Histological study of navicular bone disease.
Authors: Ostblom, Lund, Melsen
Journal: Equine veterinary journal
Summary
# Editorial Summary: Histological Study of Navicular Bone Disease Ostblom, Lund and Melsen examined navicular bone tissue from eight affected horses and used tetracycline labelling in two cases to determine whether navicular disease resulted from bone death (necrosis) caused by poor blood supply. Contrary to the prevailing ischaemic theory of the era, they found no evidence of dead bone or devitalised tissue; instead, all diseased bones showed markedly elevated remodelling activity characterised by numerous osteoclasts and osteoblasts, abundant osteoid formation, and exceptionally high tetracycline uptake—indicating the bone was metabolically active and vital. The researchers concluded that navicular disease arises from abnormal pressure transmission through the deep flexor tendon and altered loading of the caudal foot, triggering excessive bone turnover rather than tissue death. This distinction carries significant clinical weight: if navicular disease is fundamentally a remodelling problem driven by biomechanical factors, it should be reversible through corrective shoeing and load management in early stages, with irreversibility only developing once secondary changes like adhesions and bone spurs become established. This work challenges the fatalistic view of navicular disease as inexorably progressive and supports the rationale for early intervention through farriery and rehabilitation rather than acceptance of permanent decline.
Read the full abstract on PubMed
Practical Takeaways
- •Navicular disease is a remodelling problem, not a death-of-bone problem—this means early intervention through corrective shoeing has genuine potential to reverse damage
- •Focus on reducing load through the caudal navicular bone via hoof conformation changes and appropriate shoeing strategies rather than assuming the condition is inevitably progressive
- •Once secondary changes (adhesions, bone spurs) develop, the disease becomes irreversible, so early detection and load management are critical to preserve function
Key Findings
- •Histological examination of diseased navicular bones showed no evidence of ischaemia or necrosis in affected areas
- •High rate of bone remodelling present in all 8 cases, indicated by increased osteoclasts, osteoblasts, osteoid formation, and tetracycline uptake
- •Navicular disease results from increased bone remodelling activation caused by altered deep flexor tendon pressure and increased caudal foot load rather than primary ischaemic necrosis
- •Disease may be reversible through load alteration via special shoeing; only secondary lesions like adhesions and spur formation render it irreversible