Osteoarthritic joint pain in dogs – part one: causes and diagnosis

Osteoarthritis (OA) is being increasingly recognised as the most common cause of progressive chronic pain in canines and affects approximately 20% of middle-aged and geriatric dogs (Johnston, 1997). Practitioners treating dogs will therefore inevitably be presented with some affected with OA.

Joint pain in dogs related to osteoarthritis – part 3

Early recognition and diagnosis is essential so appropriate treatments can be started to alleviate the pain associated with the condition. NSAIDs are the mainstay of treatment, although a number of options for these cases are increasingly available.

The first part of this two-part article will discuss the different causes of OA and its diagnosis in dogs, while the second part will focus on non-surgical and surgical management of the condition.

Mechanisms of pain

OA is a complex disease of the whole joint that manifests as joint pain and loss of joint function. The underlying mechanisms that produce OA-related pain are extremely complex and incompletely understood (for reviews, see Schaible, 2012; Zhang et al, 2013; Mantyh, 2014), with changes in sensory processing occurring at all levels of the nervous system, from the periphery to the CNS.

Normal articular cartilage lacks innervation by sensory nerve fibres, therefore pain resulting from OA is thought to originate from activation of sensory nerves in the periosteum, synovial membrane, subchondral bone and bone marrow. However, it is important to understand nerve fibres may undergo sprouting, such that damaged articular cartilage may become innervated by nociceptors following injury and inflammation, contributing to chronic OA-associated pain.

The aetiology of synovitis in OA is also poorly understood, but is associated with high concentrations of pro-inflammatory cytokines, such as tumour necrosis factor alpha, interleukin 6, and interleukin 1 beta in the synovium and joint capsule that contribute to the sensitisation of peripheral nociceptors. Other inflammatory mediators, such as bradykinins, prostaglandins and substance P, are also important in the mechanical sensitisation of joint sensory afferent fibres, leading to enhanced pain on joint movement as well as spontaneous pain, manifesting as constant resting pain that may even occur at night.

Pathological neuronal input from joints affected by OA results in central sensitisation, a hyperexcitability of nociceptive processing in the spinal cord and higher brain centres manifest as secondary mechanical hyperalgesia and allodynia. Human OA patients therefore report widespread pain beyond the OA joint and exhibit lower pain thresholds to pressure around the joint, as well as pain caused by innocuous stimuli such as touch. The extent of widespread pain is very poorly understood in dogs with OA, but given the similarity of the pathology of OA in the two species, widespread pain is also likely in canine OA patients.

Another important change in sensory processing in human patients with OA pain is an imbalance between descending inhibition and facilitation of pain, such that descending influences become predominantly facilitatory rather than inhibitory, contributing to the enhanced pain state.

Advanced OA is also likely to have a neuropathic pain component, as evidence suggests neuronal damage also occurs during the development of OA. This may explain the utility of gabapentin – a drug licensed for management of neuropathic pain states in people – in the management of OA-associated pain in dogs.

Primary and secondary canine OA

OA can be classified as primary or secondary:

• Primary OA (also referred to as idiopathic OA) is typically associated with ageing and is commonly a symmetrical disease affecting, for example, both carpi, stifles or elbows (Innes, 1995).
• Secondary OA is by far the most common form of OA seen in dogs. Causes of secondary OA are listed in Table 1.

Investigating cases

It is important to be aware most cases of canine OA are secondary and therefore the clinical signs exhibited may be a result of either the primary underlying disease process and/or the developing OA. For example, a dog with hip dysplasia and associated hip instability may present initially with a pelvic limb lameness and a “bunny hopping” gait, but may have only very mild radiographic signs of OA. However, as the course of the condition progresses, the developing OA will become the predominant cause of discomfort.

History

OA patients typically present with a variety of signs, including chronic lameness, reluctance to exercise, stiffness after a period of rest or behavioural changes (which can include aggression). Owners may be unaware of the signs of OA and pain in their dog and usually think their pet is just getting old. These factors can culminate in their pets becoming silent sufferers of OA-associated pain.

Practitioners have a responsibility to alleviate this, if at all possible. On the other hand, owners are usually very aware of what their pet can or cannot do, therefore owner observations are important. While acquiring a history, we need to be able to ask appropriate questions regarding their pets’ activities to assist with reaching a diagnosis as owners will often not provide this information without prompting. Such opportunities typically arise during annual routine health check consultations.

Diagnosis

Information gained from appropriate questioning of a dog owner is an invaluable component of diagnosing canine OA. A thorough history relating to other conditions that could present with similar signs, or concurrently, in older patients, must also be obtained as this may influence treatment choices.

A thorough physical examination should be followed by a complete orthopaedic examination. The orthopaedic examination consists of a number of steps and it is worth logically working through them. Distant observation to assess general behaviour and body condition is important. The dog should be observed while walking and trotting (Figures 1).

It is important for practitioners to have their own system of logically working through the orthopaedic examination. With compliant patients, the authors usually begin with the dog standing and palpate to assess muscular symmetry, joint swelling/thickening or effusion, asymmetry and pain responses. They then assess the neck and vertebral column.

Asymmetry can often be used to confirm which leg is most affected, remembering, however, some conditions such as elbow dysplasia may be bilateral, making them feel symmetrical. Following a standing assessment, the authors usually lay the dog on to its side and assess each limb individually. The long bones are palpated to determine whether there is any swelling, inflammation or pain. Each joint is moved (including the joints in the digit) through the complete range of movement to identify any crepitus, pain or abnormalities.

Specific tests are also performed for joints such as the shoulder (for example, abduction), stifle (for example, cranial drawer) and hip. The soft tissues should not be forgotten.

The dog is then turned and the procedure repeated. Once pain has been localised, further tests can be pursued. The repeatability of any pain elicited should be determined. Patience and allowing adequate time is essential. If localising the source of discomfort proves challenging, repeating the examination a few times throughout the day, which necessitates admitting the dog, can be worthwhile. This allows full assessment of the repeatability of any clinical findings. It also allows a staged examination throughout the day, which can be useful in less compliant patients.

Dogs afflicted with OA occasionally present with severe lameness. This may represent a flare up. In these cases it is important to rule out complicating factors such as trauma or infection.

Diagnostic imaging

Radiographs will often be the next stage of investigation. Well-positioned orthogonal radiographs, selected based on the findings of the physical examination, are essential. In some cases, oblique and stressed views may be beneficial.

The radiographic features of OA are listed in Table 2. These features are useful markers for diagnosis, but caution must be employed when using them for staging the severity of the condition.

It is important to remember radiographic evidence of OA, physical examination findings and signs consistent with pain are not well correlated. It is therefore important to read the patient and not the radiographs (Figure 2).

CT and MRI are becoming more readily available investigative tools. As with any diagnostic test it is important to consider whether their use will actually change the clinical management and/or outcome of the condition. CT provides excellent information pertaining to bony changes and mineralisation, but is less useful when assessing soft tissue structures.

MRI is the modality of choice for assessing soft tissue structures (such as menisci, ligaments and tendons). However, the costs associated with its use can be considerable.

Arthroscopy is commonly used during assessment of joints including the shoulder, elbow and stifle. It can also be used in the tarsus and carpus. Arthroscopy allows a thorough evaluation of the cartilage within joints and can be useful in the staging of OA (Figure 3).

Arthrocentesis

Arthrocentesis is a simple, but underused, procedure when striving to reach a definitive diagnosis in cases of OA. Cytological examination allows important differential diagnoses including septic arthritis or immune-mediated polyarthritis to be ruled in or out. In cases of OA, synovial fluid typically demonstrates a mild to moderate increase in mononuclear cell numbers. Where septic arthritis is suspected, culture is indicated (Table 3).

Conclusions

Obtaining a correct diagnosis of OA is fundamental to treatment. Pain on joint manipulation is a cardinal sign of the disease, which can then be confirmed using radiography and further diagnostic tests, if appropriate.