Paulina González-Aguilar, Mario Aurelio Martínez-Jiménez, Arturo Ortiz-Álvarez, Jose L Ramirez-Garcialuna
Background and Clinical Significance: Dystrophic calcinosis cutis involves calcium deposition in damaged or chronically inflamed tissues despite normal calcium and phosphate metabolism. Although typically associated with systemic sclerosis and dermatomyositis, it is rare in rheumatoid arthritis. Ulceration over calcified deposits may impair healing and function. This case highlights a staged reconstructive strategy to remove calcified tissue and achieve definitive wound closure. Case Presentation: A 73-year-old woman with a 22-year history of rheumatoid arthritis presented with painful, partially confluent pretibial ulcerations, purulent drainage, impaired mobility, and extrusion of chalk-like material. Radiographic and histopathological findings supported dystrophic calcinosis cutis. Deep-tissue culture grew Escherichia coli, treated with intravenous ertapenem. Tangential excision of necrotic tissue and accessible calcific deposits resulted in an irregular full-thickness defect extending to the pretibial fascia. A synthetic polylactic acid matrix was applied with single-use negative pressure wound therapy for 14 days, followed by split-thickness skin grafting on day 21. Graft take exceeded 90%, and residual areas epithelialized without regrafting. At 12 months, the wound remained completely epithelialized without recurrent ulceration, with pain resolution and return to baseline activities. Conclusions: In this patient with ulcerated dystrophic calcinosis cutis associated with rheumatoid arthritis, staged reconstruction using surgical excision, a polylactic acid matrix, single-use negative pressure wound therapy, and split-thickness skin grafting facilitated recipient-bed preparation and definitive cutaneous closure of the post-excisional defect. This case supports the feasibility of this sequence for wound reconstruction in selected complex ulcerated lesions. Further studies are needed to define its comparative role.