Canine osteoarthritis is a progressive and debilitating disease affecting approximately 20% – 40% of the canine population and up to 80% of patients over 8 years old.  It requires continual assessment with appropriate updating and modification to the treatment plan as the disease evolves.  

OA is a disease of diarthrodial (synovial) joints and is characterised by inflammation of the synovium, degeneration of cartilage and formation of osteophytes at joint margins.  In later stages it extends ‘outside the joint’ with involvement and pathology affecting both the peripheral and central nervous systems and the supporting musculoskeletal elements.  Clinically, it manifests as stiffness or lameness due to joint pain and on clinical exam veterinarians may notice a reduced range of motion, joint effusion, muscle wastage and thickening of the joint.  Pain is the main clinical feature, and it is the most common cause of chronic pain in dogs and cats. 

There are many ways to manage osteoarthritis, and a multimodal approach is necessary for the best outcome for the patient.  The goals of managing arthritis are:

 

• Recognising the clinical signs as early as possible in the disease process
• Alleviating the patient’s discomfort and avoiding pain sensitization (see later)
• Minimising the occurrence of further pathological changes
• Restoring the affected joint/joints to as near a normal and pain free function as possible

 

The disease relies on owner engagement and them being willing to be proactive to get the best long-term results.  Routine monitoring and assessment are critical to achieving the goals.

 

Aetiology

 

There is no one aetiology causing the pathological changes that occur in arthritis, and the cause of the disease can be multifactorial.  It can affect dogs of any age, although it is more common in older cats, and susceptibility is related to developmental factors including genetics or acquired factors such as diet, history of trauma and infection or a combination of both genetic and acquired factors.

 

The genetic component of OA is linked to various developmental disorders such as hip dysplasia, elbow dysplasia, joint confirmation due to breed and osteochondrosis dissecans (OCD).  Variables within joint conformation can lead to increase in secondary problems such as patellar luxation and cruciate ligament deficiency.   Some of the breeds predisposed to these genetic components are summarised in the table below.

Genetic Component	Predisposed Breeds
Hip Dysplasia	Labrador Retriever, German Shepherd Dog, Rottweiler, Great Dane, Golden Retriever, St Bernard, Newfoundland, Pug, Chow, Bulldogs
Elbow Dysplasia	Labrador, Golden Retriever, English Setter, English Springer Spaniel, Rottweiler, German Shepherd Dog, Burnese Mountain Dog, Chow, Shar-Pei, Newfoundland.
Osteochondrosis	Labradors, Rottweiler, Border Collie Giant breeds (Great Dane, Irish Wolfhound)
Patellar Luxation	Pomeranian, Chihuahua, Yorkshire Terrier, French Bulldog
Cruciate ligament deficiency	Labrador, Rottweiler, West Highland White Terriers, Newfoundland, Boxer

Coupled with this genetic susceptibility, other extrinsic factors can play a role in the development of OA including trauma, body weight and diet, which can determine the severity of disease and age of onset.

 

Acquired factors have an impact in dogs that don’t have any genetic susceptibility and may include age, trauma, body weight and nutrition.

 

As a dog ages, the quality of cartilage declines, which can then result in mechanical failure of the cartilage matrix. [1] This normal change due to ageing can further increase laxity of the joint and exacerbate the progression of OA. [2]

 

Repetitive joint forces or a single severe injury or surgery to the joint or surrounding structures can lead to inflammation and development of arthritis.  Trauma or surgery to a joint disrupts its normal function and leads to inflammation and resultant secondary changes.  Severity of trauma, management of the joint at the time of trauma and which joint is involved, all play a role in the progression of OA.

 

Bodyweight can have a significant effect in developing OA and lead to more severe signs of OA in dogs that already have it.  A study [3] found that obese dogs with OA showed a significant decrease in lameness when they lost 6.1% or more of their body weight, which was supported by kinetic gait analysis from 8.85% or more loss in body weight.  Earlier studies have reported that dogs that are fed a restricted diet for life can have a reduced severity and/or prevalence of OA in certain joints when compared to control dogs [4][5][6][7].

 

A suitable balanced diet is especially important in the giant breeds of dogs.   Over feeding a high carbohydrate diet predisposes to OCD lesions which can lead to the development of OA.  The overstimulation of skeletal growth and bone remodelling due to over-nutrition leads to inadequately supported joint surfaces coupled with an increase in muscle mass and body weight, increasing the risk of an OCD lesion forming during skeletal development [8].

 

If OA is left unmanaged, it can lead to chronic pain, discomfort and debilitation but if treated early and managed correctly, can enable the dog to lead a happy, comfortable life with secondary changes occurring much later.

References

1.       N. Verzijl, DeGroot J, Zaken CB, Braun‐Benjamin O, Maroudas A, Bank RA, Mizrahi J, Schalkwijk CG, Thorpe SR, Baynes JW et al. Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: a possible mechanism through which age is a risk factor for osteoarthritis.  Arthritis & Rheumatism 2002; 46 (1): 114-123
2.       Vincent KR, Conrad BP, Fregly BJ, Vincent HK. The pathophysiology of osteoarthritis: a mechanical perspective on the knee joint. PM R 2012; 4(5 Suppl): S3-9.
3.       Marshall W, Hazwinkel H, Mullen D, De Mayer G, Baert K, Carmichael S.  The effect of weight loss on lameness in obese dogs with osteoarthritis.  Vet Res Commun. 2010; 34(3): 241–253.
4.       Kealy RD, Lawler DF, Ballam JM, Mantz SL, Biery DN, Greeley EH, Lust G, Segre M, Smith GK, Stowe HD.  Effects of diet restriction on life span and age-related changes in dogs. JAVMA 2002; 220:1315-20
5.         Kealy RD, Lawler DF, Ballam JM, Lust G, Biery DN, Smith GK, Mantz SL. Evaluation of the effect of limited food consumption on radiographic evidence of osteoarthritis in dogs. JAVMA 2000; 217 (11):1678-1680
6.       Kealy RD, Lawler DF, Ballam JM, Lust G, Biery DN, Olsson SE.  Five-year longitudinal study on limited food consumption and development of osteoarthritis in coxofemoral joints of dogs. JAVMA 1997; 210(2):222-225.