Bilateral calcareous bursitis at the elbow.

A close correlation exists between the pathomechanism and localisation of calcareous bursitis and calcification of tendons and tendon sheaths. Recent descriptions emphasise this fact and give calcifying bursitis. tendinitis and paratendinitis the common name of periarthritis calcarea (Mark#{243} 1956, B#{225}nki1964). Calcareous bursitis is frequently encountered in the shoulder region but it is rarely found elsewhere. Eufinger (1957) mentioned only the subdeltoid bursa as being affected. Hamilton (1951) described thirteen cases of bursitis under the name ofcalcinosis; in six ofhis cases the shoulder was affected; in the rest other parts were involved. Calcification ofa bursa is viewed by pathologists as a dystrophic process (Anderson 1961). Deposition of calcium-holding material in the wall and cavities of the bursa is preceded by regressive changes in the tissues. The oxygen supply and nutrition of the walls of the bursa decrease with an increase of their calcium-holding capacity. According to Rabb (1923) increased carbon dioxide saturation of damaged tissues leads to calcium deposition. This occurs most commonly in infective and degenerative conditions. Claessens and Faure (1963) divided bursitis into two major groups: post-traumatic and infective. Rheumatic bursitis belongs to the second group and includes cases in which bacterial infection cannot be proved. In the course of chronic inflammation the wall of the bursa thickens and in consequence of insufficient nutrition degenerative changes take place. Frequently inflammatory and degenerative changes are present simultaneously (Abbertini 1929). Para-articular calcification and ossification occur in neurotrophic disorders. Symmetrical bursitis (GUnther 1913, Holzweissig 1925) and bilateral tendon calcifications (Albertini 1929) suggest a possible neurological basis for the lesions. Exner (1957) regarded neurovegetative dysfunction as a cause of pathological calcification. Other authors too (Gaule 1895, Meyer 1927, Seifert 1930, Katthagen 1949, Reischauer 1958, Rossak 1961, Waschulewski 1963) have described the relationship of abnormal calcification to an underlying neurological cause.