Osteoarthritis is a slowly evolving chronic degenerative disease which disables people in mid forties, is widely prevalent all over the world and is characterized by pain and discomfort round big joints making the life of individual miserable. It is a continuous process of aging where the normal repair mechanism of the joint is not able to keep up with the destructive aspects of the joint.
More than 10% of the elderly suffer from osteoarthritis and it is twice as common in women as compared to men. Classically osteoarthritis is characterized by abnormalities in articular cartilage, subchondral bone and soft tissues surrounding the joint. Multiple joints may be involved and though it is not an inflammatory process, yet discomfort bordering on dependency occurs by causing painful involvement of surrounding soft tissues.
Most cases of osteoarthritis have no known cause. This is called primary form of osteoarthritis while the secondary form is caused by number of conditions ranging from congenital abnormalities of joints. Trauma, obesity, metabolic abnormalities of cartilage to neuropathic causes.
Though no known causes are operative in a case of primary osteoarthritis yet there are number of factors which inter act to cause the disorder.
It is an important risk factor. As age advances the frequency of the condition is markedly increased. The incidence of osteoarthritis increases rapidly in elderly people and many elders have clinical as well as radiological evidence of disease.
The incidence of O.A. increases rapidly in women than men after the age of 50. Females are found to have more severe form of disease with more joints being involved. Loss of oestrogens at the time of menopause takes away their protective role thus increasing in women the risk of getting osteoarthritis.
Obesity or overweight has a direct bearing to the development of O.A. especially of the knees. It is also an important risk factor in the rapid progress of disease. Weight loss provides symptomatic relief in a case of O.A.
There are racial differences in both the prevalence of O.A. and the pattern of joint involvement. Thus O.A. is uncommon in Chinese, Black and East Indians and when it does occur it affects more commonly the knees as compared to hip. Native Americans have a higher incidence of O.A as compared to whites. Indians are affected in the range of 22 to 32% and it is the second most frequent joint disease in India.
Heredity has an important role to play in the causation of osteoarthritis. Heberdens nodes are inherited in an autosomal dominant trait in women whereas in men the inheritance is autosomal recessive. Even primary generalized O.A has been linked to its inheritance as autosomal dominant trait.
Mutations of type II collagen gene (COL 2AJ) on chromosome 12 have been linked to chondrodysplasias and vitamin D receptor gene polymorphism and included as genetic risk factor in cases of familial OA.
Repeated injury to the joint, hyper mobility or instability, prolonged immobilization, abnormal joint shape (congenital or acquired) and stress with physical activity and sports are other risk factors in the aetiology of osteoarthritis. Miscellaneous. Osteoporosis is negatively at the hip.
Osteoporosis is characterized by a loss of bone mineral density (BMD) and as it depends on bone integrity, inverse relationship between the two may be considered. Patients with low bone mineral density are more likely to suffer progressive disease.
Some studies have suggested protective influence of smoking on knee osteoarthritis. Chondrocalcinosis, alteration in chondrocyte responsiveness to different cytokines and crystals in joints fluid are other factors incriminated.
The main pathology is loss of integrity of cartilage, the elasticity of articular cartilage and its ability to stand repeated load bearing. As the disease progresses articular cartilage thins and vertical clefts (fibrillation) extend into it.
Cartilage matrix has several macromolecules including complexes containing proteins, glycosaminoglycan (Proteoglycans) and type II collagen and its degradation is central to the pathogenesis of osteoarthritis.
Matrix depletion of the cartilage manifests as decrease in proteoglycan content and increase in water content. ‘With joint motion, shreds of fibrillated cartilage are shed unmasking a thickened bone.
Joint capsule is thickened and subchondral cysts and sclerosis takes place in underlying bone. Reactive proliferation of new bone and the cartilage at the joint margins lead to the fonnation of boney spurs (osteophytes).
In response to these changes the normally quiescent chondrocytes are triggered into proliferation and they form clusters known as ‘broad nests’. These attempt to replenish the matrix by increasing its synthesis.
Along with it there is stiffening of cartilage of subchondral bone resulting in reduction of its shock absorbing capacity. It becomes hypocellular and fibro cartilage replaces hyaline cartilage. Marked fibrosis of the joints capsule may further restrict joint movement.
Biochemical studies show increased activity of chondrocyte proteases relative to their natural inhibitors and cause release of proteoglycans, collagen and enzymes like collagenase, interleukinI, pro-inflammatory cytokines like tumour necrosis factor alpha (TNF-ct), Insulin like growth factor (IGF-I) and IL-6. These play important role in articular cartilage metabolism and in its degradation.
Joint pain is the predominant complaint. The disease usually involves a single joint but may involve number of joints. The onset is insidious. Joints commonly involved include those of hands knees, hips and spine. It is the pain which brings the patient to the doctor.
Typically the pain is relieved by rest and increased by exertion. As the disease progresses pain occurs at rest as well. Though stmctural changes in the cartilage occur but pain does not arise from there since cartilage is aneural. Cause of pain is due to raised pressure in subchondral bone, muscle spasm, synovitis and stretching of joint capsule.
Stiffness is another complaint and occurs commonly after rest and inactivity. Some degree of joint swelling and deformity may be present in some. Physical examination of joints reveals bony or soft tissue swelling. Localized tenderness is present.
Swelling round the joint may be due to soft tissue swelling or effusion or synovitis. Coarse crepitus is felt on palpation. Because of pain there is disuse atrophy of muscles, bony deformity and restricted joint movements.
Involvement of specific joints
These are involved in polyarticular form of osteoarthritis. Bony enlargement of the distal inter phalangeal joints (Heberden’s nodes) and proximal interphalangeal joints (Bouchard’s nodes) are the commonest manifestation. These develop gradually but may present acutely. There is pain, redness and swelling. Second important involvement in hand is of thumb.
It is the most commonly affected joint. The involvement may be of one knee joint, but often both knees are involved. There is bony tenderness and patient experiences pain while sifting in squatting posture. Crepitus is felt. Involvement of medial tibiofemoral compartment or patello femoral compartment (lateral > medial) leads to functional impairment and deformities (genu varus & valgus).
It is less commonly involved as compared to osteoarthritis of knee. Patient generally presents with pain referred to inguinal region, buttocks or thigh. Movements of hip (internal rotation, extension, adduction and flexion) produce pain. Osteophyte formations are prominent at lateral acetabular and medial femoral margins.
In majority usually one hip joint is involved but in small percentage (20%) both hip joints may be involved.
Involvement of the spine goes under the name of spondylosis. Here degenerative changes affect the apophyseal joint, intervertebral discs and vertebral bodies. Symptoms include localized pain and stiffness.
When there is a compression of the nerve or prolapse of a degenerated disc symptoms of nerve root compression in the form of radicular pain may appear. When spondylosis occurs in the cervical region, features of vertebrobasilar artery insufficiency may appear.
Nodal generalized osteoarthritis
It presents as generalized involvement of three or more joints. Typically patient is a female in the age group of 40- 60 years, with a strong family history who develops swelling of interphalangeal joint followed by involvement of another I.P. joint within a few months and then resulting in polyarthritis of proximal and distal interphalangeal joints. Heberden’s and Bonchard’s nodes are seen prominently in this form of osteoarthritis.
It is uncommon but IS of more severe form, and characterized with involvement of I.P. joints inflammatory signs and radiographic evidence of erosions and collapse in subchondral plate. There is a tendency for bony ankylosis. Swelling of joints and functional impairment is severe.
It is mainly clinical as well as radiological. Radiological evidence of osteoarthritis does not go along the clinical picture. An asymptomatic person may have radiological picture like osteophyte formation.
Main differentiation is from rheumatoid arthritis when it affects the wrist and small joints of the hand. There is rise of ESR, C-reactive proteins and rheumatoid factor in such cases. In some cases of inflammatory O.A. some difficulty may rise.
In primary osteoarthrits laboratory investigation are not helpful. Rheumatoid factor is absent. ESR, C-reactive proteins, serum chemistry analysis are normal.
Radiology is the main tool in making a diagnosis. Plain radiograph of the involved joint will show joint space nan owing, subchondral sclerosis, osteophytes and subchondral cysts. Effusions, loose bodies, joint alignment, subluxation chondrocalcinosis, collapse due to avascular necrosis are other signs. Bony ankylosis is uncommon.
In some cases MM, radionucleide studies and arthrocentesis may help in identifying underlying cause of secondary O.A. In moderate to severe cases of O.A. synovitis is common and there is accumulation of joint fluid.
Aspiration of this fluid will show a clear or pale yellow fluid, of moderate to high viscosity and mild leucocytosis (<200 white blood cells per micro liter) with predominance of mononuclear cells. Sometimes cartilage fragments and calcium containing crystals may be found in the synovial fluid.
The main aim in management of a patient of osteoarthritis is:
1. Improve the quality of life
2. Relief of pain and discomfort
3. Prevention of disability
Most of the patients are obese. One should ensure a reduction in weight by diet control, physical measures like exercising etc. Weight reduction is important since it shall take away the unnecessary extra load the obese patients have to cany thus putting more stress on the joints.
At the same time the patient must be given adequate amount of calories by giving a diet consisting of proteins, minerals, vitamins etc. Patient should be advised to take adequate rest.
Walking should be encouraged but not to the extent of fatique. Excessive and wrong usage of the joint should not be allowed. Strenuous exercises be prohibited since these are likely to further damage the already painful joints.
Heat applied to joints before exercising them reduces pain and stiffness. Heat therapy in the form of hot water baths, short wave diathermy and infra red therapy is helpful.
Attempt should be made to maintain joint range movement. Muscles round about the joints be exercised to maintain strength. Exercise is an important part of treatment. In this regard Isometric exercises are preferable to isotonic exercises as they minimize stress on the joint.
Relief of pain and discomfort
Basic aim of the treatment should be to give relief from pain which is probably the main complaint. Surprisingly pure osteoarthritis is painless. It is the involvement of surrounding soft tissue which produces pain.
Patients of OA obtain relief from analgesics. NSAIDs are to be used when simple analgesics fail to improve. Acetaminophen is often effective in a simple early osteoarthritis. Salicylates and traditional NSAIDs are considered only for patients who do not obtain adequate relief from paracetamol.
Non-steroidal anti- inflammatory drugs (NSAID5) form the mainline of treatmen of a patient of chronic osteoarthritis. They exert their effect through inhibition of prostaglandin synthesis. Those commonly used include:
Ibuprofen, naproxen, ketoprofen, fenoprofen and flurbiprofen. These are propionic acid derivatives and have similar pharmacodynamic properties but vary considerably in potency and to some extent in duration of action. Tablets and capsules are available.
Dosage of ibuprofen (200-600 mg thrice daily), naproxen (250 mg twice daily), ketoprofen (50 mg twice daily), fenoprofen (300-600 mg thrice daily), flurbiprofen (150-200 mg daily in divided doses).
It is an indole derivative and a potent anti inflammatory agent. Dosage 25-50 mg two to three times a day. It interacts with salicylates, lithium, anticoagulants B-blockers, anticoagulants and corticosteroids.
Its anti-inflammatory potency is similar to indomethacin and analgesic action greater than aspirin. Dosage 20 mg as single dose daily.
It has powerful anti-inflammatory action besides its analgesic and anti-pyretic actions. It is an inhibitor of prostaglandin synthesis. Dosage 100-150 mg daily in 2-3 divided doses. In cases with severe pain and discomfort Inj. DICLOFENAC sodium (25 mg/ml) can be given initially and then switch over to oral tables.
Besides its anti-inflammatory action, it is analgesic and antipyretic. Unlike other NSAIDS, its chemical structure does not contain a carboxylic group but a sulfonanlide moiety as the acidic group. It is absorbed rapidly and quickly after oral administration. Dosage 100 mg twice daily.
NSAIDs are to be used with caution in cases with impaired renal or hepatic function, hypertension, compromised cardiac function and are contraindicated in patients of peptic ulcer, active gastrointestinal bleeding or active inflammatory disease of the gastrointestinal tract. In patients with known hypersensitivity to aspirin these drugs should not be used since cross sensitivity may be existing.
Side effects include epigastric discomfort, constipation, diarrhoea, dizziness, headache, palpitation, hypertension, anorexia, vomiting drowsiness, depression, tremors, oedema, stomatitis and rarely tinnitus and vertigo.
Non steroidal anti-inflammatory gels
These are also of great use since judicial use of these gels on the joints involved does give some relief. Most of the time local application of the drug achieves good results as the patient in addition to having the drug absorbed locally gets some degree of psychological satisfaction.
These include celecoxib (100 mg twice a day) rofecoxib (50 mg once a day) etoricoxib (60 mg/day) and valdecoxib (10 mg/day). These are non-steroidal anti- inflammatory drugs which act by inhibition of prostaglandin synthesis through selective inhibition of COX-2 insoenzyme which is unregulated during inflammatory processes. These agents have better gastrointestinal tolerability. However, because of their cardiovascular safety they should be used with caution.
Systemic carticosteroids have no role in the treatment of O.A. However, ultraarticular corticosteroid injection may benefit patients with evidence of inflammation, effusion or both.
Judicious use of this treatment is desirable and not more than four injections per year are to be given in a particular joint. Indiscriminate use may effect local cartilage metabolism and aggravate the disease process.
Glucosamine sulphate with chondroitin sulphate
Glucosamine sulphate is an amino sugar which builds up the volume of naturally present glucosamine in the body. The increased glucosamine level, in tum accelerates the biosynthesis of blinding blocks of cartilage ie proteoglycans and collagens. Chondrotin Sulphate similarly provides additional substance for formation of healthy joint matrix.
Most of the time combination of the two is used. Dosage (one capsule contains glucosamine sulpate 250 mg. Chondrotin sulphate 200 mg) 2 capsules three times daily for three months. They give relief of the symptoms in 3-4 weeks. Side effects include epigastric pain, heart burn, tiredness drowsiness, headache and insomnia.
Surgery. Patients with persistent pain and progressive disability where drugs and other measures have failed, are referred for surgical intervention.
Procedures available for knee includes osteotomy, arthodesis, arthroplasty and total knee replacement.
Arthroscopy is done in some cases to do debridement and washout of the damaged joint. Removal of loose cartilage ligaments can prevent locking. Relief may occur lasting for several months.
Although articular cartilages can not repair themselves, small defects in the articular surface may be filled by fibrocartilage that is attempting to function as scar tissue. The only contraindication to this procedure is local sepsis.
In arthroplasty a sub total procedure is performed on medial compartment of the knees which is the most troubled part. Results are good if infection is avoided. Partial replacements with one of the many designs available can avoid the need for total knee replacement. Fusion of the knee can give relief to those unsuitable for total knee replacement.
Sometimes hyaluronic acid injections in arthritic joints on weekly basis may help.
Total knee replacement is the ultimate procedure. But the range of movement is not increased beyond the pre-operative level. Procedures for hip also include osteotomy, arthoplasty and total hip replacement.
Where there is failure of primary surgery, revision surgery can be preformed.