Osteoarthritis: A review for the primary physician
The Diagnosis of Osteoarthritis - by drdoc on-line

An Update
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Osteoarthritis (OA) has in the past been considered a predominately degenerative joint disease, affecting more people than any other arthritis. It is characterized by progressive loss of cartilage and bony margin overgrowth. However, it is now realized that the problem is not simply a degenerative cartilage disorder, but a problem of all the tissues involved in maintaining joint stability - the functional joint unit. In addition, there is no doubt that inflammation and synovitis is present in a significant percentage of patients, and indeed, a more aggressive form, erosive osteoarthritis may occur, associated with significant synovitis, and may be confused with inflammatory arthritis, such as rheumatoid arthritis.

The problem is acquired as a consequence of metabolic, genetic, mechanical and other influences. The involvement by the disease on the cartilage, results in secondary effect on the joint capsule, synovium, and periosteal nerve endings. It is these processes that result in pain, with further impact by stress, depression or other psychological factors that influence chronic pain.

The cartilage consists of predominantly collagen type 2 fibres linked by covalent bonds, conferring tensile strength. The matrix of the cartilage is formed by the chondrocytes which are embedded within it. The matrix consists of proteoglycans and non collagenous glycoproteins. Within the matrix, is water, tightly bound to the glycoprotein macromolecules. The chondrocytes get their nutrition from the surrounding fluid. The chondrocytes communicate via the fluid within the matrix by diffusion. The macromolecules give the cartilage the capacity for reversible deformation. They are hydrophilic and allow water molecule adherence between the collagen fibrillary network. The largest glycoprotein molecule is aggrecan. This consists of glycosaminoglycan chains predominantly made of keratan sulphate (KS), N-Acetyl glucosamine-galactose sulphated dimer, and chondroitin sulphate (CS), a dimer of N-acetyl galactosamine and glucuronic acid.

In disease there is loss of matrix, release of cytokines including IL-1, TNF and mixed metalloproteinase's as well as prostaglandins by the chondrocytes. Fibrillation of the cartilage surface and attempted repair with osteophyte formation then occurs. The adjacent synovium is frequently observed to be inflamed and symptoms of inflammation, with rest pain and stiffness and findings of swelling, heat of joints and effusions may be present.

The incidence of OA is not an inevitable consequence of ageing, although it is more prevalent the older one gets, and will affect about 80% of citizens over age 65. Other aggravating factors include obesity, gender - females, post menopause, Caucasian race, trauma, sports injuries, over-use syndromes and most importantly, family history.

The disease may be classified in several ways, but most commonly we divide it into primary or secondary OA. ( Table 1).

The diagnosis may be either clinical or radiological. It is important to realize that there is poor correlation between symptoms and radiological appearance.

 

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Clinical: History and Examination.

The clinical method remains the most important aspect of the assessment, as the laboratory investigations and radiology may be entirely normal.

Symptomatically the disease is characterized by pain with activity and through the day, and transient / short-lived stiffness, known as gelling, associated with rising in the morning and after inactivity, lasting minutes rather than hours. The greater the degree of inflammation, the greater the complaint of stiffness. In addition rest pain reflects inflammation.

Therefore the history should focus on several key questions:

When is the pain maximal?
What duration is the stiffness on walking?
Is there stiffness after resting - Gelling?
Is there swelling? v Distribution of involvement
Any predisposing factors.
Trauma or sports injury.
Family history.
Obesity.
Underlying medical disease.

The joints may become tender on minor impact and become increasingly restricted and may have a subjective sensation of crepitus of opposing irregular surfaces rubbing against each other.

Each joint is then examined with particular focus on the distribution of involvement as well as the exclusion of synovitis, more typical of inflammatory arthritis such as RA. In OA the usual finding is the presence of bony swelling and the finding of only a comparatively low amount of soft tissue swelling. Typically the examiner finds bony thickening, reduced range of movement of the joints, crepitus and if advanced, mechanical derangement of the joint with instability. Mild synovitis may be noted. The typical joints involved, are the distal interphalyngeal (DIP) joints, the proximal interphalyngeal (PIP) joints, the joints at the base of thumb, the cervical and lumbar spine, and the hip and knee (Table 2). In the case of the spine, as a consequence of facet joint arthritis, there is a restriction in range of movement. Such limitation is usually asymmetrical, compared to the symmetrical restriction of inflammatory backache. The peripheral neurological examination is done to exclude nerve root entrapment, with particular reference to sensory loss in a dermatomal distribution and reduction in power or reflexes. The straight leg reflex is also useful to assess root compression. A disc protrusion causing nerve root compression produces a radiation of pain to the affected dermatome, whilst facet related symptoms are more vague in distribution and tend to remain in the axial skeleton without radiation to the periphery.

Soft tissue rheumatism is common in patients with osteoarthritis and a simple examination of the affected muscles and tendons is done to differentiate from joint disease. Passive movement of the joint is pain free, whilst active movement in the direction of the affected muscle reproduces the discomfort.

 

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Laboratory

The laboratory remains an unreliable diagnostic method, and if anything is useful as it assists with the exclusion of other pathologies and also or for the diagnosis of secondary causes. In general, standard blood tests are normal. The most useful screening tests for inflammation include the erythrocyte sedimentation rate, ESR and the C-Reactive protein, CRP. These are classically elevated in inflammatory arthritis such as rheumatoid arthritis, but are usually normal or only slightly elevated in osteoarthritis. Secondary causes of osteoarthritis for which blood tests might help include hypothyroidism, hyperparathyroidism,acromegaly and Hemachromatosis. Aspiration of the joint fluid is unreliable but tends to have a low cell count and show less inflammatory changes, but is useful in certain clinical situations of acute flare to exclude crystal arthropathy such as pseudogout (pyrophosphate crystals), and gout (uric acid crystals) that may be coexistent clinical problems. In addition sepsis can be investigated by aspiration and doing microscopy and cultures where clinically indicated.

 

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Radiology

The radiological appearance provides the easiest method for diagnosis and classification of osteoarthritis. ( Table 3.)The typical changes are joint space narrowing, marginal osteophytes, sclerosis of Subchondral bone as well as subchondral cyst formation. The pattern in large joints is typically unicompartmental or mainly weight bearing surface involvement. In inflammatory arthritis such as RA, changes are usually bicompartmental or throughout the joint surfaces.

 

 
Arthroscopy

Arthroscopy provides a direct method to view the synovium and classification of severity is possible depending on the appearance of the cartilage. (Table 4.)

 

 
An assessment of function and impact of daily life

This is essential to determine how to manage the patient. Functionally there is enormous impact of the disease in terms of social, domestic, occupational and psychological aspects. The impact makes it imperative that ongoing research into meaningful therapies continue.

 

 
Therapy

The therapeutic aim is to treat pain, maintain motor strength, joint range of movement, mobility and therefore function. Strategies include a pharmacological and non-pharmacological approach. Surgical intervention requires strict indications.

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Nonpharmaceutical therapy includes weight loss, orthotics, assistant devices, braces and canes and physical therapy with exercise, aimed at muscle strengthening.

Pharmacological therapy largely consisted of analgesia, and Antiinflammatories. With the gastrointestinal safety component of COXIB drugs, such as Celecoxib, the latter are potentially first line in management of pain and inflammation and are likely to replace the older conventional NSAIDS. MERCK has introduced another Coxib - Etoricoxib, Arcoxia, following withdrawal of Rofecoxib / Vioxx, and Bextra, valdecoxib (due to a reported increase in incidence of myocardial infarction). Although no major association has been determined with the other COXIBs, compared to older antiinflammatory drugs, they should be used with low dose aspirin if there is risk of cardiovascular events.

Disease modifying therapy:

In addition a greater role is now foreseen with disease modifying drugs including Antimalarials, glucosamine sulphate, chondroitin sulphate and hyaluronan where appropriate.

Antimalarial therapy : Many Rheumatologists now try low dose anti-malarial for those patients who have an inflammatory variant of osteoarthritis, with stiffness and soft tissue swelling. This is often the case in the early perimenopausal phase. Also strong family history may influence me to use this as a disease modifying therapy to reduce the long term damage.

Glucosamine Sulphate and chondroitin sulphate have received wide publicity, and are now under trials for management of osteoarthritis. Results suggest that there is some efficacy and benefit for patients with osteoarthritis. There is good evidence for Glucosamine SULPHATE and NO evidence for Glucosamine CHLORIDE. Dose of the Glucosamine sulphate should be 1500mg taken in one dosing. Remember - it is made from shrimp and crab shell, so beware in shellfish allergy. Use with chondroitin increases price but there is NO evidence that it improves the response. I therefore recommend the cheapest Glucosamine sulphate from a reputable supplier.

 

 
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March 2003 Dr David Gotlieb Rheumatologist Constantia Arthritis Clinic Plumstead Cape Town www.arthritis.co.za
Updated 201
1

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Table 1: Classification of OA

 

Primary   Secondary: Common causes
     
Genetic   Metabolic / Endocrine
Erosive / progressive   Acromegaly
    Ochronosis
    Hemachromatosis
    Hyperparathyroidism
    Crystal deposition
    Trauma / Surgery
    Fracture
    Post meniscectomy
    Occupational
    Sport related injury
    Inflammatory joint disease
    Sepsis
    Inflammatory arthropathy
    Anatomic / Developmental
    Slipped epiphysis
    Congenital dislocation of the hip
    Perthes
    Hypermobility

Table 2: Joint Distribution of OA (Adults age 70).

Joints    Frequency Percentage
     
DIP   40
PIP   15
CMC   30
Knees   30-40
Hips   10

Table 3: Radiological Classification of Osteoarthritis (OA)

Grade   Classification    Description
         
0   Normal   No features of OA
1   Doubtfull   Minute osteophyte
Doubtful significance
2   Mild   Definite osteophyte. Normal joint space
3   Moderate   Moderate joint space reduction
4   Severe   Joint space greatly reduced Subchondral sclerosis

The epidemiology of chronic rheumatism, Kellgren ,vol. 2. Atlas of standard radiographs. Oxford: Blackwell Scientific; 1963.

Table 4: Arthroscopic classification of severity of OA

Grade    Description
     
1   Swelling and softening of cartilage. Edema and cellular infiltrate
2   Superficial fibrillation
3   Deeper and large cartilage fibrillation
4   Visualisation of underlying subchondral bone

Ayral X, Dougados M, Listrat et al. Chondroscopy:a new method for scoring chondropathy. Semin Arthritis Rheum 1993; 22:289-97

Figures:
Figure 1: Prevalence of Asymptomatic - radiological OA
Felson DT. The epidemiology of osteoarthritis: results from the Framingham Osteoarthritis Study. Semin Arthritis Rheum. 1990;20:(Suppl. 1):42-50.

Figure 2: Prevalence of symptomatic OA.
Felson DT. The epidemiology of osteoarthritis: results from the Framingham Osteoarthritis Study. Semin Arthritis Rheum. 1990;20:(Suppl. 1):42-50.

Figure 3: Finger involvement - Clinical - showing bony thickening.
Figure 4: XRAY appearance showing joint space narrowing, sclerosis and osteophyte formation.
Figure 5: Hand joint involvement showing bony thickening of the DIP (Heberden nodes) and PIP joints (Bouchard nodes).

 
Figure 6: Large joint involvement showing varus deformity at the knee
Figure 7: Distribution of joint involvement


 
Figure 8: Neck involvement showing disc narrowing, sclerosis and osteophytes.
Figure 9: Appearance of the cartilage at hip surgery showing cartilage loss.

Figure 10. : Osteoarthritis of the hip showing joint space narrowing at the weight bearing surface and osteophyte formation.


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