The disruption of normal joint mechanics may lead to or result from injury to the various components of a joint. Frequently, this injury results in osteoarthritis (OA),1 which often leads to physical incapacity, pain and reduced quality of life for the affected pet. OA is the most common form of arthritis and is recognized in humans and in all veterinary species. It is often a slowly progressive condition characterized by two main pathologic processes: degeneration of articular cartilage with a loss of both proteoglycan and collagen, and proliferation of new bone. In addition, there is a variable, low-grade inflammatory response within the synovial membrane.2
In North America, OA prevalence is reported to range from 20% in dogs older than 1 year up to 80% in dogs over age 8.3 The objectives of OA treatment are multifaceted: reduce pain and discomfort, decrease clinical signs, slow disease progression, promote repair of damaged tissue and improve quality of life.
It has been suggested that the best results in dogs with chronic pain due to OA result from a combination of anti-inflammatory and analgesic medications, disease-modifying OA agents, specific nutrients, nutraceuticals, weight reduction, exercise programs, physical therapy and therapeutic diets. Applying an individualized combination of these management options to each patient will enhance quality of life, which is the ultimate goal of therapy.4
Obesity as a risk factor
It is well recognized that obesity is epidemic in companion animals. In 2018, the Association for Pet Obesity Prevention estimated that 56% of dogs in the United States were overweight or obese.5 In addition, a long-term study has documented that the prevalence of OA is greater in overweight/obese dogs compared with ideal weight dogs (83% vs. 50%).4,6 Given these data, it is reasonable to assume that a significant portion of arthritic dogs will be overweight/obese and vice versa. Managing these comorbid conditions presents a variety of challenges.
As disease entities, OA and obesity present diagnostic challenges for very different reasons. Clinical signs of OA may not be obvious on examination, particularly early in the disease process. Although signs of pets being overweight or obese are readily apparent, these signs are often overlooked or dismissed as inconsequential. Diagnosis of OA generally requires a combination of history, physical examination findings and radiographic evidence of degenerative joint disease. Although this seems straightforward, historical clues, which are vital to creating an index of suspicion, may be elusive and clinical signs are often subtle and not evident on routine veterinary examination. Owners may attribute many signs of OA to normal aging and therefore fail to report them unless prompted (see Stages of osteoarthritis).
Stages of osteoarthritis
OA is a progressive disease consisting of four stages:
- Stage 1: Patient experiences early signs, which are often difficult to identify and most likely to occur in growing or young adult dogs. The signs are typically sporadic, lasting a few seconds/minutes.
- Stage 2: Patient experiences intermittent signs that are considered the first flare-ups. These signs, which last a few hours, are easy for owners to rationalize and ignore. This stage is typically seen in young adult dogs.
- Stage 3: Patient experiences progressive loss of the ability to perform activities of daily living. This stage is more impactful and recognizable by the owner. It is often seen in adult dogs and is evident through exercise intolerance and difficulties for the dog in performing activities of daily living.
- Stage 4: Patient experiences loss of mobility, strength and fitness. As the patient has lost the ability to walk, this stage is much harder for the owner to manage.
It is important to remember that both young and old dogs can be in any of these stages. Historically, most dogs with OA have been diagnosed in stage 3 or 4. Ideally, however, veterinary teams must be cognizant of the earlier stages so they recognize the signs of OA sooner.
Owners of dogs at risk for obesity and OA should be educated on the importance of lifelong weight management. The incidence and severity of OA secondary to canine hip dysplasia can be influenced significantly by environmental factors such as nutrition and lifestyle.3,4
Clinical signs
Clinical signs of OA include difficulty rising from rest, stiffness and lameness. A thorough disease-specific history may reveal evidence of subtle changes early in the course of OA, such as reluctance to walk, run, climb stairs, jump or play. Signs may be as inconspicuous as lagging behind on walks. Veterinary teams must listen to owners when they are describing that their dog is reluctant to walk on tile or hardwood floors, or that their pet no longer wants to go for car rides—something that was once a favorite activity.
Owners are often unaware of the correlation between behavior changes and OA. Yelping or whimpering, and even personality changes such as withdrawal or aggressive behavior may be indicative of the chronic pain of OA. Additionally, the veterinary team may uncover subtle signs caused by OA pain that the owner did not notice, such as longer nails (indicating that the dog is not walking and so nails are not being worn down by hard surfaces) or abnormal fur patterns over joints (indicating the dog has been licking the area). Consistent use of an owner questionnaire may facilitate early detection of OA.
Managing mobility with nutrition
Dietary factors can potentially modify some of the underlying processes involved in OA, including modulation of the inflammatory response, provision of nutrients for cartilage repair and protection against oxidative damage. Where effective, dietary management may help reduce or eliminate the need for conventional drugs, some of which are associated with adverse effects.
Amino acids
As the building blocks of proteins, amino acids play a role in the makeup of tissues and organs throughout the body. Methionine is a unique amino acid that produces several molecules that are essential for proper cell function. Methionine, which contains sulfur, can produce other sulfur-containing molecules in the joint and is involved in protein production. Manganese is an essential nutrient involved in many chemical processes in the body, including bone formation. Manganese plays a role in the health and maintenance of bone and cartilage in joints. In addition, manganese supports collagen formation for joint strength. Methionine and manganese are building blocks for cartilage in joints.
Carnitine is an amino acid that enables the body to turn fat into energy. Carnitine aids in muscle maintenance and transports long-chain fatty acids and their derivatives into the mitochondria of cells. By strengthening skeletal muscle and turning fat into energy, the severity of OA may be lessened.