18 Jun 2024
Image © Reddogs / Adobe Stock
A common misconception exists regarding canine OA.
It is held by some dog owners and by some veterinary practitioners alike, and relates to the aetiology of the disease.
The misconception is that OA in dogs is a primary condition. The belief that this disease is a natural part of age-related deterioration such that, for example, OA affecting a dog’s elbow is associated with OA affecting its metatarsophalangeal joints is not correct.
This misunderstanding justifies inappropriate blanket treatment of OA using analgesia and exercise recommendations without investigation. It also harms client engagement with OA management.
In this article, I will attempt to interweave issues of medical management, client compliance and this underlying misunderstanding of OA in dogs. Firstly, an introduction to OA.
OA is the chronic degeneration of joints at the molecular, cellular and gross levels.
Grossly, we recognise reduced exercise tolerance and lameness, with palpation revealing muscle atrophy, and joint manipulation revealing resentment alongside reduced ranges of motion. This is why we begin our consultations with history gathering and a physical examination.
Radiographic signs of OA include effusions and peri-articular new bone formation. The combination of history and examination findings (which indicate a clinical relevance) and radiographic features is diagnostic of OA.
“[We] must avoid falling into the trap of diagnosing “osteoarthritis” and stopping there.”
At the cellular level, chondrocytes alter their metabolism such that the balance swings in favour of degradation of type II collagen and large proteoglycans. Alterations in the normal molecular structure of the cartilage matrix negatively influence the function of the articular cartilage, leading to impact on the subchondral bone (pain). Peri-articular thickening (stiff joints) and eventual osteophyte formation are further consequences of interactions between the inflamed cells of the joint.
We understand the cellular and molecular events that result in the gross changes that we observe clinically in our patients.
Greater depth of knowledge of the involvement of nitric oxide, matrix metalloproteinases and transforming growth factor-β, to mention a small number of the involved molecules, is not necessary to give appropriate advice to clients.
But, we must avoid falling into the trap of diagnosing “osteoarthritis” and stopping there.
If you are a Labrador retriever, you are unfortunate indeed. Your breed is over-represented for OA of the elbows, hips and stifles. But this is not because of an innate susceptibility to OA. It is due to an innate susceptibility to diseases that trigger OA.
These include elbow dysplasia, hip dysplasia and cranial cruciate ligament disease.
With canine OA, a trigger always exists. That some dogs with OA are genetically predisposed to more rapid progression or more severe clinical signs is not in dispute.
Also, OA is more easily initiated and progresses more rapidly in older dogs. So, genes and age do contribute to OA.
But, in the dog, OA is not initiated by genes or age. Dogs can be as genetically susceptible and old as they want, but without an initiating cause, they will not develop OA.
It is brave to suggest that one rule fits all, so my statement here needs to be qualified. OA in dogs is almost never primary. It is a misconception to suggest that a large proportion of the OA cases we see represent primary disease.
The risk of this vagueness when OA is discussed between vets and pet owners is that the underlying causes (the primary diseases) are overlooked. See Table 1 for examples of statements given by pet owners that give an opening to the practitioner to inform and educate.
Table 1. Misconceptions about OA in three quotes | |
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It is part of a veterinarian’s job to inform clients and not allow misconception about OA to persist. Presented below are three sentences the author hears during consultations that are indicative of misunderstandings that should be addressed. | |
Opinion expressed | Appropriate response |
“My pet is unlucky because he is riddled with arthritis.” | This may well be the case, but dogs are only affected by multi-joint osteoarthritis if they have multiple primary joint diseases causing secondary OA in multiple joints. |
“My pet is very young to have osteoarthritis.” | Since osteoarthritis is secondary to developmental joint conditions, a large proportion of canine OA starts while the patients are juvenile. |
“My pet has osteoarthritis in the front legs.” | We cannot expect clients to know the names of the joints. However, we should inform them that OA affects specific joints as a result of a specific initiating disease. |
When we fail to take opportunities to improve their understanding, we cannot expect to engage pet owners in a treatment journey.
And, as we all know, the treatment journey for OA continues for life. Before we can treat, we must investigate.
The term “osteoarthritis” should never exist in a patient’s clinical record without two things: the joint affected (not just the limb) and some consideration of the underlying cause. That means investigation.
Concerns regarding cost, recently escalated within our profession, have an influence on this, but investigations must be discussed with clients.
Fortunately, the investigation of suspected OA is not necessarily particularly extensive or expensive.
The first component of diagnostic procedure is to compile a differential list. OA is commonly triggered by only a small number of developmental diseases in dogs. Trauma and infection are also possible triggers. Thus, conditions including hip dysplasia, avascular necrosis of the femoral head, elbow dysplasia, cranial cruciate ligament disease and osteochondrosis merit consideration. It is true that we see dogs with OA affecting the carpi, tarsi and metacarpophalangeal/metatarsophalangeal joints, which are difficult to explain. Still, we assume these joints are not affected by primary OA, since affected dogs often do not have OA in other joints.
With the differential list compiled, we proceed to discussion with clients regarding investigations. These should include examination and imaging. Examination includes palpation and manipulation of appropriate joints and peri-articular structures to record thickening, effusion and abnormal joint ranges of motion/resentment on manipulation.
CT is reported to be of superior sensitivity compared with plain radiography for certain diseases, in particular for investigation of elbow dysplasia (Kunst et al, 2014), although radiography is a reasonable first modality in all joints.
Investigations are not only aimed at identifying the underlying cause, but also at documenting which joints are affected, and the severity.
We know, for example, that the extent of peri-articular new bone formation affecting the elbows is well correlated with the severity of articular cartilage loss (Farrell et al, 2014); therefore, radiographs can indicate severity of OA.
Synoviocentesis might play a role in investigation, but only in selected cases; for example, where inflammatory arthropathy is to be excluded. If investigations are not to be performed following initial discussion with the client, then a presumptive diagnosis of OA based on examination findings should be recorded within the notes.
The examination findings on which the diagnosis is based should also be recorded.
Investigations of elbow OA in a young Labrador retriever, for example, might result in recommendations for treatment options other than joint salvage or conservative management, and these opportunities should not be missed.
However, with some frequency, surgical options other than salvage do not exist.
Perhaps it is for this reason that some practitioners might be tempted to skip investigations in favour of instituting standardised therapies during a consultation.
Conservative therapy of OA has classically involved medication, management of activity and attempts to optimise body condition. Of course, it is good health care practice to aim to manage the clinical signs of OA, so therapy should be instituted as soon as possible.
Medications are divided into symptom-modifying therapies (NSAIDs and other analgesics) and disease-modifying therapies (pentosan polysulphate, intra-articular treatment such as stem cell and platelet infusions and nutraceuticals). Symptom-modifying treatments include the historical mainstay of OA management, the NSAIDs, in addition to paracetamol, gabapentin, amantidine and tramadol, as well as the more recent, and highly popular, additions to our armamentarium: bedinvetmab and grapiprant. Remember the veterinary medicines licensing regulations.
Evidence for some of the disease-modifying treatments is slowly mounting, although even in human medicine a persistent lack of high-level evidence is recognised (Jones et al, 2018).
In addition to medical management, conservative therapy includes advice regarding exercise. In the past, we would describe a threshold of exercise, with activity above this threshold resulting in clinical signs of OA (lameness and reluctance to exercise) and activity below the threshold being recommended to minimise the signs.
However, it is now understood that the negative aspects of exercise restriction (increasing joint stiffness, reducing muscle mass and deteriorating general health and fitness) outweigh the benefits in people and pets. Therefore, the current recommendation is to maximise exercise without unduly exacerbating the clinical signs of OA.
We recognise that some patients will show some lameness after rest after exercise and, indeed, during exercise, but this is not necessarily as great an insult to their experience of life as an avoidance of exercise itself.
Short periods (a few weeks) of moderately restricted exercise might be beneficial in allowing flare-ups of clinical signs to abate, but long periods of exercise restriction are to be avoided.
We are aware that bodyweight optimisation is of significant importance in managing OA in dogs. Obesity is a significant risk factor for OA (Kealy et al, 1997), and reductions of body fat content have been shown to reduce the clinical signs of OA (Marshall et al, 2010).
To conclude the discussion of non-surgical management, we should recommend conservative treatment of OA involving exercise modulation and body condition optimisation. Medications should be administered where appropriate. These aspects of management should continue for the dog’s entire life, and the client must be part of this process.
“We recognise that some patients will show some lameness after rest after exercise, and, indeed during exercise, but this is not necessarily as great an insult to their experience of life as an avoidance of exercise itself.”
If we are to expect client compliance with the treatments we institute, we must be prepared to justify our recommendations and clarify our aims.
A situation should not exist in which a dog has a diagnosis of OA of an unspecified joint, with no investigations, consultations every few weeks with different vets, each of whom has added a different analgesic, recommendations for strict restriction of exercise with no particular timescale provided and limited or no advice on optimisation of body condition.
Clients in this situation – and many exist – are disappointed, disengaged and often disgusted. They do not understand the cause of their dog’s OA. The aims of therapy were never made clear to them.
They do not perceive improvement with the treatments they have pursued and they cannot explain their failure to treat the disease. They wonder if all of the medications they have been prescribed are necessary and safe. The money and time they have spent at the vets have not been justified, and they consider writing a negative online review.
Client compliance and gratitude do not stem from lists of medications and advice on exercise restriction. We need to be better at managing OA.
In addition, we cannot hope that clients will engage in treatment of OA without the facts about the disease. We need to be better at communicating with clients.
OA is common in young dogs, inevitable in dogs with a primary joint disease and rarely present in the absence of such a condition; therapy will be lifelong and requires maximisation of activity (not avoidance of activity), optimisation of body condition and medical management matched to the clinical signs; OA is to be managed, not treated.
OA is not a primary disease, and management aims to limit the negative impact of its clinical signs on quality of life. If we can communicate appropriately with our clients and employ a reasonable strategy of conservative management, our clients will engage with treatment, resulting in satisfaction among our patients and their owners.
Clinical Assist