Objective—To compare the duration of clinical signs in dogs prior to total hip replacement (THR) for 2 time periods and to determine whether a previous THR influenced the duration of clinical signs prior to THR of the contralateral hip joint.
Design—Retrospective cohort study.
Animals—833 dogs that underwent unilateral THR (334 dogs between 1992 and 2000 [group 1] and 499 dogs between 2001 and 2009 [group 2]; part 1) and 272 dogs that underwent staged bilateral THR between 1992 and 2009 (part 2).
Procedures—Duration of pelvic limb lameness prior to THR was recorded in an in-house data registry. Mean duration of clinical signs was determined for both groups of dogs in part 1. For part 2, duration of clinical signs prior to the first THR was compared with the interval between surgeries in dogs that underwent bilateral THR.
Results—In part 1, duration of clinical signs was significantly longer for group 2 dogs than for group 1 dogs. In part 2, the duration of clinical signs prior to the first THR was significantly longer than the interval between surgeries.
Conclusions and Clinical Relevance—Between 1992 and 2009, the duration of clinical signs prior to THR in dogs increased significantly. In dogs that underwent bilateral THR, the interval between surgeries was shorter than the duration of clinical signs before the first THR. Developments in medical treatments of osteoarthritis, surgical preferences, and veterinarian recommendations may influence the interval between initial clinical signs and surgery.
A 15-month-old 6.5-kg (14.3-lb) castrated male mixed-breed dog was evaluated because of a 4-month history of progressive intermittent non–weight-bearing lameness of the left pelvic limb.
Orthogonal radiography of the hip joints revealed a 4-mm atypical radiolucent lesion on the distal caudomedial aspect of the left femoral head and a disproportionately large-diameter femoral medullary canal with a low canal flare index. Prolonged unresponsiveness to medical management and progressive enlargement of the lesion prompted the recommendation for total hip replacement (THR).
TREATMENT AND OUTCOME
THR was performed to restore pain-free function of the left pelvic limb and normal activity. A circular osteochondral flap was grossly evident on the femoral head. Histopathologic findings for this portion of the bone indicated an arteriopathy-induced focal subchondral osteonecrosis that had resulted in articular surface collapse. The noted idiopathic arteriopathy had disrupted the normal blood supply to the affected area. On reexamination and radiographic evaluation 13 months after THR, the dog appeared to have pain-free function of the affected limb and had returned to normal activity with no reported complications or problems.
To the authors’ knowledge, this report represented the first description of arteriopathy-induced focal osteonecrosis of the caudomedial aspect of the femoral head and its successful treatment in a young dog. This type of lesion may more commonly be the cause of hip joint osteoarthritis in young dogs than previously recognized because establishing a definitive diagnosis requires early recognition and histologic evaluation before advanced degenerative changes develop that obscure the underlying etiology.
Objective—To assess effects of in vitro meloxicam exposure on metabolism in articular chondrocytes from dogs with naturally occurring osteoarthritis
Sample—Femoral head cartilage from 16 dogs undergoing total hip replacement
Procedures—Articular cartilage samples were obtained. Tissue sulfated glycosaminoglycan (SGAG), collagen, and DNA concentrations were measured. Collagen, SGAG, chondroitin sulfate 846, NO, prostaglandin E2 (PGE2), and matrix metalloproteinase (MMP)-2, MMP-3, MMP-9, and MMP-13 concentrations in culture medium were analyzed. Aggrecan, collagen II, MMP-2, MMP-3, MMP-9, MMP-13, ADAM metallopeptidase with thrombospondin type 1 motif (ADAMTS)-4, ADAMTS-5, tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, TIMP-3, interleukin-1β, tumor necrosis factor-α, cyclooxygenase-1, cyclooxygenase-2, and nducible nitric oxide synthase gene expression were evaluated. Comparisons between tissues cultured without (control) and with meloxicam at concentrations of 0.3, 3.0, and 30.0 μg/mL for up to 30 days were performed by means of repeated-measures analysis.
Results—Meloxicam had no effect on chondrocyte SGAG, collagen, or DNA concentrations. Expression of ADAMTS-5 was significantly decreased in all groups on all days, compared with the day 0 value. On day 3, culture medium PGE2 concentrations were significantly lower in all meloxicam-treated groups, compared with values for controls, and values remained low. Culture medium MMP-3 concentrations were significantly lower on day 30 than on day 3 in all meloxicam-treated groups.
Conclusions and Clinical Relevance—Results suggested that in vitro meloxicam treatment of osteoarthritic canine cartilage for up to 30 days did not induce matrix degradation or stimulate MMP production. Meloxicam lowered PGE2 release from this tissue, and effects on tissue chondrocyte content and matrix composition were neutral.