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Chapter 9

OSTEOARTHRITIS

Definition:

Osteoarthritis (osteoarthrosis, degenerative joint disease) is the most common disease of central and peripheral diarthodial joints. It is characterized pathologically by degeneration and loss of articular cartilage, bony sclerosis and osteophyte formation. It is not accompanied by constitutional signs or systemic manifestations.

Aetiology

Osteoarthritis (OA) has been divided into primary and secondary forms, depending on the absence or presence of some clearly evident underlying local or systemic etiological factor.

- Genetic factors play a role in the development of OA of the distal interphalangeal joints of the hands (Heberdens nodules). The role of obesity remains controversial. Some studies demonstrated increased frequency of OA in obese patients particularly when weight bearing joints are evaluated.

Primary OA:

No aetiological agent can be identified, it can affect single joint or can be generalized. The latter usually affects postmenopausal females and is believed to be inherited as an autosomal dominant.

Secondary OA

Trauma              Fracture, occupational, sporting

Endocrine           Diabetes mellitus, Acromegaly

Metabolic              Alkaptonuria, Wilson’s disease, Haemochromatosis, eating cereals infected   with a fungus.

Dietary               Obesity, Kashin Beck disease, Rickets

Joint                   Sepsis, inflammation, crystal deposition disease.

  Hypermobility

  Perthe’s disease

  Avascular necrosis

Congential          Hip dysplasia

                          Slipped upper femoral epiphysis

Neurological      Tabes dorsalis

                          Syringoznyelia

                          Charcot joint

                          Meningomyeiocele.

Pathology:

The initial lesion of OA takes place in the articular cartilage. The normal blue translucent cartilage takes an opaque yellowish appearance, surface irregularities due to loss of chondrotin sulphate resulting in softening of the matrix and fissuring and pitting of the superficial layers followed by erosions initially focal, become confluent and lead to large areas of denuded surface. Initial involvement of superficial and middle layers is followed by full thickness loss of cartilage down to bone.

Osteophyte formation, proliferation of bone is seen most prominently at joint margins. Subchondral bone becomes thickened and sclerotic.

Cyst formation in the juxta articular bone is common.

Secondary synovitis may result from release of crystals from cartilage and inflammatory mediators initiated by cartilage breakdown components.

Clinical features:

Osteoarthritis may present in a number of ways:

u There may be pain and stiffness in many joints (small and large). This is generalised OA, which seems to present most often in women around the menopause. The terminal interphalangeal joints of the fingers, the first carpometacarpal joint at the base of thumb, the spine and the metatorsophalangeal joints of the big toe are most often affected.

v There may be pain and stiffness in any one joint, usually a large joint such as the knee, the onset, can be gradual or sudden.

w The 3^rd form of presentation is with symptoms due to some complication of osteoarthritis e.g. parasthesiae in the medial side of arm, little & ring fingers due to entrapment of the ulnar nerve by bone hypertrophy from osteoarthritis of the elbow.

Pain early in the course of disease occurs after joint use and is relieved by rest. Later pain occurs with minimal motion or even at rest, at this stage of the disease, night pain is common. Cartilage has no nerve supply and is insensitive, pain arises from other intra-articular and pen articular structures (synovial membrane. joint capsule and ligaments).

Acute inflammatory flares may be precipitated by trauma or in some cases by crystal induced synovitis in response to crystals of calcium pyrophosphate or apatite.

Joint stiffness is relatively short lived and localized. Local tenderness may be elicited at ligamentous attachments.

Pain on passive motion and crepitus, a feeling of crakling as the joint is moved, are prominent findings.

Swelling of joint results from synovitis, increased amounts of synovial fluid or proliferative changes of bone.

Heberden’s nodes are characterized by spur formation at the sides of the distal interphalangeal joints of the fingers. Similar changes at the proximal interphalangeal joints are called Bouchards nodes.

Complications of OA

uEntrapment syndromes e.g. ulnar nerve in OA of the elbow.

vDeformities such as genu valgum or varum due to excessive wear of the cartilage in either the medial and lateral compartment of the knee producing abnormal bad stresses.

wThe affected joints may be subluxated.

Investigations:

X-ray may be normal if pathologic changes are mild. Characteristic changes include joint space narrowing. subchondral bony sclerosis, marginal osteophyte formation and cyst formation.

Laboratory investigations are usually normal and they are helpful primarily in exc1udin other joint diseases. The erythrocyte sedimentation rate is normal, synovial fluid study shows minimal abnormalities.

Synovial fluid aspirated from joint effusion are clear, of high viscosity with normal concentration of glucose and lysosomal enzymes, unless associated with deposition of crystals in such case a closely, non viscous fluid may be obtained which when examined by polarized light microscope shows hydroxyapatite crystals.

Arthroscopy, thermography and radioisotopic appearance will display clearly the cartilage loss, alteration in the normal macroscopically smooth articular surface, alteration in congruity and slight synovitis. Osteophytes may be seen and loose bodies may be visualized and sometimes removed.

The osteoarthritic joint usually displays a normal intra-articular and skin temperature and a normal thermorgram. Radioisotopic uptake of intravenously injected technetium (Tc 99 m) (reflecting synovial blood flow) is normal.

Treatment of osteoarthritis:

The aims of management of OA are:

u Control of joint pain.

v Improvement of joint mobility and functions.

w Correction and alleviation of deformity and removal of aggravating factors.

A- General:

The majority of patients with osteoarthritis are only mildly affected. Firm reassurance that they d not have rheumatoid arthritis and that they do have an excellent prognosis. Coupled with general advice on the maintenance of optimum physical and mental health and activity is all that is required in many patients. Protection of joints from overuse is important, especially if weight bearing joints are involved, weight reduction should be carried out.

B- Physical:

Heat or ice packs are useful before starting physiotherapy exercises, they relieve pain and associated muscle spasm and maintain and regain joint range of motion.

Isometric exercises in which the muscles are strengthened against weight resistance while the joint is kept in a normal anatomic position, maintain muscle function and strength.

Isotonic exercises in which the joints are put through a range of motion while being exercised should be used without resistance.

Appliances such as canes (sticks) are beneficial for joint protection when indicated also cervical collars and lumbar supports.

Transcutaneous electrical nerve stimulation which involves delivery of electrical current through the skin to a peripheral nerve, may provide pain relief in patients with osteoarthritis.

C-Medical:    

Analgesic agents help the patients by relieving pain, examples are aspirin and paracetamol. Non steroidal anti-inflammatory agents are available for patients who are allergic to or intolerant of or not responding to salicylates. Indomethacin, ibuprofen, naproxen, diclofenac and piroxicam are available. These agents share a number of toxic side reactions including rash, gastrointestinal upset, peptic ulcerations occasional vague psychic reactions and tinnitus.

Oral or parentral steroid therapy is contraindicated in the treatment of degenerative joint disease. However, intra-articular injection of steroids may he useful in management of acute joint flares. Injections should be infrequent, especially if given into weight bearing joints, Joint deterioration may be accelerated due to masking of pain with subsequent joint overuse. Pericapsular & ligamentous injection in areas of tenderness around involved joints provides relief with less hazards.

D- Surgical:

Orthopeadic surgical procedures of use in patients with osteoarthritis include arthroplasty, osteotomy, fusion and partial or total prosthetic replacement. Angulation oteotomy is particularly helpful in correcting joint malignment, when significant varous or valgus deformities of the knee are present in unicompartmental disease. Pain is relieved by bringing healthy articular cartilage into position. Hip replacement (arthroplasty) produce striking symptomatic relief and improved range of motion.

OSTEOARTHOROSIS OF THE SPINE

(SPONDYLOSIS)

The joints of the spine consist of:

a.Posterior apophyseal joints between the articular facets which are lined by synovial membrane.

b.Intervertebral, non synovial joints composed of flbrocartilagenous discs between the vertebral bodies.

Degnerative changes may occur at either site, osteoarthritis occurring in the spine is known as spondylosis. In contrast to inflammatory spinal joint disease or spondylitis.

Osteoarthrosis is the commonest cause of pain and stiffness of the spine, whether cervical, thoracic or lumbar. Symptoms are the results of supervening or complicating events e.g. minor derangement of intervertebral joint. Slipping of one vertebra on its neighbour (Spondylolisthesis) or secondary ligamentous strain.

An important point is that:

Anterior lumbar spondylosis involving discs and vertebral bodies, may be asymptomatic or at least amenable to treatment. On the hand, osteoarthritis of the posterior (apophyseal) joints is very different matter, here pain may be quite intractable and not relieved by any thing other than analgesics and anti-inflammatory drugs.

Cervical spine (cervical spondylosis)

Age: usually middle age.

The commonest level to be affected is C5-C7 in contradistinction to rheumatoid arthritis which affects mainly the upper cervical region.

Symptoms:

Pain vary from dull ache to severe attack of pain in the neck and may radiate to the upper limb.

* Limitation of neck movements.

* Symptoms are aggravated by movements of the neck.

If there is compression of the nerve roots there may be pain radiating down the arm, paraesthesia in the fingers tips, and reflex and motor changes in the distribution of the compressed nerve root.

If the disc or new bone (central prolapse) compress the spinal cord posteriorly there may be signs of upper motor neuron or other long tracts lesion affecting the legs.

Interference with the blood supply to the brain by kinking of the vertebral arteries as they run upward through the foramina before entering to foramen magnum to form the basilar artery ---> transient blackouts and visual disturbances may then be precipitated by neck movements.

Investigations:

I. Radiology:

The characteristic radiological signs of O.A. are:

u Narrowing of the joint space due to loss of the articular cartilage.

v Marginal osteophytes formation.

w Subchondral sclerosis.

II. Other investigations:

The ESR and other routine blood tests are all normal.

Treatment:

uPsychological consideration.

vMedical: Analgesics as acetyl salicylic acid (aspirin) and non steroidal anti inflammatory drugs are used to control pain and suppress inflammations but they are less effective than other situations.

wGeneral measures: These include advice on dietary habits to prevent or reduce obesity, avoidance of occupational aggravation and advice on stress relieving posture during activities of daily living.

xPhysical therapy:

Aims:

* Prevent further strain or trauma on the affected joint.

* To improve the muscle power.

* To improve nutrition of the cartilage by restoration of physiological movement.

Methods:

uExercises.

vMobilisation.

wProvision of aids adjuncts; ice and heat.

Exercises:

Increase the strength of muscles acting over the affected joint and therapy improves the body natural splinting mechanism to prevent further trauma and strain on the joint.

Chapter 10

LOW BACK PAIN

Pain in the lower part of the back is experienced at some time by virtually every adult. It is estimated that about 80% of the adult population experience LBP at some time during their life, so LBP is the commonest symptom related to the musculoskeletal system.

Definition:

LBP is defined as acute or chronic pain in the lumbar region with or without sciatic radiation.

Causes:

The cause of LBP may originate from structures of the lumbo-sacral spine (local) or referred from structures away from the lumbo-sacral spine (referred

The cause of LBP may be classified as follows:

u Spondylogenic: (The commonest causes)

The commonest causes of LBP, with or without sciatica, are disorders of the lumbo-sacral spine:

a) Trauma:

Muscle strains, residual effects of fractures and dislocations, tendon sprains, sacroiliac strain.

b) Infection:

Non specific ---> osteomyelitis

Specific ---> T.B. (Pott's disease)

c) Inflammatory:

Seronegatve arthropathies e.g. Ankylosing spondylitis

d) Degenerative:

IVD prolapse, lumbar spondylosis and osteoarthrosis of facet joints

e) Metabolic bone diseases:

Osteoporosis and osteomalacia

f) Bony deformities:

Spondylolysis and spondylolisthesis

g) Neoplasm:

Benign      ---> Osteoma and haemangioma

Malignant  ---> 1ry: Multiple myeloma

                ---> 2ry: Thyroid, lung, breast, kidney, prostate

 v Viscerogenic:

Lesions of the genito-urinary tract, pelvic organs as well as lesions intra-peritoneal or retro peritoneal, that irritate the posterior peritoneum may cause LBP.

w Vasculogenic:

Abnormalities of the descending aorta and iliac arteries, such as vascular occlusions or dissecting aneurysms, may cause pain that is referred to the back.

x Neurogenic:

Infections and neoplasms that involve either the spinal cord or the cauda equina may mimic disc herniation examples ---> transverse myelitis, radiculitis and neurofibromatosis.

y Psychogenic:

Although LBP is sometimes a manifestation of psychosomatic illness, an underlying organic cause of the pain must always be sought.

Lumbar Intervertebral Disc Prolapse

Disc herniation is due to degeneration and trauma to annulus fibrosus resulting in protrusion of nucleus pulposus. Herniation is either:(

u Posterolateral: (the commonest) with displacement of posterior longitudinal ligament and compression of emerging nerve root causing LBP & sciatica.

v Posterior: Causing LBP, large protrusion ---> rarely compress the cauda equina.

w Vertical: Symptomless herniation occurs above and below through cartilage plates into adjacent vertebral bodies (Schmorl's nodes).

Chronic back pain may be due to chronic nerve-root compression which results form granulation tissue and the scarring within nerve-root canals, known as arachnoiditis.

Clinical Features:

LD lesions cause acute LBP with or without sciatica, or chronic backache sometimes with sciatica Typical acute “lumbago and sciatica” occurs at any age and commonly, but not always, follows slight trauma or strain. This is known as mechanical back pain, as opposed to inflammatory back pain (as in ankylosing spondylitis).

Sudden severe LBP which persists several hours or days and then gradually subsides, associated with Lumbar spasm. Occasionally onset of pain is insidious and builds up.

- Sciatica is severe, shooting pain in one or both legs in distribution of sciatic nerve, usually aggravated by coughing, sneezing or bending

- Pain in the lumbar region and of sciatic distribution, usually unilateral.

- Acute symptoms usually follow severe bending, lifting or twisting stresses.

- At this stage all movements are very painful and restricted, with marked spasm of spinal extensor muscles, and pain on coughing, sneezing and straining

- Straight leg raising is restricted and neck flexion may produce the pain

- Femoral nerve stretch in 3^rd l4th lumbar disc lesions ---> passive knee flexion (in prone position) causes pain in fronts of thighs

- Parasthesias and neurological signs in legs: Muscle weakness, reflex or sensory changes according to root involved.

Investigations:

- Clinical examination of back, legs and abdomen.

- Rectal and/or vaginal examination.

- Urine analysis

- ESR ----> normal, Latex fixation test ----> negative

- Biochemistry---> especially serum calcium, alkaline phosphatase

- x-ray (plain)---> may show narrowing of disc space and exclude other lesions. Other investigations include CSF, myelography, discography.

Table 4 Differences between mechanical and inflammatory low back pain:

Treatment:

a) General:

u Complete bedrest for 1-2 weeks in acute cases.

v Hard bed with low pillow.

w Instruction in correct posute and back discipline (bending, carrying, ...etc.).

x Change to more suitable work (not involving bending, lifting or climbing).

y Reduction of weight in obese patients.

b) Medical:

u Analgesics and muscle relaxants for pain and spasm.

v Caudal epidural injection (50 ml of 0.5% procaine or lignocaine in normal saline) for persistent sciatica. This separates nerve roots from protruding disc.

w Chemonucleolysis (intradiscal injection of chymopapain, a proteolytic enzyme to break chondromucoprotein ---> scarring(.

c) Physical:

u Strengthing exercises (back extension and/or flexion exercises) preceded by local heat or ice.

v Lumbosacral support: corset or brace.

w Intermittent lumbar traction: 30-60 kg for 30-60 minutes at a time for persistent sciatica. Continuous lumbar traction may be applied in hospital for acute cases.

d) Surgical:

Indications

u Failure of conservative treatment.

v Cauda equina.

w Progressive muscle weakness due to root pressure.

w Sphincteric disturbances.

y Congenital defect with severe disc lesion e.g. spondylolisthesis & spinal canal stenosis.

The usual operation is lamenectomy. Postoperatively, patient stays one week in hospital, then one month of intensive rehabilitation before allowed to return to work.

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   END OF THE BOOK

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Thank you Dr. Abd ElSamad Elhewala

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