagnosis can be made by excising a segm ent of the affected vessel, exam ining it histologically, and integrating the inform ation gained with o th e r c lin ic a l fin d in g s.9 M icroscopic fin d in g s, w hile d istin c tiv e, are n o t pathognom onic and they may be observed
in Wegener’s granulomatosis, polyarteritis nodosa, and T akayasu’s disease. T he la tte r vascular diso rd er, also referred to as the aortic arch syndrome or pulseless disease, ap p ea rs id e n tic a l to c ra n ia l a rte ritis except th a t it m ain ly affects y o ung w om en a n d the a o rtic arch branches rather than elderly women and the cranial arteries.10 Early in the disease process, the fibers of the internal elastic m em brane break dow n and becom e su rro u n d e d by a chronic inflammatory response, predom inantly consisting of lymphocytes, mac rophages, and foreign body giant cells.8 Later, the vessel lum en becomes o b lit erated w hen the in tim a th ick en s and the endothelial and subendothelial fibro blasts proliferate. D eterioration of the tu n ic a media vasorum th en occurs as a consequence of extension of the gran ulomatous reaction into the arterial wall. Intravascular thrombosis and subsequent fibrosis may be the final outcome. T rea tm en t of the disease is u su ally favorable; how ever, serious sequelae in c lu d in g blindness, deafness, stroke, or even death can occur. The occurrence of blindness, secondary to obliteration of the central retinal artery or posterior ciliary arteries, is a serious risk in patients with cranial arteritis, and provides the rationale for rapid diagnosis and aggres sive treatm ent.1 A pproxim ately half of the patients w ith cranial arteritis have visual disturbances. Involvement of other vessels m anifests in sym ptom s related to the area w hich the vessels serve JADA, Vol. 119, November 1989 ■ 621
CLINICAL
REPORTS
(occipital symptoms from vertebral artery disease or central nervous system disorders from cerebral artery arteritis). Treatm ent of cranial arteritis requires steroids started in large doses and then tapered to relatively low m aintenance levels when symptoms have disappeared and the ESR has returned to norm al.11 P re d n iso n e is u su a lly the p referred medication, beginning with 40 to 60 mg per day, orally, and tapering slowly for several weeks to a level of 7 to 12 mg, daily. T h e patient may be kept at this dosage for 2 to 5 years, depending on the c lin ic a l response. M o n ito rin g the sedim entation rate may be used as an indicator of progress.
Fig 1 ■ S w elling of left su b m a n d ib u la r area as a result of adenopathy.
Fig 2 ■ Appearance of erythematous skin overlying involved temporal artery, and infraorbital edem a.
Report of case A 65-year-old female patient was referred to an e n d o d o n tist for tre a tm e n t of maxillary left facial pain of 1 to 2 weeks’ duration. T he patient’s medical history included arthritis and a heart m urm ur re q u irin g p ro p h y la x is. She h ad no allergies and took diazepam (V alium , R oche P rod u cts) for anxiety. D u rin g exam ination, a “ persistent” periapical radiolucent area on the mesial root of the maxillary left first m olar was found. It was termed “persistent” as conservative endodontic therapy had been completed. An apicoectomy was performed. After surgery, phenoxym ethylpenicillin (pen ic illin V) an d a c e ta m in o p h en w ith codeine were prescribed. The patient returned the next day with increased p ain . M ild s u b m a n d ib u la r adenopathy was noted, on the left side. T he dosage of penicillin was increased to 500 mg four times per day, and she was seen daily. T he patient’s condition continued to deteriorate and 3 days after the o rig in a l surgery she was referred for o ral an d m a x illo fa c ia l su rg ical evaluation with a presumptive diagnosis of deep space infection. At th is p o in t, the p a tie n t re p o rte d general m alaise, fever, b lurred vision, and increased anxiety. She stated that her scalp hurt so m uch that she could not brush her hair. Slight trismus was noted, but there were no indications of d ysphag ia. H er oral tem p eratu re was 100.2 F. Physical exam ination revealed bilateral temporal erythema and edema, bilateral infraorbital edema, and severe subm andibular adenopathy on the left side (Fig 1). T he term inal portions of the temporal arteries appeared prom inent and were firm and tender to palpation (Fig 2). F unduscopic an d otoscopic 622 ■ JADA, Vol. 119, November 1989
Fig 3 ■ P h o to m icro g rap h of biopsied tem poral
F ig 4 ■ P h o to m ic r o g ra p h of g ia n t c ells, fr e
artery sh o w in g acute and c h ro n ic in flam m ato ry
q u e n tly seen in c ra n ia l a rte ritis (H & E stain ,
in filtra te w ith in the vessel w all (H & E sta in ,
orig m ag
x
100).
o rig m ag x 100).
examinations were normal. T h e d ifferential diagnosis in clu d ed c ra n ia l a rte ritis, p a n s in u s itis w ith a tem p o ral space infectio n , and a n g io neurotic edema. W ater’s view and p an oram ic radiographs did not show any air-fluid levels. L aboratory values ob tained were: hem atocrit, 43.7%; hem o g lo b in , 14.4 g /d L ; w hite blood cells, 17,500/m L3; platelets 358,000/mm3; nor mal differential, Westergren method for erythrocyte sedimentation rate 33.0 m m / h (0-30), C-reactive p ro te in 13.5 m g / dL (0-5). T he clinical exam ination and lab o rato ry studies strongly suggested a diagnosis of cranial arteritis. Therefore, biopsy of the left tem poral artery was perfo rm ed the fo llo w in g day in the hospital. T h e term in al p o rtio n of the left su p e rfic ia l tem poral artery was approached by a 6-cm incision in the hairline, p aralleling the course of the vessel. After sharp and blunt dissection, the artery was easily identified and noted to be grossly occluded and firm . T he vessel was ap p ro p ria te ly lig ated , and a 5-cm section was excised. Histological exam ination revealed acute and chronic inflam m atory cell infiltrate w ithin the w alls of the artery ex ten d in g beyond the walls into the surrounding adventitia
(Fig 3). The cellular com ponent consisted of lymphocytes, plasma cells, and neu trophils; and occasional giant cells were id en tified (Fig 4). D estru ctio n of the elastic lam in a an d th ic k e n in g of the arterial wall with narrow ing of the lumen were seen (Fig 5). The patient’s physician was consulted and prednisone 60 mg per day was started with a dosage schedule that diminished by 10 mg every 6 days. W ithin 8 days, the patient was asym ptom atic and her sedim entation rate had dim inished to 10 m m /hr.
Discussion W hen a 65-year-old patient treated for pain of odontogenic origin did not heal in the expected time, other diagnostic “ avenues” were explored. In patients with cranial arteritis, these actions must be promptly accomplished or irreversible blindness can occur. T his was recently reiterated by Lamey and coworkers4 in their report of four patients with cranial a rte ritis w hich first ap p eared to be o ro facial co n d itio n s to th e ir dental practitioners. In a study that was cited by Freedman and G old,10 the risk of visual impairm ent was related to the presence or absence
CLINICAL
of giant cell arteritis on temporal artery biopsy. When arteritis was not present, there was a 15% chance of visual im pair m ent; how ever, w ith a rte ritis , v isu al disturbances developed in 53% of patients. Temporal artery biopsy also allows the practitioner to make a definitive diagnosis before co m m ittin g a p a tie n t to lo n g term steroid th erap y . T h is w o u ld be especially im p o rtan t in those patients w ith a h ig h likelihood of steroid side effects (patien ts w ith m o rb id obesity, diabetes m ellitus, hypertension, peptic ulcers, osteoporosis, an d w om en and the elderly). Many physicians believe, however, that as soon as a diagnosis of cranial arteritis is considered clinically, they are obligated to start steroid therapy im m ediately to avoid blindness. However, the surgical procedure is relatively sim ple and can be performed using local anesthesia for cachectic patients as described previously in th is case rep o rt. M cD onnell and coworkers12 reported that in a series of 265 temporal artery biopsies performed, there were no complications. Lesions of the vessel may be in te r mittent, and areas of healthy tissue may be interspersed w ith diseased tissue.13-14 It is, therefore, imperative that a sufficient specim en be o b tain ed by the surgeon and m ultiple serial sections be examined by the path o lo g ist. M inim um lengths of 2.5 to 4.0 cm have been suggested.1315 In patients for whom there is high clinical su sp ic io n , an d the frozen section is negative, it is suggested that biopsy of the c o n tra la te ra l tem p o ral artery be p e rfo rm e d .16 It is also im p o rta n t to recognize that previous unilateral biopsies have m issed u p to 14% of a rte ritis diagnoses w hich were later iden tified by bilateral procedures.17 T he two laboratory tests that can be useful a d ju n c ts in the d ia g n o sis an d treatment of cranial arteritis are the ESR and the detection of C-reactive protein in the serum . T h e ESR is a relatively nonspecific examination, useful in detect ing occult disease, confirm ing a diagnosis or differential diagnosis, or follow ing the course of certain diseases. There are two m ain m ethods of p erfo rm in g the test, the Westergren and the W introbe. T he form er is m ore accurate, an d the latter is considered more convenient.18 As in this case report, the ESR rises in cranial arteritis, and as the disease is appropriately treated, the ESR slows.
REPORTS
T h e a u th o r s th a n k N ic h o la s C acciab ev e, M D, c h ie f, d e p a r tm e n t o f p a th o lo g y , C a p ito l H ill H o s p ita l, W a s h in g to n , D C , fo r h is a ss is ta n c e in the p re p a ra tio n of this m anuscript.
Fig 5 ■ P h o to m icro g ra p h of th ick en in g arterial w all w ith n arro w in g lum en (H & E stain, o rig m ag x 40).
It is, therefore, useful during both the diagnostic and treatment phases of this disease. C-reactive protein (CRP) is normally detected in very small am ounts in the serum or not at all. In acute inflammation or necrosis, the CRP increase will occur before the rise in the ESR, and in recovery it tends to disappear before the return of the ESR to normal. A significant rise in serum C R P was seen in the case discussed in this clinical report.
Summary When a patient in pain comes to a dental office or is referred from one dentist to a dental specialist, it is reasonable to assum e th at the p ain is tooth-related. However, this phenom enon would also ap p ly to the o p h th a lm o lo g ist or otorhinolaryngologist who would explore every possible eye, ear, nose, or throat cause of pain before considering a dental origin. Because of its severe m orbidity and possible mortality, a possible diagnosis of cranial arteritis m ust be considered when supposed odontogenic pain does n o t decrease after a p p ro p ria te dental intervention. A case of this disorder has been presented and the disease process and diagnostic and treatment modalities have been described. T he diagnosis of c ra n ia l a rte ritis was d eterm ined by distilling information gathered from the medical history, physical exam ination, tem poral artery biopsy, and laboratory studies. P ro m p t in itia tio n of steroid medication is the preferred treatment.
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D r. G u tte n b e r g is s e n io r a tte n d in g s u rg e o n , W a s h in g to n H o s p i ta l C e n te r; c h ie f, O ra l a n d M a x illo f a c ia l S u r g e r y , C a p ito l H ill H o s p ita l, W ash in g to n ; a n d is p riv a te p ra c titio n e r in W ash in g to n . Dr. E m ery is staff, W a s h in g to n H o s p ita l Center; staff, C ap ito l H ill H ospital; an d is p rivate o ra l a n d m a x illo f a c ia l s u rg e ry p r a c titio n e r in W a s h in g to n . D r. M ilo b sk y is sta ff, W a s h in g to n H o s p i ta l C e n te r; s ta ff, P r o v id e n c e H o s p i ta l in W a s h in g to n ; a n d is p r iv a te o ra l s u rg e ry a n d e n dodontic p ra c titio n e r in W ashington. Dr. G eballa is p riv a te e n d o d o n tic p r a c titio n e r , W a s h in g to n . A ddress re q u e sts fo r re p r in ts to D r. G u tte n b e rg , 916 19th St, N W , Suite 728, W ashington, DC, 20006.
1. Siemssen SE. O n the occurrence of n e crotising lesions in arteritis tem poralis: review of the literature w ith a n o te o n the p o te n tia l risk of a biopsy. Br J P last S urg 1987;40:73-82. 2. P a u lle y JW , H u g h e s J P . G ia n t cell a rte ritis , or arteritis of the aged. Br M ed J 1960;2:1562-7. 3. B eeson PB , M c D e rm o tt W , W y n g a a rd e n JB . T e xtbook of m edicine. P h ilad e lp h ia : WB Saunders, 1979:216-8. 4. L am ey P -J, T a y lo r JA , D evine J. G ia n t cell arteritis. A forgotten diagnosis? Br D ent J 1988; 164:4850. 5. J o n a s so n F, C u lle n JF , E lto n RA. T e m p o ra l a rte ritis . A 14 year e p id e m io lo g ic a l, c lin ic a l a n d prognostic study. Scott M ed J 1979;24:111-7. 6. H o rto n BT. H eadaches an d in te rm itten t c la u d i c atio n of the ja w in te m p o ra l a rte ritis. H e ad a c h e 1962;2:29-40. 7. R osem an BB, G ra n ite E. Massive tongue necrosis secondary to te m p o ra l a rte ritis. J O ral M axillofac Surg 1984;42:682-4. 8. R o b b in s SL. T e x tb o o k of p a th o lo g y . P h il a d elp h ia: WB Saunders, 1962:452-3. 9. P o n g e T , B a rrie r J H , G ro lle a u J-Y , P o n g e A, V lasak AM, C o ttin S. T h e efficacy of selective u n ila te ra l te m p o ra l a rte ry b io p sy versus b ila te ra l b io p s ie s fo r d ia g n o s is o f g ia n t c e ll a r te r itis . J R h eu m ato l 1988;15:997-1000. 10. Freedm an SO, G old P. C linical im m unology. H agerstow n, MD: H a rp e r 8c R ow , 1976:274-7. 11. F re ita g J J , M ille r LW . M a n u a l o f m e d ic a l therapeutics. B oston: L ittle, B row n, 1980:391-2. 12. M c D o n n e ll P J , M o o re G W , M ille r N R , H u tc h in s G M , G re e n W R. T e m p o r a l a rte ritis . A clin ic o p ath o lo g ic study. O p h th a lm o lo g y 1986;93:51830. 13. K lein R G , C am pbell R J, H u n d e r G G , Carney JA . S kip lesions in te m p o ra l a rte ritis. M ayo C lin P roc 1976;51:504-10. 14. A lbert DM, R u c h m a n MC, K eltner JL . S kip a re a s in te m p o ra l a r te r itis . A rc h O p h th a lm o l 1976;94:2072-7. 15. C ohen DN, S m ith T R . Skip areas in tem poral a rte ritis : m y th versus fact. T r a n s A m A cad O p h th a lm o l O tolaryngol 1974;78:772-83. 16. N a d ea u SE. T e m p o r a l a rte ritis : a d e cisio n a n aly tic a p p ro a c h to te m p o ra l artery biopsy. Acta N eurol Scand 1988;78:90-100. 17. H a ll S, H u n d e r G G . Is tem poral artery biopsy prudent? M ayo C lin Proc 1984;59:793-6. 18. W allach J. In te rp re ta tio n of d ia g n o stic tests. B oston: L ittle, B row n, 1978:105-7.
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