Histopathology zyxwvutsrqponmlk 1991, zyxwvutsrqpo 19, 169-172 AUONIS zyxw 030901h79100137C Dystrophic amyloidosis: a local complication of tissue damage with heterogeneous distribution L. M.LOOI zyxwvutsrq Department of Pathology, Faculty of Medicine, University of Malaya, Kuala zyxwvu Lumpur, Malaysia Date of submission 18 March 1991 Accepted for publication 1 1 April 1 9 9 1 1,001 L.M. (1991) Histopathology 19, 169-172 Dystrophic amyloidosis: a local complication of tissue damage with heterogeneous distribution Seventeen consecutive patients with dystrophic amyloidosis are reported here (eight Chinese, three Indian, three Iban, two Malay and one Caucasian).Ten were females and seven males, with ages ranging from 12 to 80 years (mean of 48 years). Five instances of dystrophic amyloidosis occurred in areas of tissue damage in the cardiovascular system, including fibrotic cardiac valves and an atheromatous plaque. Three occurred in osteoarthritic joint tissue. Of note were three occurrences in endometriotic cyst walls, four in the fibrotic walls of epidermal cysts, one in a hernial sac and one at the edge of a skin ulcer. All deposits were congophilic and exhibited green-birefringence and permanganate-resistance. Immunohistochemistry did not reveal reactivity for AA protein or immunoglobulin 2 or K light-chains. AP protein was detected in 35% of cases. Our results show that, besides the usual sites of osteoarthritic joints and damaged heart valves, dystrophic amyloidosis can complicate other areas of chronic tissue damage and fibrosis such as walls of cysts and ulcers. While the pathogenesis and biochemical nature remain unresolved, immunohistochemistry indicates that neither AA nor AL proteins are present in the deposits, and suggests that a different amyloid protein is involved. Keywords: dystrophic amyloid, fibrosis, calcification Introduction The term ‘dystrophic amyloidosis’ was first used by Goffin in 1980’ to describe a form of localized amyloido- sis that occurred in damaged and scarred cardiac valves. Since then, several other workers have investigated this phenomenon, and its reported prevalence within damaged valves has ranged from 15 to The amyloid was not associated with systemic disease and occurred independently of age, differentiating it from senile cardiac amyloidosis. Histologically, the deposits appeared as irregular small floccules or plaques in close proximity to foci of calcification or within areas of dense fibrosis. Electronmicroscopy has shown typical amyloid fibrils mixed with collagen fibrils’.4. Cooper4pointed out that it was unlikely for a dystro- phic form of amyloidosis to occur only in heart valves, and drew attention to other localized amyloidoses, Address for correspondence: Professor L.M.Looi, Department of Pathology. Faculty of Medicine, University of Malaya. 59100 Kuala Lurnpur, Malaysia. representing the same or analogous forms of the disease, that have been reported in arthritic joint^^-^. Various investigations showed it to complicate between 2 3 and 56% of osteoarthritic joints8-l*. A significantly frequent occurrence of this form of amyloidosis in pyrophosphate arthritis and chondromatosis was also notedh,”.’’. The amyloid deposits were present in the joint capsules and/ or articular cartilage and a close association with fibrosis and chondrocytes was common. In a study in the Department of Pathology, University of Malaya, the occurrence of dystrophic amyloidosis has been found to be more heterogeneous than has previously been reported. Its clinicopathological, mor- phological and immunohistochemical characteristics are described here. Materials and methods Congo red screening of surgical biopsies received by the Department of Pathology. University of Malaya over a 5.5-year period, as part of a larger study to determine the 169