Objective: The etiology of temporal arteritis (TA) and polymyalgia rheumatica (PMR) is unknown, but the sudden onset and the wide variation in incidence reported from various parts of the world suggest the existence of environmental and/or genetic factors. We studied the incidence of TA and PMR during a 12 year period in different regions of Denmark.
Methods: For the period 1982 to 1994, data were obtained on the incidence of PMR and TA prospectively recorded in 2 general hospitals, and for 1982 to 1993 on the incidence reported by legal requirement to the national patient register by all hospitals in 13 of the 16 counties in Denmark. In 2 counties data on all temporal artery biopsies were obtained. Serological epidemiological surveillance data on infections causing epidemics in Denmark were obtained from the Statens Seruminstitut.
Results: We analyzed data on 10,818 patients from 13 counties and 2651 temporal artery biopsies from two counties. The incidence rate for TA for the population aged 50 years and older was 20.4/100,000 (95% CI, 19-23), the rate for PMR was 41.3/100,000 (95% CI, 30-67). Significantly higher incidence rates were found in locations with high population density. Median number of temporal artery biopsies performed was 109/100,000 population aged 50 years and older, and the number increased linearly with time; a positive biopsy result was observed in 15.0%; the incidence rate of histologically proven TA in 2 counties was 15.1/100,000 population aged 50 years and older (95% CI, 11-20). Pronounced quarterly and annual variations of the incidence of TA and PMR were found in each of the 13 counties, and in the 2 hospital regions, with a clustering in 5 peaks. These cyclic fluctuations were seen simultaneously in several regions irrespective of the origin (hospital based, register derived, or temporal artery biopsy) of the data. Distinct peak incidences of TA and PMR occurred in close association with 2 epidemics of Mycoplasma pneumoniae infection. Two peaks were seen, partly related to 2 epidemics of parvovirus B19 and to an epidemic of Chlamydia pneumoniae.
Conclusion: The synchronous variations in the incidences of TA and PMR recorded in several regions of Denmark strongly indicate that an environmental infectious factor influences the frequencies. The close concurrence with epidemics of M. pneumoniae and the coincidence of 2 epidemics of parvovirus B19 and of one epidemic of C. pneumoniae in some locations with peak incidences of TA and PMR suggest that TA and PMR may be triggered by certain virus and/or bacterial agents.