Vital bone and increased osteoid in equine osteochondrosis dissecans of the proximal phalanx: A controlled study indicating a mineralization deficit rather than vascular failure.

Abstract

Osteochondrosis and osteochondrosis dissecans (OCD) are among the most common orthopaedic disorders in young horses. Although traditionally explained by vascular failure and ischaemic necrosis, recent findings in human juvenile OCD suggest that impaired bone mineralization may play an important role. Horses are known to have relatively low circulating vitamin D metabolites, raising the question of whether insufficient mineralization contributes to equine OCD. This study investigated the bone vitality and mineralization status of osteochondrosis dissecans fragments (OCDFs) collected from the dorsomedioproximal aspect of the proximal phalanx and compared them with control bone from the corresponding anatomic region in non-affected horses. Micro-CT, undecalcified histology, histomorphometry, and quantitative backscattered electron imaging (qBEI) were used to assess bone vitality, osteoid accumulation, and mineral content. All OCDFs showed vital bone tissue without any evidence of osteonecrosis. Histomorphometry revealed a pronounced accumulation of osteoid by means of osteoid per tissue volume (control: 0.49% ± 0.36% vs. OCD: 2.85% ± 1.45%, p = 0.0001). Micro-CT demonstrated reduced bone tissue mineral density in OCD (control: 843.7 mgHA/cm³ ± 31.3 mgHA/cm³ vs. OCD: 779.0 mgHA/cm³ ± 37.0 mgHA/cm³, p < 0.0001) confirmed by qBEI. Our results indicate that equine OCDFs contain vital bone with impaired mineralization rather than necrotic tissue. This pattern mirrors findings in human juvenile OCD and supports the hypothesis that a metabolic mineralization disorder contributed to the pathogenesis of equine OCD.