New approaches to osteoarthritis in dogs: etiology, detection, diagnosis

Introduction – the what, how and why of osteoarthritis

This paper looks at osteoarthritis (OA) in dogs by taking statements from various web pages and review articles, posing questions as to their validity, and then responding in order to provide the reader with a comprehensive understanding of the current knowledge around canine OA, and to highlight what lies ahead in tackling this condition.

How common is osteoarthritis?

“Osteoarthritis (OA) is a very common problem in small animals, as it is in humans; it has been estimated that around 30-50% of dogs and cats will be affected by OA at some point in their lives.” 

So is this correct? What is the actual prevalence of canine OA in Western countries? 

Estimates range from 6.6% (based on a primary care database of 3,884 dogs in UK 1) to 20% of dogs over one year of age 2,3. However, this latter figure was based on the North American referral dog population from 1997 (and the study data were not accessible), and it must be anticipated referral populations will have an apparently higher prevalence of disease 4. Recently, one study based on a questionnaire to 504 owners at 9 US practices gave a prevalence of 37.3% (confirmed by veterinarian examination +/- radiographs) 3. This is higher than previously reported, but the population sample size was low and susceptible to bias. Finally, from a population of 455,557 dogs attending primary-care practices in UK, an annual prevalence of 2.5% was calculated 4. Therefore, it would be reasonable to suggest that in a country such as Canada, with around 8 million dogs in 2023, around 200,000 dogs are affected by OA annually, with an overall prevalence between 10.0 and 20.0%. 

More importantly, these epidemiological studies reported a median age at first diagnosis of 10.5 years 4, which differed significantly from the median age of the overall denominator population of disorders at 4.8 years 1. Other risk factors are clearly revealed, the first being the dog’s bodyweight and size 4,5,6. Neutering is also associated with increased OA occurrence 7; the gonadal hormones are recognized to protect against OA, and/or neutering will indirectly lead to weight gain. Genetics is supposed to be an influential risk factor 5, and requires further investigation where conformation defects (particularly relating to body and leg size) and joint angles (as required by breed standards) are a major cause of canine OA. However, the influence of breed (there is no significant difference between cross- and pure-breed 1,4 and the effects of size (there is a higher incidence of medium/large breeds) and gender (males may be slightly more often affected 4) are less clear.

The author believes that OA is most frequently diagnosed at 8 years of age, and dogs over 12 years have the highest likelihood of OA diagnosis compared to other age groups 4. So is it a disease of aging in dogs, as in humans 8? Given that OA has been diagnosed in young dogs (1.5-2 years old), it is suspected that signs are generally only noticed by owners and/or investigated at the stage when there are more advanced, more evident, signs later in life 4,5. Could the failure to identify early-stage OA be related to insufficient public awareness – including dog owners 9 and veterinarians – and/or the use of unvalidated methods of detection, leading to a false association of OA disease with normal aging? As reported 5, findings related to age should be interpreted with caution, and longitudinal studies are warranted to explore the relationship between age and OA development more thoroughly. 

What is osteoarthritis?

“Osteoarthritis is a progressive, degenerative disorder of synovial joints. It is characterized by pain and low-grade chronic inflammation, with long-term structural and functional deterioration of the joint. The condition involves many tissues, including cartilage, subchondral bone, joint capsule, and synovial fluid.” 

Is this correct? What about other structures involved in OA? 

The definition is partially correct, but OA also impairs the ligaments and tendons in an affected joint, as recently highlighted by magnetic resonance imaging studies 10. Conversely, previous joint deterioration or loss of muscle mass, such as sarcopenia in geriatric animals, could increase the risk of developing OA 5. Although OA initially affects the cartilaginous matrix, it ultimately involves total joint degeneration involving the subchondral bone, joint capsule, synovial fluid, as well as the menisci, ligaments, tendons, and muscles. Once the cartilage begins to thin, tendons and ligaments are put under greater stress and eventually stretch abnormally, contributing to synovial effusion and osteophyte formation. Structural changes contribute to joint pain during movement by the release of inflammatory and catabolic factors. However, as described in humans 11, the intensity of the pain is not necessarily associated with the anatomical damage observed on radiography 12. 

Pain is the most important clinical manifestation of canine OA, and the degree of pain is linked to the entire joint, including its innervation and vascularization. Although the cartilage is aneural, the periosteum, subchondral bone, soft tissues (including ligament insertion), menisci and synovium are all innervated (Figure 1). Inflammatory and neurotrophin factors released at the joint (e.g., nerve growth factor (NGF)) will contribute to increased responsiveness of the pain fibers. OA dogs with chronic lameness have been shown to have elevated levels of NGF in their synovial fluid when compared to healthy joints 13. Peripheral sensitization could occur, characterized by hypersensitivity at the level of affected joint, and neovascularization at the osteochondral junction contributes to the spread of inflammation and sensitization. The continuous recruitment and high-frequency input from nociceptors to the brain lead to the “wind-up” phenomenon, and ultimately could induce neuroplasticity, central sensitization and endogenous pain modulation impairment 14. Structural joint damage will make movement more difficult, resulting in pain, stiffness and lameness. Reduced mobility will aggravate muscle and ligament weakness, contributing to further immobilization and muscle atrophy, which fuels the vicious circle of pain (Figure 2) 10. This is one reason why controlled exercise is recommended in the early stages of canine OA 15. 

OA is therefore a progressive disease of the synovial joint, but a simplistic definition is misleading; a single structural lesion will often lead to hypersensitized nociplastic pain, and eventually the neurological expression can encompass biological, psychological and social dimensions (Figure 3). 

Is osteoarthritis mainly due to aging?

“Unlike humans, where OA is usually related to aging and ‘wear and tear’ of joints, OA in dogs usually has a specific underlying cause and is therefore often seen earlier in life. Causes can include developmental conditions (e.g., elbow or hip dysplasia), ligament rupture, and traumatic problems (e.g., a humeral condylar fracture where the broken bone involves the joint). Diet, obesity, genetics, age, breed, and environment are risk factors that can influence OA development and progression.” 

So what evidence exists to support this statement? Isn’t OA an “aging disease”, and what are the consequences if older animals have a 60-90% risk of developing OA? 

The statement is correct, but contrary to popular belief, OA is not limited to elderly populations, especially in companion animals. The association of normal aging with OA is often wrongly made, caused by limitations in diagnostic methods (see below), and should no longer be automatic. Owners also frequently consider the emergence of OA signs as “normal” for an aged dog. Such perception is deleterious for OA detection, and delayed diagnosis greatly limits treatment options – such that euthanasia may frequently be proposed (and accepted by the client) 16. This is fueled by the view that OA is an incurable and progressive degenerative process, which will require the patient to have life-long treatment. 

As highlighted above, the risk of developing OA with age is significant in companion animals. One study showed that the occurrence of OA in a cohort of Labrador dogs (N=48) was 15% at 2 years, but increased to 67% by 14 years of age 17. Other studies also report that prevalence increases with age; one study claimed up to 80% of dogs over 8 years old 5, whilst another (in a small cohort of 48 dogs) reported 91% to have histopathologic changes consistent with shoulder OA at end of life 18. 

The appendicular skeleton – hip, stifle, hock, shoulder and elbow joints – is commonly affected in dogs, and risk factors for OA are well documented, as noted above. The literature illustrates that OA can develop at any age and can be due to an undetermined cause (primary OA), or to a specific underlying cause (secondary OA) 5. This latter can for example occur after cruciate ligament rupture or damage to the menisci (e.g., from slipping on ice or repeated activity such as agility). On the other hand, longitudinal studies have shown that the onset of OA has not only been delayed, but also prevented in animals fed a restricted diet 17,18. This indicates that early dietary intervention (in this case a 25% reduction in overall intake) can be beneficial for the health-related quality of life (HRQoL), which encompasses the physical, psychological (mental, emotional) and social wellbeing of an OA-affected dog (Figure 3). 

Although there is a high risk of developing OA in older pets, owners are generally not proactive, and any adaptation to the animal’s lifestyle once signs appear is too late. Practical pre-emptive interventions include increased monitoring by the owner, more regular visits to the veterinarian with in-depth monitoring, adaptation to diet and physical activity, and specific environmental alterations 15. Longitudinal studies (as evidenced in human pain patients) are the key to help identify if a dog will show either slow or rapid progression with its OA, and help predict the onset of persistent, deleterious pain 19. This should help minimize the risks of central sensitization, preserve the animal’s HRQoL and maintain the human-animal bond. One problem, however, is the limitation of detection methods. Despite their lack of sensitivity, radiography and clinical examination remain the diagnostic references, making it difficult to concur on the age of commencement for OA and the benefits of earlier intervention 20. 

What are the signs of osteoarthritis?

“The key signs of OA are stiffness, lameness and pain. Stiffness and lameness are often particularly evident after a period of rest, especially if there has been previous exercise. The stiffness often ‘warms out’ after a few minutes. Joint pain associated with OA may manifest in a number of ways, including groaning, abnormal sleep patterns and altered behavior (including aggression). Reluctance to climb, jump and exercise are additional features.” 

Is this right? What pushes an owner to consult when they suspect OA in their animal, and what could improve OA detection?

In affected dogs, orthopedic alterations such as lameness and stiffness are frequent, and when present are easily recognized in dogs of middle and larger size. Specifically in young adult dogs, owners (and veterinarians) will observe abnormal changes to movement-based behaviors in day-to-day activities 21. In the early stages these are usually subtle, intermittent and insidious, before becoming permanent in the later stages 22. Observing protective postural (limb or pelvic flexion, unbalanced weight-bearing) and gait (speed, limb stiffness, range of motion) changes require careful application. With time, certain actions (e.g., reluctance or refusal to perform activities, more hesitant running, difficulty in climbing on a chair or entering a car, in going up/downstairs) make OA more easily identifiable. Decreased tail wagging and lowered ear-tail positions may also be signs of chronic pain in dogs 21. Dogs may also show some form of psychological alteration, with emotional depression (Figure 3), anxiety (either acute, or manifested by over-reaction, aggressive protection of a body part, or self-injury with excessive licking or tail chewing), or prolonged sleeping time. Such changes will also frequently lead to social modifications, such as reduced sociability and playing (with the owner or other dogs), or a delayed welcoming of the owner at the door 23. A study with 23 owners of dogs with OA demonstrated that the most visible signs were reduced mobility after exercise and a slow ability to change posture after rest or in the morning 22. 

On another note, a recent qualitative study 9 of 10 owners with OA dogs mentioned that owners often have a “wait-and-see” attitude towards the first signs of the problem. The exceptions were if the dog expresses acute pain, the owner feels he/she has a strong bond with his/her pet, is aware of the limits of his/her knowledge or has confidence in the veterinarian. 

In summary, canine OA is a chronic degenerative disease that is under-detected and under-diagnosed 15, and little is known about how dog owners recognize its early manifestations 9. Given that OA has a direct impact on how owners and dogs interact, it could be interesting to investigate the daily routines they carry out together that may be affected by OA; this may help identify the point(s) that make owners notice their dog’s malaise and motivates them to seek veterinary advice. 

Are all dogs with osteoarthritis in pain and lame?

“Once OA has started in a joint it cannot be cured and will affect an animal for the rest of his or her life. However, there are broadly two forms; chronic active OA which causes pain and lameness, and chronic silent (asymptomatic) OA which may cause transient /occasional stiffness but not pain or lameness. It is possible for a dog to have the silent form of OA for long periods with occasional bouts of the active form which may develop, for example, due to over-exercising and stressing/spraining of the osteoarthritic joint.” 

Is this true? Are pain and lameness systematic in canine OA? 

An OA joint is characterized by the progressive and irrevocable loss of tissue integrity. The whole joint will then be subjected to chronic failure 5. However, long-term prospective studies in naturally occurring OA are needed to better understand the complex interrelationship that prevails between joint structural changes and functional impairment associated with nociceptive sensitization (Figure 2); the rate at which a damaged canine joint progresses over time, as well as how the damage evolves, is not well established. Such uncertainties are exacerbated by the complex etiopathogenesis of the disease, the joint involved, use/overuse of the joint and a multitude of intrinsic factors at the level of the tissues. As with other diseases, early detection is of the utmost importance to help both owner and animal to better cope with the condition. Where the clinically recognizable OA signs (mostly pain and lameness) relate to the spectrum of changes within the joint is also unknown 20. Do they occur at the onset of the molecular changes, or when obvious joint degradation is reached? Are they related to sensitization? Moreover, we do not know how strong the damage revealed on imaging reflect the intensity of clinical signs. In other words, do radiographic changes correlate with the functional impairment? These weaknesses in knowledge are amplified by the need to develop sensitive methods of detecting pain expression, joint discomfort and assessing quality of life. One could also argue that no imaging scoring system has been accepted as the standard-of-care to document OA, a situation that further confounds the situation. 

Some veterinarians claim that the clinical course of OA is marked by waxing and waning of clinical signs. The notion that animals with OA can have “good days and bad days” appears simplistic and we should be prudent with such an assumption. Without good evidence from prospective studies in naturally occurring OA and a refined method of assessing pain expression and joint discomfort, the ambiguity remains: is any improvement/worsening of the signs genuine, or is it due to inherent variation in measurement? For clinicians, this unknown compromises precise discernment of therapeutic efficacy, as it could be part of the natural course of the disease. 

What is the best method of diagnosis?

“Arthritic joints are often thickened, with a restricted range of movement, and muscles on the affected limb are invariably atrophied. Detecting pain on manipulation of arthritic joints is an important feature that helps distinguish the active and silent forms of the disease. Radiographs are the most common method of diagnosing OA and excluding other possible causes of joint pain and lameness. Radiographic features typically include the presence of effusion (increased synovial fluid in the joint), fibrosis (increased capsule and synovium depth) and the formation of abnormal bone (osteophytes, sclerosis) around the joint.” 

Is this true? How useful is detection of pain on manipulation, and how should we use radiography? 

Pain, crepitus, joint effusion, joint thickening and abnormal range of motion are all distinctive signs of canine OA 15, and can be useful to estimate the severity of the condition. However, in a qualitative study of 26 general practice veterinarians, all participants felt this scoring to be subjective and to have high variability between practitioners 9; most participants found it difficult to describe how these elements were used in their decision-making, and some disputed their relevance. Indeed, an orthopedic exam to detect the presence of OA in dogs remains challenging; observing the animal walking (gait analysis) and standing (posture), along with its ability to change position, and also after strenuous physical activity, is not an easy task in a clinic. This crucial information must be provided by the owner, and although time-consuming, a complete and accurate history, set aside the signalment, will be helpful, particularly with a focus on the previously described risk factors. Most clinicians will diagnose OA after identifying a joint conformation problem, laxity, reduced range of movement, muscular atrophy, effusion, pain and crepitus, but in most cases a suspicion will and possibly must be confirmed using radiographs. 

Radiography is the gold standard for OA clinical diagnosis, but it is not sensitive enough to detect the early stages 20, and poor positioning and/or contrast can affect radiographic interpretation. There is also little correlation between radiographic signs, limb function 12,24 and pain assessment 25. In the qualitative study previously cited 9, radiography was only used in certain cases (usually in young dogs with acute lameness, or elderly dogs that showed a rapid painful deterioration). The clinicians admitted to relying on owner information and clinical examination for a diagnosis, justifying their choices by citing limited time for consultations, and saying that they believe radiography will not change their final opinion. 

Insurance status is also a significant “risk factor” for OA diagnosis, with insured dogs being twice as likely to have an OA diagnosis compared to non-insured individuals 4. Appropriate imaging for OA confirmation, as well as the long-term nature of the condition and therefore expected treatments and costs, are likely to explain much of the increased rate of diagnosis. More importantly, it may be the case that uninsured individuals (i.e., most owners) are more likely to receive an uncertain diagnosis and/or no follow-up post-diagnosis, and no potential treatment or recommendations for the condition – which in turn could suggest compromised welfare for these affected dogs 4. 

Radiographs are usually sensitive enough to recognize some OA structural changes and remain the first step in the diagnosis of a joint problem 10,20, and the modality is affordable, readily available and safe. Given that breeders will use radiographic screening to assist in making breeding decisions, should we not consider routine imaging at middle age to inform an owner about their animal’s joint health? Instead of being used primarily to confirm a tentative diagnosis, routine radiographs at this life stage could and should be used as a screening tool for OA, and will act as a basis to monitor potential OA progression. Although this may be costly, it cannot be interpreted as unnecessary – given the high prevalence of radiographic evidence for OA in adult dogs, and the difficulty in recognizing the clinical signs of the condition 5. Where clinical signs of OA are absent, this approach can prompt the owner to take proactive preventative measures, instead of being reactive only when pain and lameness, and other dramatic biological, psychological or social alterations, become obvious.

Conclusion 

A positive approach by the veterinary profession to osteoarthritis is required to fight the current false belief that OA is a normal expression of aging. With early detection, including radiographic evidence and categorization of a dog’s functional impairments, more can be done to limit the development of further clinical signs. Introducing routine imaging of middle-aged dogs will allow clinicians to have a concrete basis to initiate discussion about OA and its treatment, and should help improve an owner’s understanding on what can be done for their pet. In turn this eases the burden on the owner and improves the veterinarian – client relationship.