• trismus
• giant cell arteritis

In the September issue of the journal, Nir-Paz et al described six patients who developed reduction in jaw opening in association with giant cell arteritis.¹ These authors found that patients with such a complaint seem to have a more severe disease with a higher prevalence of eye involvement.

Although the precise pathological mechanism underlying reduction in jaw opening is unknown, this symptom probably results, like jaw claudication, from partial failure in blood supply to masseter muscles. However, the value of jaw claudication as a harbinger of visual loss has been debated.^2–7 We sought to determine, in a large series of patients with temporal (giant cell) arteritis, the prevalence and clinical associations of reduction in jaw opening.

Between January 1977 and August 2002, 222 consecutive patients were diagnosed as having temporal arteritis in the Department of Internal Medicine. Clinical, laboratory, and pathological data were recorded prospectively before treatment at the time of diagnosis in 217 patients (178 biopsy proven), using a specifically designed, comprehensive questionnaire. The following items pertaining to jaw-mouth-throat problems were included in the questionnaire: jaw claudication, reduction or difficulty in jaw opening, maxillary or tooth pain, lingual discomfort or ischaemia, sore throat, dysphagia, hoarseness, and dry cough. Various jaw-mouth-throat complaints were present in 126 patients, including typical jaw claudication in 80 (63%), reduction or difficulty in jaw opening in 45 (36%), maxillary pain in 28 (22%), sore throat in 27 (21%), dysphagia in 22 (17%), dry cough in 14 (11%), hoarseness in 11 (9%), lingual discomfort in 7 (6%), and multiple complaints in 60 (48%).

Table 1 shows that reduction or pain in jaw opening was associated with pain over temples, occipitalgia, jaw claudication, and other jaw-mouth-throat complaints but not with other pretreatment variables, including the delay in diagnosis, permanent visual loss, extracephalic signs, constitutional symptoms, and inflammatory response. Finally, reduction or pain in jaw opening was the only jaw-mouth-throat complaint in 13 patients and the sole cephalic symptom in one patient.

Thus, our study only partially confirms the findings of Nir-Paz et al. Reduction in jaw opening seems to delineate, along with jaw claudication and other jaw-mouth-throat symptoms, a subset of giant cell arteritis characterised by a constellation of symptoms or signs indicating the involvement of multiple branches of the external carotid artery. Of importance is our finding of no association between reduction in jaw opening and visual symptoms, contrary to the Israeli study. This result is not surprising, because reduction in jaw opening involves vasculitis lesions in the external carotid artery system, whereas visual loss is due to vasculitis in distal branches of the ophthalmic artery—that is, in the internal carotid artery system.⁸ In our opinion, the observed differences between our results and those presented by Nir-Paz et al may be related to different study designs. Furthermore, we did not separate patients with true reduction in jaw opening and those with pain upon jaw opening but without obvious trismus, which may account for further discrepancies. Finally, we agree with Nir-Paz et al that jaw-mouth-throat complaints, including reduction of jaw opening, should be better known to doctors because such symptoms may speed up the diagnosis of giant cell arteritis. In our experience, jaw-mouth-throat complaints represented, along with laboratory abnormalities, the keystone of diagnosis in five patients with biopsy-proven disease—that is, 2.3% of the series.