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Osteoarthritis

June 10, 2024

Osteoarthritis (OA, osteoarthrosis or degenerative joint disease) is not a single disease. Rather it is the end result of a variety of patterns of joint failure. To a greater or lesser extent it is always characterised by both degeneration of articular cartilage and simultaneous proliferation of new bone, cartilage and connective tissue.

Etiology

The daily stresses applied to the joints, especially the weight-bearing joints (eg, ankle, knee, and hip), play an important role in the development of osteoarthritis. Most investigators believe that degenerative alterations in osteoarthritis primarily begin in the articular cartilage, as a result of either excessive loading of a healthy joint or relatively normal loading of a previously disturbed joint. External forces accelerate the catabolic effects of the chondrocytes and further disrupt the cartilaginous matrix. Etiological factors for the primary osteoarthritis include the following:

1. Advancing age

With advancing age come reductions in cartilage volume, proteoglycan content, cartilage vascularization, and cartilage perfusion. These changes may result in certain characteristic radiologic features, including a narrowed joint space and marginal osteophytes. However, biochemical and pathophysiologic findings support the notion that age alone is an insufficient cause of osteoarthritis.

Primary osteoarthritis is mostly related to aging. With aging, the water content of the cartilage increases, and the protein makeup of cartilage degenerates. Eventually, cartilage begins to degenerate by flaking or forming tiny crevasses. In advanced cases, there is a total loss of cartilage cushion between the bones of the joints. Repetitive use of the worn joints over the years can irritate and inflame the cartilage, causing joint pain and swelling. Loss of the cartilage cushion causes friction between the bones, leading to pain and limitation of joint mobility. Inflammation of the cartilage can also stimulate new bone outgrowths (spurs, also referred to as osteophytes) to form around the joints. Osteoarthritis occasionally can develop in multiple members of the same family, implying a hereditary (genetic) basis for this condition.

2. Obesity

Obesity increases the mechanical stress in a weight-bearing joint. It has been strongly linked to osteoarthritis of the knees and, to a lesser extent, of the hips. Higher body mass index (BMI) at year 1 and a significant increase in BMI over 15 years is predictor of bilateral knee pain at year. In addition to its mechanical effects, obesity may be an inflammatory risk factor for osteoarthritis. Obesity is associated with increased levels (both systemic and intra-articular) of adipokines (cytokines derived from adipose tissue), which may promote chronic, low-grade inflammation in joints.

3. Other causes

Trauma or surgery (including surgical repair of traumatic injury) involving the articular cartilage, ligaments, or menisci can lead to abnormal biomechanics in the joints and accelerate osteoarthritis. Although repairs of ligament and meniscal injuries usually restore joint function, osteoarthritis has been observed 5-15 years afterward in 50-60% of patients. Insults to the joints may occur even in the absence of obvious trauma. Microtrauma may also cause damage, especially in individuals whose occupation or lifestyle involves frequent squatting, stair-climbing, or kneeling. Muscle dysfunction compromises the body’s neuromuscular protective mechanisms, leading to increased joint motion and ultimately resulting in osteoarthritis. This effect underscores the need for continued muscle toning exercises as a means of preventing muscle dysfunction.Valgusmalalignment at the knee has been shown to increase the incidence and risk of radiographic progression of knee osteoarthritis involving the lateral compartment.

4. Genetics

A hereditary component, particularly in osteoarthritis presentations involving multiple joints, has long been recognized. Several genes have been directly associated with osteoarthritis, and many more have been determined to be associated with contributing factors, such as excessive inflammation and obesity. Genes in the BMP (bone morphogenetic protein) and WNT (wingless-type) signaling cascades have been implicated in osteoarthritis. Two genes in particular,GDF5 (growth and differentiation factor 5) and FRZB (frizzled related protein) have been identified in the articular cartilage in animal studies and share a strong correlation with osteoarthritis. Genetic factors are also important in certain heritable developmental defects and skeletal anomalies that can cause congenital misalignment of joints. These may result in damage to cartilage and the structure of the joint.

Etiological factors for secondary OA:

A. Miscellaneous

Frostbite

Caisson’s disease

Hemoglobinopathies

B. Congenital or developmental

Localized diseases: Legg-Calve ´-Perthes, congenital hip dislocation, slipped epiphysis

Mechanical factors: unequal lower extremity length, valgus/ varus deformity, hypermobility syndromes

Bone dysplasias: epiphyseal dysplasia, spondyloepiphyseal dysplasia, osteonychondystrophy

C. Metabolic

Ochronosis (alkaptonuria)

Hemochromatosis

Wilson’s disease

Gaucher’s disease

D. Endocrine

Acromegaly

Hyperparathyroidism

Diabetes mellitus

Obesity

Hypothyroidism

E. Calcium deposition diseases

Calcium pyrophosphate dihydrate deposition

Apatite arthropathy

F. Other bone and joint diseases

Localized: fracture, avascular necrosis, infection, gout

Diffuse: rheumatoid (inﬂammatory) arthritis, Paget’s disease, osteopetrosis, osteochondritis

G. Neuropathic (Charcot joints)

H. Endemic

Kashin-Beck

Mseleni

Pathogenesis

OA is a chronic degenerative disorder related to but not caused by aging, as there are people well into their nineties who have no clinical or functional signs of the disease. As a person ages, the water content of the cartilage decreases due to a reduced proteoglycan content, thus causing the cartilage to be less resilient. Without the protective effects of the proteoglycans, the collagen fibres of the cartilage can become susceptible to degradation and thus exacerbate the degeneration.

one changes, together with the inflammation, can be both painful and debilitating.

Classification

· Idiopathic

· Secondary

Localization of OA

1. Hands:

Heberden’s and Bouchard’s nodes (nodal),

erosive interphalangeal arthritis,

1st carpometacarpal joint

2. Feet:

hallux valgus,

hallux rigidus,

contracted toes (hammer/cock-up toes),

talonavicular

3. Knee:

Medial compartment

Lateral compartment

Patellofemoral compartment

4. Hip:

Eccentric (superior)

Concentric (axial, medial)

Diffuse (coxaesenilis)

5. Spine:

Apophyseal joints

Intervertebral joints (disks)

Spondylosis (osteophytes)

Ligamentous (hyperostosis, Forestier’s disease, diffuse idiopathic skeletal hyperstosis)

6. Other single sites, e.g., glenohumoral, acromioclavicular, tibiotalar, sacroiliac, temporomandibular

Сlinical forms

1. Polyarthritis (5 and more joints)

2. Oligoarthritis (2-4 joints)

3. Monoarthritis

4. In combination with spinal osteochondrosis, spondyloarthrosis.

Synovitis:

– present;

– absent.

Kellgren-Lawrence XR-Grading Scale

Grade I: doubtful narrowing of joint space and possible osteophytic lipping.

Grade II: definite osteophytes, definite narrowing of joint space.

Grade III: moderate multiple osteophytes, definite narrowing of joints space, some sclerosis and possible deformity of bone contour.

Grade IV: large osteophytes, marked narrowing of joint space, severe sclerosis and definite deformity of bone contour.

The functional ability of the patient:

1. Limited ability to work temporarily (FA I).

2. Lost working capacity (FA II).

3. Needs constant care (FN III).

Clinical features

Clinical symptoms of OA may include

· joint pain

· stiffness

· “crepitus” of joints

· Inflammation

The main symptom is acute pain, causing loss of ability and often stiffness. “Pain” is generally described as a sharp ache, or a burning sensation in the associated muscles and tendons. OA can cause a crackling noise (called “crepitus“) when the affected joint is moved or touched, and patients may experience muscle spasm and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Humid and cold weather increases the pain in many patients.The patient increasingly experiences pain upon weight bearing, including walking and standing. Due to decreased movement because of the pain, regional muscles may atrophy, and ligaments may become more lax.

Periarticular muscle atrophy may be due to disuse or reﬂex inhibition of muscle contraction. Physical examination of the OA joint may reveal localized tenderness and bony or soft tissue swelling. Palpation may reveal some warmth over the joint.

In some patients with OA, joint pain may be due to synovitis. In advanced OA, histologic evidence of synovial inﬂammation may be as marked as that in synovium of a patient with rheumatoid arthritis. Synovitis in OA may be due to phagocytosis of shards of cartilage and bone from the abraded joint surface (wear particles), release from the cartilage of soluble matrix macromolecules, or crystals of calcium pyrophosphate or hydroxyapatite. In other cases, immune complexes, containing antigens derived from cartilage matrix, may be sequestered in collagenous tissues of the joint, leading to lowgrade chronic synovitis. In contrast, in the earlier stages of OA, synovial inﬂammation may be absent, suggesting that the joint pain is due to one of the other factors mentioned above.

The joints most frequently involved are those of the spine, hips, knees and hands. The disease is confined to one or only a few joints in the majority of patients. Common patterns of joint of primary generalised OA with prominent involvement of the knees and hands (distal interphalangeal joints, proximal interphalangeal joints, carpometacarpal joints of thumbs) involvement, as well include next types:

· nodal

· non-nodal

SIGNS AND SYMPTOMS CHARACTERISTIC OF OSTEOARTHRITIS IN THE MOST FREQUENTLY AFFECTED JOINTS:

Hands: squaring of the base of the hand; medial and lateral deviation at the DIPs (distal interphalangeal joint) and PIPs (proximal interphalangeal joint), affects:

· DIPs (Heberden nodes)

· PIPs (Bouchard nodes)

· CMC (carpometacarpal joints)

Bouchard’s nodes are hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints (the middle joints of fingers or toes). Seen commonly in osteoarthritis, they are caused by formation of calcific spurs of the articular (joint) cartilage. Bouchard’s nodes are comparable in presentation to Heberden’s nodes, similar osteoarthritic growths on the distal interphalangeal joints, but are significantly less common.

Heberden’s nodes are hard or bony swellings that can develop in the distal interphalangeal joints (DIP). They are caused by formation of osteophytes (calcific spurs) of the articular (joint) cartilage in response to repeated trauma at the joint.

Classification Criteria for Osteoarthritis of the Hand:

Hand pain, aching, or stiffness and 3 or 4 of the following features:

Hard tissue enlargement of 2 of 10 selected hand joints*
Metacarpophalangeal joint swelling in 2 joints
Hard tissue enlargement of 2 distal interphalangeal joint joints
Deformity of 1 of 10 selected hand joints

* The 10 selected joints are the second and third distal interphalangeal (DIP), the second and third proximal interphalangeal, and the first carpometacarpal joints of both hands. This classification method yields a sensitivity of 94% and a specificity of 87%.

MCP = metacarpophalangeal.

Knees:Patellofemoral joint symptoms worse on the stairs than on the flat; varus changes with medial compartment disease, valgus with lateral; Baker’s (popliteal) cysts and tenderness of the pes anserine bursa are common.

EULAR Criteria of knee OA

–Persistent Knee pain (1 month, most days)

–Limited Morning Stiffness (< 30 min.)

–Impaired Function

–Crepitus

–↓ ROM LR

–Bony enlargement

Criteria for Classification of Osteoarthritis (OA) of the Hip

Hip pain and at least 2 of the following 3 features:

ESR<20 mm/hour
Radiographic femoral or acetabular osteophytes
Radiographic joint space narrowing (syperior, axial, and/or medial)

*This classification method yields a sensitivity of 89% and a specificity of 91%. ESR = erythrocyte sedimentation rate

Cervical spine: Local spine pain, muscle spasm, and limited motion (lateral flexion and extension); radicular pain with pain, sensory loss or muscle weakness/atrophy ierve root distribution; cervical myelopathy with long tract signs, bladder dysfunction

Lumbar spine: Local pain and muscle spasm, limited extension, buttock pain, worse in PM, but not nocturnal; radicular pattern with pain, sensory and motor changes in nerve root distribution; spinal stenosis pattern pain with back/leg pain with standing, walking relieved by sitting

Laboratory and instrumental findings

The diagnosis of OA is usually based on clinical and radiographic features. In the early stages, the radiograph may be normal but joint space narrowing becomes evident as articular cartilage is lost. Other characteristic ﬁndings include subchondral bone sclerosis, subchondral cysts, and osteophytosis. A change in the contour of the joint, due to bony remo-deling, and subluxation may be seen. Although tibiofemoral joint space narrowing has been considered to be a radiographic surrogate for articular cartilage thinning, joint space narrowing alone does not accurately indicate the status of the articular cartilage in patients with early OA who do not have radiographic evidence of bony changes (e.g., subchondral sclerosis or cysts, osteophytes).

The Kellgren-Lawrence grading systemis radiological classification osteoarthritis. It is based on x- rays and consists of normal, Grade I, Grade II, Grade II and Grade IV.This categorical scale incorporates important radiographic features of osteoarthritis:

· Joint space narrowing – bone is visible on x-ray but the articular cartilage that covers it is not. A normal joint therefore appears to have a space between the bones. Any decrease in space implies a reduction in cartilage cover.

· Osteophytes – small bony projections that from around joint margins. They are responsible for limiting range of motion and can cause pain.

· Sclerosis – this means ‘hardening’ and is a sign of osteoarthritis, seen as increased white areas in the bone at the joint margins.

Magnetic resonance imaging and ultrasonography have not been sufﬁciently validated to justify their routine clinical use for diagnosis of OA or monitoring disease progression. The diagnosis of OA is usually based on clinical and radiographic features. In the early stages, the radiograph may be normal, but joint space narrowing becomes evident as articular cartilage is lost. Other characteristic radiographic findings include subchondral bone sclerosis, subchondral cysts, and osteophytosis. A change in the contour of the joint, due to bony remodeling, and subluxation may be seen.

Treatment

No single treatment is considered sufficient for managing OA. The consensus is that a multifaceted approach that involves both nonpharmacological and pharmacological therapies should be used, especially for weight-bearing joints, where mechanics and lifestyle play a significant role in determining the symptoms.Nonpharmacological treatments should form the basis of any OA regimen, but they often are underutilized and underemphasized. The Figure shows a flowchart that summarizes the general strategy in OA management.

EULAR Evidence-based Recommendations

Non-pharmacological Therapy: include

· exercise

· body mass index (BMI),

· prevention of injury,

· misalignment (e.g. orthesis)

· local measures (e.g. thermal modalities, transcutaneous electrical nerve stimulation [TENS], acupuncture).

Among these treatment options, exercise may help by improving motion and strengthening muscles, weight loss could reduce disease progression, especially in overweight patients with knee or hip OA, while prevention of injury may help to prevent the development of OA.

Strength of Recommendation for Hand, Knee Osteoarthritis Interventions

SOR Intervention:

A – Glucosamine, chondroitins sulphate, exercise, education,

paracetamol, conventional NSAIDs, coxibs, topical NSAIDs,

topical capsaicin

B – Diacerin, ASU, nutrients, herbal remedies, telephone, acupuncture,

laser, pulsed EMF, opioid analgesics, antidepressants

C – Minerals/vitamins, sex hormones

Strength of recommendation (SOR) is based on both evidence and expert opinion.

A = fully recommended, B = strongly recommended, C = moderately recommended.

ASU = avocado soybean unsaponifiable; EMF = extracellular fragment matrix;

NSAID = non-steroidal anti-inflammatory drug.

Recommendations for the Management of Hip Osteoarthritis

Combination of non-pharmacological and pharmacological

treatment modalities.

Treatment should be tailored according to:

hip risk factors;
general risk factors;
pain intensity;
disability and handicap;
degree of structural damage;
wishes and expectations of the patient.

A. Regular education, exercise, appliances and weight reduction if obese

or overweight.

B. Paracetamol (up to 4g/day) is the oral analgesic of first choice, and is the

preferred long-term oral analgesic.

C. NSAIDs, at the lowest effective dose, in paracetamol non-responders. In patients

with increased GI risk, non-selective NSAIDs plus a gastro-protective agent or

coxibs according to the GI risk.

D. Opioid analgesics, with or without paracetamol.

E. SySADOAs (glucosamine, chondroitins 4 and 6 sulphate, diacerin, ASU and

hyaluronic acid) have symptomatic effect and low toxicity.

F. Intra-articular steroid injections (guided by ultrasound or X-ray) in patients with a refractory flare.

G. Consideration of osteotomy and joint-preserving surgical procedures, preferably

in young adults (dysplasia or varus/valgus deformity).

H. Joint replacement with radiographic evidence + refractory pain and disability.

ASU = avocado soybean unsaponifiable; GI = gastrointestinal; NSAID = non-steroidal anti-inflammatory drug; SySADOAs = symptomatic s

Surgery

If the above management is ineffective, joint replacement surgery may be required. Individuals with very painful OA joints may require surgery such as fragment removal, repositioning bones, or fusing bone to increase stability and reduce pain. Surgical intervention for osteoarthritis of the knee may be no better than placebo at relieving symptoms.

Prognosis

The most common course of OA is an intermittent, progressive worsening of symptoms over time, although in some patients the disease stabilizes. Prognosis also varies depending on which joint is involved.

Factors associated with progression of OA: