Osteoarthritis

 

Osteoarthritis

PKGhatak, MD

Osteoarthritis is a degenerative disease followed by inflammatory disease of the joints.

In the initial stage of Osteoarthritis (OA) the wear and tear produce damage to the cartilage covering the ends of the bones forming a joint. When cartilage is destroyed, the bones are exposed and rub against each other causing pain. Subsequently, the bones and joint capsule also undergo inflammatory changes. Osteoarthritis (OA) is distinct from Rheumatoid Arthritis (RA) where inflammation primarily is in the synovial membrane of the joints and then spreads to bones and the rest of the joint structures. RA is an autoimmune disease and affects the lungs and other collagen vascular structures of organs.

OA is a disease of the elderly. Young people also develop OA from sports injuries, in addition, OA develops secondary to other diseases and a few hereditary diseases which damage the cartilage.

Cartilage.

The ends of bones forming a joint are covered by a layer of cartilage called Articular cartilage. Articular cartilage has a unique ability to withstand high loads with little damage. Cartilage is connective tissue and provides structural support like bone. In fact, in the animal kingdom the development of the backbone, the cartilaginous vertebral column appeared first, then came the bony vertebrae, even then currently the oceans are full of cartilaginous fishes- sharks for example.

The cartilage is composed of a dense extracellular matrix. In the matrix a few sparsely distributed cells called Chondrocytes are present. The extracellular matrix is composed of water, collagen(protein), proteoglycans (protein+carbohydrate) and other glycoproteins. These structural components make cartilage retain water and provide a cushion and absorb the body weight and pressure during joint movements.

Blood supply to cartilage is absent, this results in poor healing properties of cartilage. It is devoid of nerves and so insensitive to pain.

The part of the bone next to the cartilage layer is known as the subchondral pate and is very vascular. Nutrition to articular cartilage is provided by synovial fluid.

Commonly affected Joints in OA.

OA can start in any joint, but the joints commonly affected joints are Knee, Lumbosacral and Cervical Spine, Hips and thumb.

The thumb and distal finger joints are commonly affected in elderly females. Knee, Lumbosacral, Cervical Vertebrae and Hip joints are equally affected in both sexes. OA of shoulders and fingers are generally spared, unless overused, for example, manual laborers and coal miners.

The middle joints of fingers are typically affected in RA. This is an important distinction between the RA and OA. RA patients show associated systemic symptoms and x-ray evidence of erosion of bone ends of the finger joints and elevated acute phase reactants in the blood.

Risk factors to OA.

Injury, obesity, manual workers, sports injuries, diabetes, in addition, OA develops secondary to a number of diseases. Closely resembles but distinct from OA are Gout, Pseudo gout and Peripheral sensory neuropathic arthritis.

Secondary causes of OA.

Metabolic defects of cartilages:  Ochronotic arthropathy, Alkaptonuria, chondrocalcinosis, or pseudo gout.

Connective tissue metabolism:    Hurler syndrome, Moquino disease, Marfan syndrome, Poly-epiphyseal dyslexia.

Congenital bone defects:   Scoliosis, Spina bifida, Club foot, Leg-Parthese disease.

Hereditary gene mutation:    Hemochromatosis. Sickle Cell Anemia.

Blood clotting abnormality:   Hemophilia.

Autoimmune disease:   RA, Psoriatic arthritis. Crohn's disease, Ulcerative colitis,

Leukocyte Antigen gene mutation:    Ankylosing spondylitis due to inherited HLA-B27 gene.

Endocrine disease:    Acromegaly, Cretinism, Dwarfism, Hypothyroidism, Menopause.

Neurogenic:   Muscular dystrophies. Syringomyelia. Charcot arthropathy. Reflex sympathetic dystrophy.

Vascular:    Aseptic necrosis of hips, Caisson disease

Symptoms of OA.

All different types of arthritis produce similar symptoms like pain, swelling, muscle stiffness, and limitation of range of motion. OA is a local disease and produces very few systemic effects. OA of the vertebral column has some unique features. In cervical spine OA - the wry neck may start even before the radiological evidence of OA. Thorns like outgrowths of bone spicules produce sharp jabbing pain. OA of facet joints limits turning of head and torso side to side and specially backward. Stenosis of the cervical spine can produce spastic paralysis of the legs. In the lumbar area, OA produces muscle spasms. Lumbar stenosis can interfere with bladder and bowel functions, in addition to muscle weakness of lower legs, often seen as foot drop and mark limitation of climbing stairs.

Diagnosis.

History and clinical examination are sufficient to make a diagnosis of OA. There is no blood test to confirm OA, however, blood tests are done to exclude other forms of arthritis. X-rays are an essential part of diagnosis showing loss of joint space, subchondral bone sclerosis and small outgrowths from the ends of bones in OA.

In the weight bearing joints, like knees, an x-ray is used to stratify OA into early, intermediate and advanced stages. In the advanced stage of OA knee, surgical replacement of the knee is advocated.

Medical treatment of OA.

There is no cure for OA. The non-steroidal anti-inflammatory drugs are the mainstay of the treatment of OA. These drugs produce relief of pain and limit bone inflammation.

In addition to medication, physical therapy, daily exercise and weight reduction, where applicable, are advised. When pain is acute, rest of that joint is essential till the pain is tolerable then physiotherapy is helpful. Use of other anti-inflammatory drugs, narcotics and muscle relaxants are discouraged.

In some European countries intra-articular lubricant, a visco-supplementation containing Hyaluronic acid, is injected into the knee to lessen friction and pain. Use of it in the USA is generally not recommended because the beneficial effects last only a few months, if at all. and a chance of infections in repeated injections is a real possibility.

Surgical Treatment.

In advanced knee OA, joint emplacement is commonly advised. Corrective surgery of various kinds is done for cervical and lumber vertebral stenosis.

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