Histopathology in horses with chronic palmar foot pain and age-matched controls. Part 1: Navicular bone and related structures

Authors


Centre for Preventive Medicine, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk CB8 7UU, UK.

Summary

Reasons for performing study: Causes of palmar foot pain and the aetiopathogenesis of navicular disease remain poorly understood, despite the high incidence of foot-related lameness.

Hypotheses: Abnormalities of the collateral sesamoidean ligaments (CSLs), distal sesamoidean impar ligament (DSIL), deep digital flexor tendon (DDFT), navicular bone, navicular bursa, distal interphalangeal (DIP) joint or collateral ligaments (CLs) of the DIP joint may contribute to palmar foot pain.

Methods: Feet were selected from horses with a history of unilateral or bilateral forelimb lameness of at least 2 months' duration that was improved by perineural analgesia of the palmar digital nerves, immediately proximal to the cartilages of the foot (Group 1, n = 32); or from age-matched control horses (Group 2, n = 19) that were humanely destroyed for other reasons and had no history of forelimb foot pain. Eight units of tissue were collected for histology: the palmar half of the articular surface of the distal phalanx, including the insertions of the DDFT and DSIL; navicular bone and insertion of the CSLs; DDFT from the level of the proximal interphalangeal (PIP) joint to 5 mm proximal to its insertion; synovial membrane from the palmar pouch of the DIP joint and the navicular bursa; CLs of the DIP joint and DSIL. The severity of histological lesions for each site were graded. Results were compared between Groups 1 and 2.

Results: There was no relationship between age and grade of histological abnormality. There were significant histological differences between groups for lesions of the flexor aspect, proximal and distal borders, and medulla of the navicular bone; the DSIL and its insertion and the navicular bursa; but not for lesions of the CSLs, the dorsal aspect of the navicular bone, distal phalanx and articular cartilage, synovium or CLs of the DIP joint.

Conclusions: Pathological abnormalities in lame horses often involved not only the navicular bone, but also the DSIL and navicular bursa. Abnormalities of the navicular bone medulla were generally only seen dorsal to lesions of the FFC.

Potential relevance: Adaptive and reactive change may be occurring in the navicular apparatus in all horses to variable degrees and determination of the pathogenesis of lesions that lead to pain and biomechanical dysfunction should assist specific preventative or treatment protocols.

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