Conservative management of canine osteoarthritis - part 2 - Veterinary Practice
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Conservative management of canine osteoarthritis – part 2

continues her series on canine OA
with a discussion of the types of
pain involved and a look at the
various types of treatment

IF untreated, OA is a problem to the patient in two main areas:

  1. It is often a painful condition and this affects quality of life by causing suffering.
  2. The function of the joint becomes increasingly impaired to the extent that it eventually becomes non-functional. This has an impact on the local muscles, other areas of the body (as discussed in the first article) and in other less obvious ways, such as abnormal wearing of nails and excoriation of the skin on the dorsum of the paw. These may, in some cases, cause the animal more immediate suffering than OA itself.

Veterinary intervention potentially creates problems for the patient and owner in other areas:

  1. Restriction of the dog’s resources by limiting exercise and the kinds of play in which they can engage, potentially causing frustration and confusion. This restriction can also cause problems for the owners because they feel guilty about restricting an activity from which their dog derives pleasure.
  2. Food is a major resource that is often restricted or changed. Owners will often feel guilty about limiting their animal’s food if they “look hungry” and are dissatisfied if they do not enjoy their food. The relationship between the provision of food and affection is a complex one and such feelings often negatively affect owner compliance.
  3. Potential side effects of medication may affect the well-being of the patient, yet, whether the side effects occur or not, this may worry the owners. These potential pitfalls are covered later in this article under therapeutic approaches. This section is to remind the reader of the challenges of pain in OA.

Acute pain

The experience of acute pain is vital to survival; an organism must experience the sensation we call pain to withdraw from the painful stimulus (and therefore limit the damage), protect the damaged area and learn not to repeat the experience, if possible.
However, this is not a reason to leave patients in acute pain or to use pain to limit movement and activity. Ignoring, or under-treating, acute pain not only causes immediate suffering but is likely to lead to prolonged, chronic pain and the development of chronic pain states. It is unlikely that any analgesic will provide powerful enough analgesia to allow an animal to be able to exercise normally in the face of significant pathology.

Chronic pain

The experience of pain is not a straightforward transmission-perception process from the peripheral stimulus to the brain. This is true of acute pain, where there are many levels of modulation of pain from the periphery, through spinal cord to brain. The experience of acute pain from the same stimulus will be experienced differently by different individuals. In chronic pain the picture is even less clear. Chronic pain is not adaptive, i.e. it is of no biological use to the animal. This is important to recognise, because owners often still think that pain is somehow of use to the patient and that they do not want to be giving something that “just masks the pain”. Chronic pain causes the same physiological changes as chronic stress: poor quality sleep (which leads to more pain), increased heart and respiratory rates, increased blood viscosity, muscle fasciculation and trembling.5 Untreated pain therefore exposes the patient to the physical and psychological effects of ongoing chronic stress. In chronic pain, because of the “neuronal plasticity” of the nervous system (i.e. the way that pain is perceived is not “hard wired”) the pain is not only part of the disease but can become the disease. The experience of pain may continue to get worse for the patient even if there is no change in the pathology, or sometimes even when the pathology is removed (phantom limb pain is the clearest example of this). This is due to the changes in the nervous system where increasing numbers of systems become involved in pain signalling [wide dynamic range neurons (WDR), NMDA receptors and glutamate receptors, causing the upregulation of further receptors, membrane depolarisation and the experience of further pain]. The normal physiological consequence of this is spinal “wind up” which occurs in every mammal and may
last minutes or hours depending on the cause and the current state of the nervous system. If this process continues or goes on
unchecked, then central sensitisation may result; here there are transcriptional changes in dorsal horn neurons leading to altered
neurotransmitter levels at synapses and an increased number of
receptors. This state may include an imbalance between excitatory and inhibitory influences (central disinhibition) and changes to the Abeta fibres that usually “recognise” light touch
but now produce substance P, which causes input from these receptors to be perceived as pain.6 It is not fully understood why this happens in some individuals and not in others, but at least one risk factor is likely to be uncontrolled pain. The extent of suffering in these patients is completely uncorrelated to anything one might see on imaging and may exist without significant pathology. In OA, the dynamic nature of the condition, and the difficulty of recognising pain in patients who cannot verbally complain about it, means that it is likely that dogs will experience
uncontrolled pain from time to time, even if some analgesia is given. Under-dosing, using analgesics only when the patient appears to be really suffering (what the owner tends to do), or just giving short, limited courses of analgesics, is likely to predispose at least some of these dogs to a chronic pain
state or central sensitisation. Repeated acute “flare ups” may well contribute to this problem and this is one of the best reasons to avoid a “fire fighting” approach to the treatment of OA.

Sources of pain in canine OA

The joint

In soft tissues of the joint, the synovial membrane becomes inflamed (“synovitis”), leucocytes enter the joint space and enzymes, cytokines, free radicals and prostaglandins are released, triggering further inflammation. This inflammatory process damages the cartilage. The cartilage erodes due to damage to the supportive matrix and further inflammation. This process means that it is less able to resist mechanical injury and the subchondral bone is eventually exposed. Whilst cartilage has no nerve supply, bone is richly innervated and the pain is further increased when it is exposed.

The soft tissues

Secondary muscle pain mainly consists of myofascial pain in local
muscles and those that take the strain of the postural shift off the
affected joint or limb. Note that these may continue to cause pain
for the patient even when the joint is not in a chronically active
inflammatory state.

Central changes

These include central sensitisation/disinhibition as outlined above. Note that these may continue to cause pain for the patient even when the joint is not in a chronically active inflammatory state. NB. Available evidence suggests that a reduction in central sensitisation can reduce peripheral disease and inflammation (i.e. treating pain effectively may also reduce inflammation and disease progression).7

Approach to treatment

The treatment of OA has two main aims:

  1. to drive the chronically active arthritic joint into a chronically silent state (i.e. where there is minimal inflammation and pain);
  2. to slow, as far as possible, the inevitable progress of the joint to its dysfunctional end stage

Traditionally, the approach to OA relies on diagnosis, assumed or
confirmed, followed by analgesics, usually NSAIDs. These are prescribed either shortterm to cover acute flare-ups, when the condition is first diagnosed, or, in contrast, permanently. The problem with the short-term approach is discussed above; it is likely that the patients are not receiving sufficient analgesia and are being predisposed to chronic pain states because they are exposed to repeated bouts of pain. The problem with permanent
therapy is that owners may perceive this to be “over treatment” and then either only resuming therapy (which then sometimes appears not to “work”) when the pain has become as severe as before, or revisiting the practice. There is an instinct that warns the owner against long-term medication, especially in a young dog, and this practice must be rationalised and justified to the owner. This can be achieved by: (a) assessing the extent of the patient’s suffering (see below), so that the owner understands why medication is being used (or not used); (b) recording realistic outcome measures with the owner’s help, so that the owner can look for specific improvements or deteriorations and understand why medication may be maintained or altered; (c) tailoring the dosage and frequency of treatments according to individual response. This way the owner becomes part of the treatment programme and sees the reasoning behind why their dog may sometimes be given long-term therapy, as well as understanding why that treatment is sometimes suspended or increased.


After the initial course of NSAIDs it is often hoped that this nutraceutical combination may continue to manage the patient’s problem and limit the progress of arthritis. The evidence for either of these being achieved with glucosamine/chondroitin as a sole treatment is, at best, currently equivocal (in both dogs and humans). Since safety is not a factor in treatment with these veterinaryformulated compounds, there is no reason to stop using them as part of the management of OA, but, on the strength of current evidence, it would be hard to justify them as a sole
medication if the animal is suffering OA pain.8,9


Limited exercise is the usual advice, with regular, short walks and no weekend hikes. This is correct at the time of initial diagnosis and if the dog is suffering. However, in the absence of pain, many dogs with OA manage to increase their exercise over time to normal levels. This helps to regulate weight, improve muscle tone, bulk and strength and generally improve well-being, as well as being pleasing for the owner. Advice about exercise should therefore not stop at “restricted” but, again, be tailored and adapted to the level with which the dog can cope. But the management of OA can offer so much more than this to the patient and the owner. The key is to appreciate the dynamic nature of the condition and therefore its treatment.

A NEW APPROACH TO MANAGING CANINE OA Assessment – not just of pain but also of suffering

The individual tailoring of a programme relies in part on being able to assess the patient’s suffering. This assessment guides the clinician in deciding how much should be done and how quickly, and can help balance questions of quantity versus quality of life.
All of the validated pain scores rely, to a greater or lesser extent,
on the assessment of behavioural changes in response to pain and on more than one assessment. The Glasgow Composite pain scale
uses a number of outcome measures and has an intervention
score at which additional pain relief should be considered.10 This scale is currently validated for acute pain in orthopaedic patients.
A quality of life scale, validated in orthopaedic patients with chronic pain, is currently being revised and shortened.11 This subject has been covered in detail recently by Yeates and Main.12
In this author’s pain clinic, the technique dubbed “triangulation” is used to assess the degree of suffering in the pain clinic patient. To be accurate, pain and suffering are not synonymous – pain is the sensation, but suffering is the negative way it causes the animal to feel about the sensation. For example, a dog with an arthritic stifle may have a sensation of pain in that joint when he runs or when he walks upstairs, or when the veterinary surgeon
palpates or moves it, but that does not stop him performing those
activities, nor does it cause him to have aversive feelings about
that sensation, thereby learning to avoid certain behaviours that
cause it. Neither does that sensation keep him awake, or stop him
lying comfortably, or make him anxious about other dogs coming towards him. Therefore, there is pain but no significant suffering.
However, the dog that has the sensation of pain plus all the
aversive and unpleasant associations that go with pain, is suffering. The first example needs relatively simple pain relief, such as NSAIDs, to allow as normal movement as possible and to
stop the pain progressing toward suffering. The second example needs aggressive multi-modal analgesia, attention to its comfort and appreciation of the fact that some normal experiences (such as grooming or interacting with other dogs) are unpleasant and even frightening. This is the key to approaching the pain of OA: the assessment of suffering. Once there is an appreciation of how much suffering is present, the risk-benefit analysis of using multiple, and sometimes off-licence, medications is simplified, even in the presence of concurrent disease. Few owners would want their dog suffering as much as the example above, even if treatment of that suffering created some measure of risk to organ function, but if the first dog were in an advanced stage of renal failure and being managed well, one would feel justified in carefully exploring methods of pain relief that were unlikely to further compromise renal function.


This technique starts from the premise that one can never be certain about an absolute value of the degree of suffering in an animal (or even in a human, despite our verbal dexterity), just as one can never give a certain value on an animal’s welfare. It is what John Webster, in his book Limping Towards Eden,13 describes as a “fuzzy area of science”. What is needed in such areas is a way of decreasing the uncertainty around one’s assessment. Webster uses a sailing analogy to illustrate the point: if one is trying to work out where one is whilst at sea, there is little use in taking only one bearing (or using a measure of cortisol as a single outcome measure of “stress”) because there still remains too
much uncertainty. Two bearings are better, but three further reduce the area of uncertainty about the position. The composite pain scale described earlier uses a similar approach – by measuring different expressions of animal pain, individual variation is minimised; if touching a wound is the only measure of pain, then what about those animals who are frightened or who dislike being touched by strangers anyway? The Pain Clinic uses triangulation in the following way: The presenting complaint or sign is the starting point for most consultations. In OA, for example, the owner may present a dog that can no longer jump into the car, or for whom on survey radiographs of the pelvic area, OA of the hips is identified. The dog may not want to jump into the car for a variety of reasons: it may feel car sick, it may have had a bad experience when being left in the car, the car may have been changed and now simply be much higher or more awkward to get into, the dog may have learned that reluctance to get in the car receives encouragement in the shape of a food reward, or its sibling dog may be quietly, but firmly, discouraging its entry. Similarly, the identification of arthritic changes in the hips is suggestive of pain, but does not absolutely mean that there is pain – or suffering – present. Therefore, taking this single presenting sign or complaint as an indication of pain and suffering could result in over, or inappropriate, treatment for pain. The second bearing is that of behavioural changes for that individual. Are there changes other than reluctance towards getting in the car? A list of possible changes is given in Table 1. However, it should be borne in mind that such changes alone do not indicate pain. Spending more time with the owner, or being “clingy”, may occur in response to an environmental change such as moving house, or a family member moving out, or a sibling dog dying. Such changes always need to be checked against possible environmental or social causes, e.g. trying to hide from other dogs may be the simple response to a recent dog attack. The third bearing is taken from both the examination and the gait and/or general movement. Although these could strictly be two separate bearings, the pain clinic patients are not restricted to patients with musculoskeletal pain, and non-ambulatory patients also need to be assessed for pain and suffering. The examination process has been described earlier. Gait and movement should be assessed outside, if possible: on slopes, up and down steps and at different speeds. This assessment can be limited by patient co-operation and the gait of a dog desperately pulling to get away from the clinic is not the easiest to judge. If this is a limitation, then asking the owners to video the dog at a walk, trot and run, up and downstairs, etc., can be helpful, particularly if other parts of the overall assessment are not straightforward. Slowing down the video can also make it clearer to determine on which leg the patient is lame. As well as frank lameness, stiffness, pacing, inability to pick the feet up properly, a shortened stride and difficulty in turning tight circles can also be picked up at this time and may indicate additional problems or the need for a neurological examination. This part of the assessment is a useful point at which to ensure that the owner and the assessor are in agreement about the site of lameness and getting the owner to point at which leg they think is the problem can offset a raft of potential confusion and miscommunication.

5. Lamont, L. A., Tranquilli, W. J. and Grimm, K. A. (2000) Physiology of pain. Veterinary clinics of North America Small Animal Practice 30 (4): 703-728.

6. Mathews K. A. (2008) Update on management of pain: Neuropathic pain in dogs and cats: If only they could tell us if it hurts. Veterinary Clinics of North America Small Animal Practice 38 (6): 1,365-1,414.

7. Sluka, K. A., Jordon, H. H. and Westland, K. N. (1994) Reduction in joint swelling and hyperalgesia following posttreatment with a non-NMDA glutamate receptor antagonist. Pain 59: 95-100.

8. McCarthy, G., O’Donovan, J., Jones, B. et al (2007) Randomised double-blind, positive controlled trial to assess the efficacy of glucosamine/chondroitin sulfate for the treatment of dogs with osteoarthritis. The Veterinary Journal 174: 54-61.

9. Moreau, M., Dupuis, J., Bonneau, N. H. and Desnoyers, M. (2003) Clinical evaluation of a nutraceutical, carprofen and meloxicam for the treatment of dogs with osteoarthritis. The Veterinary Record 152: 323-329.

10. Holton, L., Reid, J., Scott, E. M. et al (2001) Development of a behaviour based scale to measure acute pain in dogs. The Veterinary Record 148: 525-531.

11. Wiseman-Orr, M. L., Nolan, A. M., Reid, J. and Scott, E. M. (2004) Development of a questionnaire to measure the effects of chronic pain on health related quality of life in dogs. The American Journal of Veterinary Research 65: 1,077-1,084.

12. Yeates J and Main D. (2009) Assessment of companion animal quality of life in veterinary practice and research. The Journal of Small Animal Practice 50: 274-281.

13. Webster J. (2005) In: Animal Welfare; Limping Towards Eden. Blackwell Publishing, Oxford: p45.

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