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Ultrastruct Pathol. 2005 Mar-Apr;29(2):107-20.

Study on a nonhealing fracture from a patient with systemic lupus erythematosus and its pathogenetic mechanisms.

Author information

1
Department of Pathology, State University of New York, Downstate Medical Center, Brooklyn, New York, USA.

Abstract

Arthritis and osteonecrosis affect a large number of patients with systemic lupus erythematosus (SLE). A patient with history of SLE suffered a traumatic fracture of the left foot. Despite a long period of immobilization and internal fixation, the fracture failed to heal and required arthrodeses with removal of the phalanx. Histopathological investigation revealed destruction of cartilage, subchondral cystic degeneration, vasculitis, deposition of fibrinogen, type III collagen and fibronectin, absence of bone remolding, and detectable F-actin. The nonhealing was therefore due to lack of progression of healing process beyond the initial stage. There was deposition of immunoglobulins and complement C4b, possibly forming immune complex by autoantibodies and cellular components. The authors found that MSE55 protein, required for polymerization of actin and initiation of cellular process organization, had a similar cellular deposition as that of immunoglobulins. Autoantibodies thus may inhibit differentiation of the bone cells, and resulted in nonunion in the patient.

PMID:
16028667
DOI:
10.1080/01913120590912214
[Indexed for MEDLINE]

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