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We hypothesised that tumour necrosis factor- α  (TNF- α ) may enhance receptor activator of nuclear factor- κβ  ligand- (RANKL-) mediated osteoclastogenesis in acute Charcot osteoarthropathy. Peripheral blood monocytes were isolated from 10 acute Charcot patients, 8 diabetic patients, and 9 healthy control subjects and cultured  in vitro  on plastic and bone discs. Osteoclast formation and resorption were assessed after treatment with (1) macrophage-colony stimulating factor (M-CSF) and RANKL and (2) M-CSF, RANKL, and neutralising antibody to TNF- α  (anti-TNF- α ). Resorption was measured on the surface of bone discs by image analysis and under the surface using surface profilometry. Although osteoclast formation was similar in M-CSF + RANKL-treated cultures between the groups ( p  > 0.05), there was a significant increase in the area of resorption on the surface ( p  < 0.01) and under the surface ( p  < 0.01) in Charcot patients compared with diabetic patients and control subjects. The addition of anti-TNF- α  resulted in a significant reduction in the area of resorption on the surface ( p  < 0.05) and under the surface ( p  < 0.05) only in Charcot patients as well as a normalisation of the aberrant erosion profile. We conclude that TNF- α  modulates RANKL-mediated osteoclastic resorption  in vitro  in patients with acute Charcot osteoarthropathy.

Inhibition of TNF-αReverses the Pathological Resorption Pit Profile of Osteoclasts from Patients with Acute Charcot Osteoarthropathy