Osteoarthritis and diet: Joined at the hip

Osteoarthritis and diet: Joined at the hip


Osteoarthritis, also called degenerative joint disease, is the most prevalent joint disorder in dogs, affecting as many as 20% of adult dogs.1 Osteoarthritis is associated with inflammation and increased degradation or loss of proteoglycans from the extracellular matrix, resulting in a morphologic breakdown in articular cartilage.2 There's no known cure for osteoarthritis, so treatment is focused on controlling pain, improving joint function, and slowing the degenerative process within the joint.3 Standard veterinary medical care typically involves weight management, controlled exercise, and anti-inflammatory and analgesic medications. In addition to medical therapy, dietary management can play an important role in the clinical management of dogs with osteoarthritis.

Weight management in osteoarthritis

Obesity, or excess body weight, results from consuming more calories than are needed to maintain a lean body condition. Obesity is recognized as a risk factor for osteoarthritis in both people and dogs. Preventing obesity can help reduce the incidence and severity of osteoarthritis.4-8 Excess body weight affects dogs from puppyhood through old age. When at-risk puppies were fed ad libitum, they exhibited an increased incidence and severity of hip joint laxity and hip dysplasia compared with puppies fed 25% less.9 Over time, those dogs fed to maintain lean body condition throughout their lifetimes exhibited a delayed need for treatment and reduced severity of osteoarthritis in the hips and other joints compared with their heavier siblings.6 (For additional information on the orthopedic aspects of this study, see the article by Dr. Gail Smith.) One of the most compelling findings from this study was the observation that even a mild degree of excess body weight can adversely affect joint health. This is important, since more than 25% of dogs seen by veterinarians are overweight or obese.10

The effect of obesity on osteoarthritis may be more than just physical strain due to weight bearing. Obesity is now recognized as an inflammatory condition; adipose tissue or associated macrophages produce inflammatory cytokines.11-15 C-reactive protein, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and other inflammatory mediators are elevated in the blood and adipose tissue of obese subjects, and are thought to contribute to many complications associated with obesity such as osteoarthritis.11,13,16-18 Obesity is also associated with an increase in oxidative stress.13,19

Multiple studies have shown that weight loss helps decrease lameness and pain and increase joint mobility in patients with osteoarthritis.5,20-22 Overweight dogs with coxofemoral joint osteoarthritis demonstrated decreased lameness (as measured by objective force-plate analysis and subjective clinical and client assessment) following weight reduction to ideal body condition.

In addition to dietary energy, dietary protein may play an important role in helping achieve and maintain ideal body condition. Protein has several physiologic effects that may benefit weight control: protein stimulates metabolism and protein turnover, induces thermogenesis, and promotes satiety.23-28 During weight loss and subsequent weight maintenance, increased protein intake promotes loss of body fat with retention of lean body mass.29-31 These aspects of protein may enhance weight loss in dogs with osteoarthritis.

Fatty acids in osteoarthritis

A primary target of osteoarthritis treatment is the inhibition of cyclooxygenase (COX) enzymes—especially the COX-2 enzyme—through the use of nonsteroidal anti-inflammatory drugs (NSAIDs).32-34 COX-2 selective inhibitors can decrease prostaglandin E2 (PGE2) concentrations and block inflammatory pathways involved in osteoarthritis, as well as reduce pain and lameness.32,33,35-38 Blocking both the COX and lipooxygenase (LOX) enzymes at the active sites of 5-LOX, COX-1, and COX-2 significantly reduces matrix metalloproteinases (MMPs), IL-1β, leukotriene (LT) B4, and PGE2, resulting in decreased tissue damage in arthritic joints.39