OSTEOARTHRITIS (OA) is often defined as “a progressive, degenerative disease of synovial joints characterised by pain, disability, destruction of articular cartilage, and bony remodelling”. However, this relatively straightforward definition can often be misleading, especially when the complex biochemical, pathological and physical changes caused by OA are taken into consideration. This complexity confounds our ability to find a simple, straightforward solution to canine OA, which often frustrates clinicians and dog owners alike. Dog owners understand that canine OA can be debilitating, adversely affecting both the dog’s and the owner’s lives. However, canine OA does not always have to cause significant suffering, nor be the grim predictor of a shortened lifespan. This article details canine OA and its diagnosis, the assessment of chronic pain, and the wide range of available therapies.
Implications for patient, owner and practice
Canine OA is usually a secondary condition (i.e. secondary to conformational abnormalities such as hip dysplasia, elbow dysplasia, and osteochondrosis), differing from human OA and feline OA, which are usually primary (i.e. caused by “wear and tear”). What this means for the canine patient is that clinical signs and radiographic changes may appear when the dog is still very young (Figure 2), potentially resulting in the following implications:
- pain at a young age; n impaired exercise tolerance leading to poor development of muscle and gait;
- untreated, or undertreated, pain at any age is a chronic stressor (see below) which affects posture, behaviour and may lead to a chronic pain state;
- pain during the behavioural development phase may manifest as aggression or anxiety, avoidance behaviour and poor or inadequate socialisation;
- postural and gait abnormalities put strain on other musculoskeletal structures and predispose to pain, possibly accelerating the development of primary or secondary osteoarthritis in other joints;
- poor exercise levels will predispose to obesity, exacerbating pain.
For the owner, the implications of early development and/or diagnosis of OA are:
- shock and distress that such a young animal develops a condition that they usually associate with old age and debility;
- negative comparisons between their pet’s condition and other arthritic conditions with which they are familiar in humans (e.g. rheumatoid arthritis);
- the assumption that this diagnosis represents a death sentence, or at least a shortening and reduction in quality of their dog’s life;
- disappointment, as they cannot share the experience of their dog exercising and playing normally;
- worry that their dog is suffering;
- worry about the potential side effects of medication;
- worry that the medication will inevitably be life-long and may shorten life;
- the sense that they have no control over the problem.
For the veterinary practice, the implications of the diagnosis of OA in a young dog are:
- that the owner must be reassured and quickly given the tools with which to cope with their pet’s condition;
- involvement, for the life of the patient, in the dynamic process of managing OA;
- accepting that chronic conditions may easily become the classic “heart sink” cases;
- that the “heart sink” scenario should not be allowed to develop by always having access to resources that can add to the management plan, by frequent reassessment of the patient’s condition, by improving pain relief and by giving owners a sense of control over the problem;
- that the whole team can, and arguably should, be involved in the process.
Patients may be presented to the practice with a variety of clinical signs and at any age, including: lameness; stiffness; limping; gait abnormalities (e.g. “bunny hopping” or “crabbing”); scuffing of the nails (forelimb or hindlimb – Figure 3); excessive licking of a limb; swelling around a joint (Figure 4); inability to do one or more certain movements (e.g. jumping, going up and downstairs, getting in and out of the car, getting up, lying down, sitting down); change in exercise tolerance; changes in behaviour (see below). NB. Behavioural changes/problems may be the only sign of pain and disease in an ostensibly healthy animal.
In addition to the standard clinical examination for general health, the whole dog should be examined, not just the limb that appears to be giving the problem. An initial scan with light touch may pick up any gross abnormalities, such as masses or gross differences in muscle atrophy and swollen or deformed joints. Just as importantly, this initial scan will help to pick up areas of allodynia (response to light touch as though it were a painful stimulus). This would be indicative of the animal suffering from a chronic pain state (see below), which would be missed if the limbs were grasped firmly on initial examination. Allodynia can be identified by a shuddering or fasciculation of the affected area in response to light touch and/or by a flinching away from the touch; in severe conditions, and depending on the individual, such touch may also elicit aggression. As a general rule, examination should start at the furthest point from the area that is suspected to be the most painful. As an additional guide, if the left elbow, for example, is the joint suspected to be affected by OA, then start at the ipsilateral hindlimb, because the weight will usually be thrown back onto the contralateral hindlimb, as well as onto the opposite forelimb. The rationale behind this approach is twofold:
- If the most painful area is examined first and the patient is hurt then, effectively, the examination is over, because no further useful information will be gathered; muscles will be tense, joint movement will be restricted and the patient may react at a lower threshold than previously.
- This examination may reveal that the main source of pain is in fact in a different place than first suggested by the initial presentation. For example, forelimb lameness may be the initial presenting sign, but examination may suggest that the hindlimbs, or the lumbar area, is significantly more painful.
Forelimb lameness (except for traumatic injuries) should always prompt the clinician to look at the hindquarters. Given that the dog carries approximately 75% of its weight on its forequarters, hindquarter pain will significantly increase that burden. Weight thrown off the hindlimbs first puts strain on the lumbar muscles and then the forelimbs, causing muscle strain and presumably exacerbating the effects of any pre-existing forelimb pathology. This phenomenon should also be suggested if the dog is having more trouble going upstairs than down, into the car rather than out, and uphill rather than downhill, and/or rises by first sitting up and then obviously hauling its hindquarters off the ground with its forequarters. The examination will then continue by the examination of the joints, examining for: swelling (bony or fluid); bony distortion; heat; crepitus; pain on direct palpation and on palpation above and below the joint. NB. Not all joints with arthritis and not all joints with painful arthritis will show these changes (i.e. the absence of these signs does not rule out arthritis).
Range of movement
This can be difficult to assess and tends to improve on repetition unless the dog finds it painful in which case it may reduce with subsequent attempts. A goniometer will accurately measure range of movement and “normal” ranges of movements for the joints are available. Bear in mind that a reduced range
of movement does not necessarily equate to a painful joint. In particular, most dogs do not take every joint to the extreme of flexion and extension
during normal movement. Full extension of the arthritic/dysplastic hip may elicit a painful response, but does not mean that the dog is inevitably suffering that degree of pain except when that particular movement is carried out. Repeated “testing” of the efficacy of any analgesia by performing this extension on every examination is not only unhelpful but also unnecessary and unkind.
Muscles that are not being used properly will atrophy. A significant clue to the restriction of joint movement by pain or mechanical limitation will be the amount of muscle atrophy that is present in the relevant muscle groups.
This is harder to assess in bilateral lameness and in dogs with cachexia (neoplastic/cardiac) or concurrent disease, such as protein-losing nephropathy/enteropathy/ hepatopathy. Swapping hands so that the same
muscle mass is assessed by both hands (not just the dominant one) makes the assessment clearer since the dominant hand tends to be less sensitive.
The detailed assessment of muscle pain is not usually taught at veterinary
or medical schools. Myofascial pain is a complex area that is outside the remit of this article, but many references are available.1,2 Myofascial trigger points (MFTrPs) are areas in muscle that are hyperirritable loci within taut bands or “knots” in muscle. These bands are painful on compression, can elicit a jump sign (involuntary movement away from the pain), a twitch response in the local muscle and a characteristic referral pattern of pain (described in humans) when compressed. Essentially, they equate to the “knots” in muscles that masseurs and physiotherapists may find when examining muscle. Trigger points arise in response to muscle strain, postural strain, radiculopathy and other sources of somatic and visceral pain. A painful arthritic joint will give rise to painful MFTrPs in the muscles local to the joint. The postural shift which occurs when an animal takes the weight off a limb will also cause trigger points in other muscles (the ones which are now taking the strain), but one would not expect these to be as painful on palpation as those associated with a painful joint. Trigger points appear to arise predictably in certain muscle groups (e.g. painful elbow arthritis will be associated with painful trigger points in triceps, infraspinatus and caudal
trapezius muscles; painful hip arthritis will be associated with painful trigger
points in gluteals, rectus femoris and longissimus muscles). Muscle pain can be widespread and debilitating and will contribute to the suffering caused by OA. The more intense the pain and the longer the duration, the more widespread is the pain referral from muscle.3 Note that MFTrPs are not inflammatory and neither do they equate to “muscle spasm”. They sometimes appear to be refractory to many analgesics, although if the original source of pain is treated they may “settle down” to become “latent” rather than “active” trigger points. Palpation of these trigger points is a practical skill that needs to be demonstrated rather than described.4
Confirmation of OA diagnosis
Confirmation of OA is by radiography. In the dog the radiographic picture is usually associated with an osteophytic reaction (unlike in cats, where osteophyte production is modest by comparison). NB. A confirmation of OA is NOT a confirmation of pain and suffering (although the animal should be given the benefit of the doubt until proved otherwise). Furthermore, the severity of radiographic changes in no way predicts the degree of pain and suffering caused by the arthritis.
- Simons, D. G., Travell, J. G. and Simons, P. T. (1999) In: Travell and Simons’ Myofascial Pain and Dysfunction: The Trigger Point Manual. Volume 1: Upper half of the body. Williams and Wilkins, Baltimore.
- Gerwin, R. D. (1994) Neurobiology of the myofascial trigger point. Ballieres Clinical Rheumatology 8 (4): 747- 762.
- Kellgren, J. H. (1938) Observations on referred pain arising from muscle. Clinical Science 3: 175-190.
- Lindley, S. and Cummings M. (2006) Essentials of western veterinary acupuncture. Blackwells, Oxford.