Alternative therapies for managing mobility: Nonsurgical management of cranial cruciate ligament rupture (Sponsored by Iams)

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Alternative therapies for managing mobility: Nonsurgical management of cranial cruciate ligament rupture (Sponsored by Iams)

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Jan 01, 2011

Osteoarthritis (OA) affects about 20% of canine patients.1 However, that estimate is probably low because there are many dogs with undiagnosed OA for which owners have not sought treatment. Pain response to OA varies greatly among patients, so the management strategy must be tailored to the individual for the best response. The typical OA management armamentarium consists of weight loss, physical therapy, nonsteroidal anti-inflammatory medications, and nutritional supplements. Additional therapies available for managing patient pain from OA include specially formulated diets, synovial fluid supplementation, acupuncture, additional pharmacologic medications, and other forms of complementary medicine.

Since excessive weight or obesity is a major contributing factor to the development and progression of OA, the first line of therapy for treating patient pain associated with OA should be aimed at reducing body weight and, more specifically, minimizing body fat. (For more on the role of weight loss in managing OA, see the Related Link "Current concepts in the management of osteoarthritis" below.) Traditionally, it was thought that obesity affected the outcome of patients with OA through excessive mechanical load on the joints during normal weight bearing.2 In people, there is a strong correlation between obesity and OA of the knee. But there is also a correlation between OA of the hand and obesity, suggesting that systemic and not just mechanical stress contributes to OA development. Adipokines, inflammatory mediators released by white adipose tissue, are known to contribute to insulin resistance, cardiovascular disease, cancer, and OA. Those most commonly studied include adiponectin, leptin, and resistin.

Adiponectin

Adiponectin, identified as a 30-kDa protein, is secreted from the adipose tissue into circulating blood and influences systemic metabolism. Its expression increases insulin sensitivity. In contrast to most secreted proteins from adipose tissue, which rise with increased fat mass, adiponectin levels decrease with increasing adiposity.3 More intriguingly, adiponectin appears to decrease the obesity-related risk factors, unlike other adipose tissue secretory proteins, which contribute to the health risks associated with obesity, diabetes, and cardiovascular disease.

Leptin

Leptin, a 16-kDa protein and a product of the obesity gene, is synthesized and secreted predominantly by adipose tissue. With circulating levels directly proportional to the total amount of body fat, leptin plays an important role in whole body metabolism, regulating food intake and energy balance, as well as assisting in the control of homeostasis, reproductive function, the immune system, and numerous other body functions.4 Binding to receptors of the hypothalamus, leptin signals food satiety and reduces appetite. Evidence suggests that, in general, obese people have unusually high circulating levels of leptin. As leptin levels rise, resistance in target cells develops. Consequently, it no longer acts to control food intake. Furthermore, leptin is proinflammatory and is likely involved in the pathogenesis of OA, but at this time it is unclear whether increased levels are protective, due to the anabolic effects it has on chondrocytes. More recent studies have shown it to be detrimental, since women have higher levels of leptin and also higher incidence of OA.4

Resistin

Resistin is another proinflammatory adipokine. In humans and likely in dogs, it acts primarily by stimulating macrophages to secrete proinflammatory cytokines. Circulating resistin levels are known to increase with increasing fat mass. Resistin causes tissues to be less sensitive to insulin, and high levels of resistin are known to contribute to the development of insulin resistance and type 2 diabetes mellitus.5

Obesity greatly affects the outcome for dogs diagnosed with OA. In one lifelong study, overweight dogs with OA had more radiographic evidence and clinical signs than dogs kept at an ideal body condition score.6 Another study revealed that lameness scores improved for overweight dogs with OA of the hip with a weight loss of at least 11% of body weight.7 An additional study revealed that a combined weight loss and physical therapy program versus weight loss alone improved force plate values in overweight dogs diagnosed with unilateral OA.8 Furthermore, physical therapy reduces pain and inflammation, improves strength and balance, increases range of motion, and restores a more normal joint function. In many cases, medications can also be reduced because of improved pain relief.9

Obesity and cranial cruciate ligament rupture

In addition to the role obesity plays metabolically in the development of OA, it is also considered a risk factor for cranial cruciate ligament rupture (CCLR).10-11 CCLR is the most common orthopedic condition diagnosed in dogs and is known to lead to the development of OA and lameness. Most studies indicate that female dogs have a higher incidence of CCLR,12 which is hypothesized to be because spayed female dogs have a higher incidence of obesity.13 A recent study detected an increased prevalence of CCLR in both male and female sterilized dogs, leading to the hypothesis that a lack of sex hormones predisposes dogs to CCLR.14 However, no studies to date have prospectively determined if there is a correlation between adipokine levels and lameness assessment in dogs undergoing weight loss.