Nitrate patch prevents steroid‐related bone necrosis

Abstract

Avascular necrosis of the femoral head is a common complication with disabling effect for young patients after high-dose corticosteroid treatment. We could show that steroids have a vasoconstrictive effect on lateral epiphyseal arteries of the femoral head which could lead to ischemia and subsequent necrosis. In this study we investigated the preventive effect of a nitrate patch on steroidrelated bone necrosis in a rabbit model. New Zealand White rabbits (male; 3-4.5 kg bodyweight) were injected with 20 mg/kg bodyweight methylprednisolone (GC group; n ¼ 6). Control animals (n ¼ 6) were treated with phosphate-buffered saline. A third group (GC þ N; n ¼ 6) additionally received a nitrate patch (0.675 mg/day). Four weeks after i.m. methylprednisolone injection the animals were sacrificed. For histology and immunohistochemistry, tissue samples were fixed in 3% paraformaldehyde, embedded in paraffin, sectioned, dewaxed, and stained with Ladewig. For quantification of empty lacunae, a histologic sign of FHN, histomorphometry was performed. Histomorphometry revealed a significant increase of empty lacunae in glucocorticoid-treated animals compared to controls and GC þ N-treated animals. No significant difference in empty lacunae count was detected between the GC þ N group and controls. HE staining revealed the different osteocyte amount in the GC versus GC and nitrate patch-treated groups. This study demonstrates an increased number of empty osteocyte lacunae representing a pathologic feature of osteonecrosis, in the GC group. Less empty lacunae were counted in the GC animals after additional treatment with a nitrate patch. This finding suggests that nitrate co-treatment has the potential to prevent steroid-associated FHN. ß

Osthole stimulates bone formation, drives vascularization and retards adipogenesis to alleviate alcohol‐induced osteonecrosis of the femoral head

“…Notably, promoted adipogenic differentiation led to disordered osteogenic differentiation, and the accumulation of adipocytes might lead to a high intramedullary pressure and impair brittle blood circulation in the femoral heads . Moreover, fat emboli in vessels and sinusoids can also indirectly induce intravascular coagulation via the complement signalling pathways and deposition of immune complex, whereas antithrombotic reagents have protective effects to promote circulation and ameliorate ONFH . In this work, we found that ethanol could stimulate BMSCs towards adipogenic differentiation.…”

Nontraumatic Osteonecrosis of the Femoral Head: Where Do We Stand Today?

“…the interest in finding appropriate treatments for precollapse disease 67,72,[130][131][132][133][134][135][136][137][138][139][140][141][142][143][144][145][146] . Treating asymptomatic osteonecrosis of the hip is controversial, with 59% of such hips becoming symptomatic in three years, and 7% of small and 80% of large lesions (a Kerboul angle of >240°) collapsing by eight years.…”

Downregulated SOX9 mediated by miR‑206 promoted cell apoptosis in Legg-Calv�-Perthes disease

“…Previous studies have tried to prevent the generation of steroid-induced femoral head osteonecrosis (SANFH), for example, enoxaparin and nitrate patch could use to prevent the occurrence of SANFH (16,17), while the potential mechanism was not fully understand. Liu et al found that miR-206 regulated connexin43 that involved in the osteogenic differentiation in SANFH (13).…”