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Etiology

There is no one etiology causing the pathological changes that occur in arthritis and the cause of the disease can be multifactorial.  It can affect dogs of any age 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 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 componentPredisposed Breeds
Hip DysplasiaLabrador Retriever, German Shepherd Dog, Rottweiller, Great Dane, Golden Retriever, St Bernard, Newfoundland, Pug, Chow, Bulldogs
Elbow DysplasiaLabrador, Golden Retriever, English Setter, English Springer Spaniel, Rottweiller, Gernam Shepherd Dog, Burnese Mountain Dog, Chow, Shar-Pei, Newfoundland.
OCDLabradors
Giant breeds
Patellar luxationPomeranian, Chihuahua, Yorkshire Terrier, French Bulldog
Cruciate ligament deficiencyLabrador, Rottweiller, 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 play a role separately in dogs that don’t have any genetic susceptibility including age, trauma, body weight and nutrition.

As a dog ages, the quality of cartilage declines, which then results in mechanical failure. [1] This normal change due to ageing can 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 also 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 chance of development of formation of an OCD lesion [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 on.

Reference

  1. 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 possiblemechanism 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.

  7. Kealy RD, Olsson SE, Monti KL, Lawler DF, Biery DN, Helms RW, Lust G, Smith GK. Effects of limited food consumption on the incidence of hip dysplasia in growing dogs. JAVMA 1992; 201(6):857-863.

  8. Dammrich K. Relationship between nutrition and bone growth in Large and Giant Dogs. The Journal of Nutrition 1991; 121(11): S114-S121