Osteoarthritis, adipokines and the translational research potential in small animal patients

Abstract

Osteoartritis (OA) is a debilitating disease affecting both humans and animals. In the early stages, OA is characterized by damage to the extracellular matrix (ECM) and apoptosis and depletion of chondrocytes. OA progression is characterized by hyaline cartilage loss, chondrophyte and osteophyte formation, thickening of the joint capsule and function loss in the later stages. As the regenerative potential of cartilage is very limited and osteoarthritic changes are irreversible, prevention of OA, modulation of existing osteoarthritic joint inflammation, reducing joint pain and supporting joint function are the only options. Progression of OA and pain may necessitate surgical intervention with joint replacement or arthrodesis as end-stage procedures. In human medicine, the role of adipokines in the development and progression of OA has received increasing interest. At present, the known adipokines include leptin, adiponectin, visfatin, resistin, progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin. Adipokines have been demonstrated to play a pivotal role in joint homeostasis by modulating anabolic and catabolic balance, autophagy, apoptosis and inflammatory responses. In small animals, in terms of dogs and cats, naturally occurring OA has been clearly demonstrated as a clinical problem. Similar to humans, the etiology of OA is multifactorial and has not been fully elucidated. Humans, dogs and cats share many joint related degenerative diseases leading to OA. In this review, joint homeostasis, OA, adipokines and the most common joint diseases in small animals leading to naturally occurring OA and their relation with adipokines are discussed. The purpose of this review is highlighting the translational potential of OA and adipokines research in small animal patients.

Keywords: adipokines; dogs and cats; joint disease; joint homeostasis; osteoarthritis; translational research.

Figure 1

Mediolateral view of the antebrachium of a dog showing a translucent line parallel to the distal growth plates of radius and ulna typical for hypertrophic osteodystrophy (arrow heads).

Figure 2

Caudocranial view of a 3D-CT reconstruction of a canine shoulder joint with a typical OCD lesion in the centrocaudal part of the humeral head (arrow head).

Figure 3

Craniomedial view of a 3D-CT reconstruction of a canine elbow joint with medial coronoid disease showing fragmentation of the coronoid and osteoarthritic changes (arrow head).

Figure 4

Arthroscopic medial view of a canine elbow joint with medial coronoid disease showing a displaced fragment with clear osteonecrosis (asterisk).

Figure 5

Histological slides of a typical osteochondral fragment. Local full thickness loss of articular hyaline cartilage is present (A). Osteonecrosis with loss of osteocytes, cartilage degeneration and vasculitis are shown in larger magnification (B).

Figure 6

Sagittal CT view of a canine elbow joint showing a ununited anconeal process including severe osteosclerosis in the adjacent shaft of the ulna (arrow head).