Canine Osteoarthritis: How the Disease Develops, Why It Causes Pain, and How It Is Managed

Article Summary

• Canine osteoarthritis is a progressive, degenerative joint disease involving cartilage breakdown, subchondral bone remodelling, persistent synovial inflammation and altered pain processing.
• It is the most common chronic joint disorder in dogs, with radiographic evidence reported in around 20% of dogs over one year of age in UK primary-care populations. [1]
• The condition is recognised as a whole-joint disease in which structural, inflammatory and neurological mechanisms interact to drive chronic pain and reduced mobility.
• Pain arises not only from joint degeneration but also from inflammatory mediators, peripheral sensitisation and central sensitisation within the nervous system.
• Radiographic severity does not always correlate with clinical discomfort because imaging does not capture inflammation or altered pain processing.
• Effective management typically requires a multimodal approach addressing biomechanics, inflammation and nociceptive pathways.

Clinical Overview

This page is written for pet owners and caregivers who want a more detailed understanding of how canine osteoarthritis develops and why it causes pain, as well as for veterinary professionals seeking a concise clinical overview of the mechanisms involved.

Canine osteoarthritis is a progressive joint condition involving cartilage degeneration, bone remodelling, persistent synovitis and altered pain signalling. It is the most common chronic joint disorder in dogs and a leading cause of long-term pain and reduced mobility. Prevalence increases with age, but structural joint changes may be present earlier than clinical signs are recognised. Disease mechanisms involve cartilage, bone, synovium and pain pathways, which together drive chronic discomfort and functional decline.

In UK primary-care populations, around 20% of dogs over one year of age show radiographic evidence of osteoarthritis, with prevalence increasing as dogs age. [1] Joint changes can also develop earlier than many expect. In one study of young dogs with radiographic changes, only around one third of owners had recognised clinical signs before assessment, showing how easily early osteoarthritis can be missed. [2]

Multiple interacting risk factors contribute to disease development, including previous joint injury, orthopaedic disease, and body weight. [3] Genetic influences on joint conformation and cartilage biology have also been identified, further supporting the multifactorial nature of osteoarthritis development. [4]
Osteoarthritis affects more than joint surfaces. Over time, it influences mobility, behaviour, stamina, and daily activity. Reduced willingness to exercise, difficulty with movement, and changes in interaction patterns are frequently reported in affected dogs. [10,11]

Osteoarthritis is now understood as a whole-joint disease rather than simple "wear and tear". Cartilage degeneration, remodelling of underlying bone, persistent synovial inflammation, and alterations in pain processing all contribute to the long-term discomfort and functional decline associated with the condition. [8,14] In referral populations, 41.5% of elbows assessed have shown radiographic signs of osteoarthritis, underlining how commonly structural change is identified once dogs are examined more closely. [23]

In UK primary-care data, osteoarthritis was estimated to affect around 11% of a dog's total lifespan once diagnosed. [1]
Osteoarthritis develops gradually, and early changes are often subtle. In research settings, osteoarthritis pain is typically defined as long-standing, with some studies requiring at least a six-month history of mobility impairment before dogs are included. This reflects the chronic nature of the condition. [20]

Dogs compensate well, and progressive reduction in activity may be mistaken for normal ageing. Understanding how the disease develops, and how pain emerges from structural and neurological changes, helps explain why management usually involves several coordinated approaches rather than a single treatment.

Pathophysiology of Canine Osteoarthritis

Osteoarthritis affects the entire joint, causing cartilage breakdown, bone remodelling and persistent inflammation that together drive pain and stiffness. In a large clinical review of nearly 5,000 dogs and over 6,000 joints, elbow osteoarthritis was most common, affecting 57.4% of elbows assessed. Shoulder osteoarthritis was seen in 39.2%, stifle in 36.4% and hip in 33.1%. [23]

When both left and right joints were available on radiographs, 31.6% showed osteoarthritis in both joints, while 52.1% were bilaterally free of osteoarthritis. This highlights how uneven, but also how often symmetrical, the condition can be within the same dog. [23]

Early Cartilage Degeneration

Early osteoarthritis begins with subtle changes in cartilage structure that reduce its ability to absorb load and repair itself. Healthy cartilage is made up of a dense network of collagen fibres and water-retaining proteoglycans that give it strength and resilience under pressure. In the early stages of osteoarthritis, this internal structure begins to change before any obvious structural damage can be seen. Proteoglycan content gradually decreases. As a result, the cartilage softens, becomes more permeable, and slowly loses some of its ability to distribute load evenly across the joint surface.

Chondrocytes, the cells responsible for maintaining cartilage, initially respond to mechanical stress and inflammatory signals by increasing their activity to repair the damaged matrix. This repair response is limited and cannot be sustained indefinitely. When mechanical strain and inflammatory mediators continue, the balance shifts. Matrix breakdown begins to exceed matrix production. The cartilage surface starts to fray, a process known as fibrillation, with fine cracks forming that can extend into deeper layers over time.

Progressive Structural Joint Damage

As osteoarthritis progresses, cartilage damage deepens, inflammation increases, and underlying bone becomes exposed and stressed. Fragments of broken-down cartilage enter the synovial fluid and stimulate an immune response that sustains inflammation. With ongoing damage, cartilage can be worn away completely, exposing the underlying subchondral bone. In older dogs assessed radiographically, more advanced osteoarthritic change was recorded in 16.4% of elbows, illustrating how structural damage can become pronounced over time. [23] Comparable advanced change was documented in 10.4% of hips in the same clinical population. [23]

Cartilage itself contains no blood vessels or nerves. This means the damaged cartilage does not directly cause pain. Instead, pain arises from inflammation, pressure within the bone, and activation of pain-sensitive structures in surrounding joint tissues. [14] Understanding this helps explain why visible cartilage loss on X-ray does not always match how uncomfortable a dog appears.

Subchondral Bone Remodelling

Bone beneath the cartilage becomes denser and remodelled, contributing both to structural change and pain generation. The bone beneath the cartilage, known as subchondral bone, also changes as osteoarthritis progresses. It undergoes continuous remodelling throughout the course of the disease. In response to altered load distribution and ongoing inflammatory signalling within the joint, this bone can become denser, a process called sclerosis that is visible on radiographs. At the edges of the joint, new bone may form as osteophytes, often referred to as bone spurs. These are generally considered adaptive responses to joint instability and altered biomechanics.

Unlike cartilage, subchondral bone contains a rich supply of nerves and blood vessels. Increased pressure within the bone, small stress fractures, and bone marrow lesions can all act as sources of pain in osteoarthritic joints. These changes help explain why a dog may experience significant discomfort even when cartilage loss on imaging appears limited. [14] They also reinforce the idea that osteoarthritis affects the joint as a whole organ system, rather than a single tissue.

Ongoing Joint Inflammation (Synovitis)

Persistent inflammation within the joint lining sustains both structural damage and increased pain sensitivity. The synovial membrane, which lines the joint and produces lubricating synovial fluid, can become persistently inflamed, a state known as synovitis. When fragments of damaged cartilage enter the joint fluid, they activate both local synovial cells and immune cells that move into the area. These cells release pro-inflammatory cytokines, including interleukin-1β and tumour necrosis factor-α. These signalling molecules drive further cartilage breakdown and increase the sensitivity of nearby pain-sensing nerve endings.

In osteoarthritis, inflammation is not a brief protective reaction. Instead it becomes a sustained biological process within the joint. Continued production of inflammatory mediators accelerates structural damage while also heightening tissue sensitivity, reinforcing the link between degeneration and pain. [14]

A self-perpetuating cycle develops. Cartilage damage promotes inflammation, inflammation accelerates additional cartilage damage, and both processes contribute to ongoing pain signalling. Concentrations of nerve growth factor within the inflamed joint also rise, further amplifying pain pathways. The role of nerve growth factor in pain sensitisation is explored in the following section.

Biomechanical Consequences of Osteoarthritis

Structural joint changes alter load distribution and movement patterns, leading to compensation and muscle loss. As cartilage thins, subchondral bone stiffens, and osteophytes form, the way the joint moves changes. Range of motion decreases, and movement becomes less smooth. Load is distributed less evenly across the joint surface, placing greater stress on remaining cartilage and nearby soft tissues. In force-plate studies, dogs with osteoarthritis have been shown to place around 10–15% less weight on an affected limb. This difference can be measured even when lameness looks relatively mild. [14] Over time, this altered mechanical environment can place ongoing strain on the joint.

Periarticular muscle atrophy develops as dogs instinctively reduce weight-bearing on painful limbs. With less muscular support around the joint, stability can decline further, making controlled movement more difficult.

In some cases, pain-related changes in gait shift weight onto other limbs. When a dog consistently favours one side, compensating joints may experience increased mechanical load. Over time, this repeated stress is thought to contribute to osteoarthritic changes in additional joints. In this way, biomechanical adaptations become part of the wider disease process rather than simply a short-term response to discomfort.

In referral data, around one third of dogs with elbow osteoarthritis had changes in both elbows. When both sides are affected, compensation becomes more complex and can influence overall movement patterns. [23]

Mechanisms of Pain in Canine Osteoarthritis

Professor B. Duncan Lascelles BVSc PhD CertVA DSAS(ST) Dipl ECVS MRCVS, a veterinary pain specialist and lead author on international pain management guidelines, has noted that assessing pain in dogs with osteoarthritis requires more than radiographic evaluation. Clinical signs, owner observations and validated pain scoring tools each contribute to a fuller picture of how a dog is affected, explaining why pain levels and imaging findings frequently do not align. [6,21]

Osteoarthritis pain arises from inflammation, bone stress and long-term changes in how the nervous system processes signals. This layered complexity helps explain why pain severity often does not match the degree of structural change visible on X-ray. A review of the research in this area screened 3,697 published papers and identified 117 suitable canine osteoarthritis studies. Across those studies, outcome measures were used 618 times, with a median of four different measures per study. This variation helps explain why imaging findings and clinical signs do not always line up neatly. [13]

One reason pain and imaging findings can be hard to compare across studies is that researchers often measure outcomes in different ways. In that review, 71% of the measures assessed were used in only one study, and only 10 were reported as validated. This helps explain why consistent tools are recommended for tracking change over time. [13]

For this reason, osteoarthritis pain reflects more than visible structural damage alone. It represents the combined effect of tissue injury, inflammation, altered nerve sensitivity, and adaptive changes within the central nervous system

Inflammation and the Activation of Pain Signals

Inflammatory chemicals lower the threshold at which nerve endings trigger pain signals. The initial source of pain in osteoarthritis is the activation of nociceptors, which are specialised pain-sensing nerve endings located in the synovium, joint capsule, surrounding soft tissues, and the bone beneath the cartilage. These nerve endings respond to mechanical strain, inflammatory substances, and chemical signals that are produced within the diseased joint.

One important contributor is prostaglandin E2, a compound generated through cyclooxygenase enzymes in inflamed synovial and periarticular tissues. Prostaglandin E2 lowers the activation threshold of nociceptors and increases how frequently they fire. As a result, movements or pressures that would normally be tolerated can begin to trigger pain signals. [18].

This process is known as peripheral sensitisation. It helps explain why an inflamed joint may feel painful even during everyday activities such as walking, standing, or rising from rest. In controlled comparisons, dogs with osteoarthritis showed pain sensitivity levels that were around 25–30% lower than healthy dogs, meaning less pressure was needed to trigger discomfort. [20]

The Role of Nerve Growth Factor in Pain Sensitisation

Nerve growth factor (NGF) plays a central role in osteoarthritic pain by increasing sensitivity within affected joints. It is produced by synovial cells, cartilage cells, and immune cells as part of the inflammatory response. NGF binds to a specific receptor called tropomyosin receptor kinase A, or TrkA, which is found on the endings of pain-sensing nerves within joint tissues.

When NGF binds to this receptor, it increases the sensitivity of these nerve endings. It lowers the threshold at which they are activated and increases the activity of molecules involved in transmitting pain signals. Over time, NGF can also contribute to structural changes in sensory nerves, including an increase in nerve fibre density around the joint. The overall result is a joint that becomes more responsive to pain stimuli.

As NGF acts upstream of several sensitisation pathways, it has been identified as a therapeutic target in veterinary pain management. Monoclonal antibody approaches are designed to bind circulating NGF and reduce its interaction with pain-sensing nerve endings within the joint.

Central Sensitisation: How Chronic Pain Alters the Nervous System

Persistent pain signals from an osteoarthritic joint do not simply travel unchanged to the brain. Over time, ongoing input from the affected joint can lead to changes within the central nervous system, particularly in the spinal cord, where incoming pain signals are first processed.

These changes include increased signal transmission, reduced natural dampening of pain signals, and activation of pathways that were previously less active. The result is known as central sensitisation, a state in which the spinal cord and brain become more responsive to sensory input [22,23]. Pain can feel more intense, sensitivity may extend beyond the original joint, and stimuli that would not normally be painful can start to cause discomfort.

Research has demonstrated widespread somatosensory sensitivity in dogs with naturally occurring osteoarthritis, consistent with central sensitisation [22]. Once established, this increased central responsiveness can persist even if joint inflammation is reduced. In this situation, pain becomes partly maintained by changes within the nervous system itself rather than by joint damage alone.

Why Pain Does Not Always Match X-Ray Findings

Radiographs capture bony changes such as osteophytes, sclerosis, and joint space narrowing, but they cannot show synovitis, soft tissue inflammation, bone marrow lesions, or the extent of nervous system sensitisation. These factors all contribute to pain [13].

A dog with relatively mild radiographic changes may still experience significant discomfort if central sensitisation is present. Conversely, another dog with more extensive osteophyte formation may appear comparatively comfortable if inflammation is limited and pain processing remains more stable. This variation highlights why clinical assessment and functional evaluation are as important as imaging findings when evaluating osteoarthritis.

How Chronic Pain Affects Behaviour and Daily Life

Dogs living with chronic pain may show reduced spontaneous movement, altered resting positions, withdrawal from interaction, and changes in temperament.

Compensatory movement patterns, such as shifting weight away from a painful limb, change how muscles are used and how joints are loaded. Over time, this can lead to muscle loss, reduced joint awareness, and uneven weight distribution across the body. These secondary changes reinforce the importance of viewing osteoarthritis not only as a problem within a single joint, but as a long-term pain condition that affects the whole musculoskeletal system.

Rationale for Multimodal Management

As osteoarthritis pain has multiple causes, effective management requires combining complementary approaches, which are outlined below.

Weight Management and Exercise

Structural and biomechanical factors are addressed through weight management and appropriate exercise. Excess body weight increases the load placed on articular cartilage and contributes to low-grade systemic inflammation through adipose-derived cytokines [5,6]. Reducing body weight lowers mechanical stress on joints and decreases inflammatory drive. In controlled studies, long-term dietary restriction has also been associated with delayed onset and reduced severity of osteoarthritis [7].

In a 16-week study of 14 obese dogs with osteoarthritis, improvements in lameness were seen once dogs had lost around 6.10% of their body weight. Objective gait improvements were also recorded once weight loss reached about 8.85%, showing that even moderate weight reduction can make a measurable difference [15].

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

Synovial inflammation and prostaglandin-mediated pain are primarily targeted with non-steroidal anti-inflammatory drugs. NSAIDs inhibit cyclooxygenase enzymes, which reduces prostaglandin production in inflamed tissues. This helps decrease peripheral sensitisation and moderates inflammatory activity within the joint [18]. In UK primary-care data, around 75% of dogs diagnosed with osteoarthritis were advised to use pain-relief medication, reflecting how central pain management is to clinical care [1].

Anti-NGF Monoclonal Antibody Therapy

Monoclonal antibody approaches targeting NGF are included within contemporary multimodal management strategies for canine osteoarthritis. By reducing NGF activity, these therapies aim to decrease peripheral sensitisation and may help limit downstream amplification of pain signals. Their use is guided by veterinary assessment and is typically considered alongside weight management, exercise modification, and other analgesic strategies in accordance with consensus recommendations. [14,21].

Additional Pain Relief for Central Sensitisation

Central pain processing may require additional support in dogs with established chronic pain. Adjunctive analgesics such as amantadine act on NMDA receptors involved in central sensitisation [19], addressing a component of pain that peripheral treatments alone may not fully control.

Rehabilitation and Physiotherapy

Rehabilitation and physiotherapy help counteract the musculoskeletal consequences of chronic pain, including muscle loss, reduced range of motion, and altered gait mechanics [16,17]. Strengthening supportive musculature and improving movement patterns can reduce secondary mechanical stress on affected joints.

Environmental Modifications

Environmental modifications can also reduce daily joint strain. Ramps, supportive bedding, and non-slip flooring lower the physical demands placed on compromised joints and may help reduce episodes of increased discomfort

Together, these approaches address structural, inflammatory, and neurological dimensions of the disease. Their combined use reflects current consensus guidance on multimodal management in canine osteoarthritis. [14,21]

Long-Term Disease Course

Osteoarthritis requires ongoing monitoring and adjustment of care as structural and pain mechanisms evolve across the disease course. Its progression is gradual but variable, and effective management requires an understanding of how symptoms fluctuate over time. The disease does not typically worsen in a straight line. Instead, it tends to move through periods of relative stability interspersed with episodes of increased discomfort.

Recognising this pattern helps set realistic expectations. Day-to-day variation does not necessarily indicate rapid structural deterioration, just as temporary improvement does not mean the underlying disease has resolved. Long-term care therefore focuses on monitoring functional change, responding appropriately to flare-ups, and adjusting management strategies as the condition evolves.

Why Symptoms Fluctuate

Day-to-day variation in inflammation and nerve sensitivity causes natural symptom fluctuation. These fluctuations are linked to ongoing variations in joint inflammation, bone stress, and nerve sensitivity. Factors such as weather, activity levels, minor strains, or concurrent illness can all influence how a dog feels on a given day. This type of variability is a recognised feature of osteoarthritis and does not necessarily indicate sudden worsening of the underlying joint structure.

Understanding Flare-Ups

Flare-ups reflect temporary increases in joint inflammation rather than sudden structural collapse. These episodes usually reflect temporary increases in joint inflammation and heightened sensitivity of pain-sensing nerves within the joint. They may follow unusual exertion or environmental influences such as damp or cold conditions, although a clear trigger is not always identified. Flare-ups often settle over days to weeks as inflammation reduces, but the underlying joint changes associated with osteoarthritis remain present.

Monitoring Osteoarthritis Over Time

Tracking functional change over time is more informative than imaging alone when assessing progression. Changes in activity patterns, mobility, and interaction often provide earlier indicators of progression than imaging alone [9,10,12]. Validated owner questionnaires, such as the Canine Brief Pain Inventory and the Liverpool Osteoarthritis in Dogs instrument, offer structured tools for tracking functional change and identifying clinically meaningful treatment response over time [10,11,12,22]. Radiographs remain useful for assessing structural progression, but they do not directly measure pain burden or day-to-day impact.

Why Treatment Plans Change Over Time

As osteoarthritis evolves, management strategies must adapt to shifting pain mechanisms and structural changes. Approaches that are sufficient in earlier stages may need adjustment as the condition evolves or as clinical needs shift. Regular reassessment helps ensure that management remains aligned with the current structural changes and pain mechanisms affecting the dog.