регистрация / вход

Compare And Contrast The Changes Described In

All The Tissue Types Of The Neuro-Muculoskeletal System Associated With Rheumatoid Arthritis And Degenerative Disease Accompanying Advancing Age. Essay, Research Paper

All The Tissue Types Of The Neuro-Muculoskeletal System Associated With Rheumatoid Arthritis And Degenerative Disease Accompanying Advancing Age. Essay, Research Paper

Compare and Contrast the Changes Described in all the Tissue Types of the Neuro-Musculoskeletal System Associated With Rheumatoid Arthritis and Degenerative Disease Accompanying Advancing Age.By Daniel Gibb (3rd Year)Introduction:Arthritis is a chronic illness frequently managed in the primary care setting. It is estimated that by the year 2020, 59.4 million, or 18% of Americans, will be afflicted with the disease.1 Arthritis in the United States is estimated to cost $54.6 billion, including medical treatment, work loss, and disability. It ranks among the top five causes of long-term disability2,There are more than 100 recognized types of arthritis, with osteoarthritis (OA) and rheumatoid arthritis (RA) being two of the most common.3 However, whilst rheumatoid arthritis is considered to be auto immunological in origin, osteoarthritis is associated with wear and tear or the aging process4. As such for the most part, the discussion of degenerative changes shall primarily focus upon osteoarthritis.Both osteoarthritis and rheumatoid arthritis affect various parts of the neuro musculoskeletal system. In order to clarify their comparison, it is necessary to investigate all parts of the neuro musculoskeletal system.Normal Joint Structure:The basis for both rheumatoid arthritis and age related changes or osteoarthritis is a breakdown in the normal structure and thus function of a joint or joints. A typified joint is shown in figure 1.Any disruption to one or more elements in the joint will lead to dysfunction in the joint. Thus the changes seen in patients with rheumatoid arthritis and osteoarthritis with respect to function occur.Figure 1: A Typified Joint. Synovial Fluid:In osteoarthritis, little, if any change occurs in the Synovial fluid filling the joint space. If however the osteoarthritic changes have intertwined with them, inflammatory action, white blood cell (WBC) proliferation may be present5. Also, the viscosity of the fluid may be raised above normal levels5.With rheumatoid arthritis, the changes in Synovial fluid constitution are far more abundant. The immunological nature of rheumatoid arthritis has the result of filling the Synovial space with an inflammatory infiltrate of lymphoid follicles (mainly CD4+ and helper T cells), plasma cells and macrophages5, 6. Again, as in degenerative forms of arthritis, the viscosity of the Synovial fluid may be increased. In rheumatoid arthritis and osteoarthritis, loose bodies are sometimes able to break away from the chondral or osseous surfaces of a joint. The fibrinocytes on the outer surface of the body derive nutrition from the Synovial fluid, thus proliferating. The center however becomes necrotic. In addition to Osseo-chondral bodies, excessive fibrous exudation into the joint may cause rice bodies in the joint (especially the knee), though this is more common in rheumatoid arthritis5.Synovium:The most blatant changes in the Synovium occur in rheumatoid arthritis. In this condition the membrane undergoes a polypoid fibrovascular thickening. This is to say that it the synoviocytes undergo hypertrophy and hyperplasia, occasionally with giant cell proliferation6. Vascular growth also abounds to meet the demands of the new, highly inflamed tissue. This will give rise to hyperaemia4, 5,6. Collectively this causes the Synovium to grow into a series of papillary folds, which may be traumatized in movement of the joint5.In osteoarthritic degeneration, the Synovium is not a primary site of degeneration6. Limited inflammatory changes may possibly be seen8. As such Synovial thickening is less common and a villous pattern may apply itself to the Synovium. This is generally due to absorption of abraded fragments of cartilage and bone9. However the fact that the fronds are more delicate is a sign of the lack of any great cellular infiltrate in the subsynovium5. The increase in vascularity seen in rheumatoid arthritis is not seen in osteoarthritis. If any change occurs in the vascularity of the Synovium of an aging joint, it is most likely to be a decrease due to the various age associated pathological mechanisms7.Capsule:In early osteoarthritis the joint capsule is largely spared due to its physical distance from the bony joint4. However, in later stages of osteoarthritis, osteophyte formation and joint effusion can have the effect of tightening the capsule8 (see figures 2 and 3).Figure 2: Joint changes in mild osteoarthritis. Tightening of the capsule will have the effect of restricting joint mobility and decreasing the blood supply and lymphatic drainage8.In rheumatoid arthritis the converse is true. Synovial infiltration may lead to destruction of the capsule5. This leads to instability and the inherent possibility of subluxation or dislocation and subsequent gross deformity5, 9. Cartilage:In early osteoarthritis, the primary changes are seen in the chondral surfaces of the joint. This is similar to those signs seen in the normal aging process10. The mechanism behind this is chiefly due to the avascularity of cartilaginous tissue and its low cell to matrix ratio and thus an inability to adequately repair damaged tissue11. Cartilage removal in osteoarthritis occurs mainly in the center or at the weight/ load-bearing portion of a joint12. Flaking and fibrillation of the cartilage at the site of wear occurs, eventually exposing the subchondral bone10.

In rheumatoid arthritis, cartilage removal takes place via the growth of pannus4, 5,6,7,10. This is a granulation tissue which grows from the Synovium, releasing mediators for osteoclastic activity as well as destructive enzymes6, 9. This occurs around the periphery of the joint in preference to the weight bearing areas (as in osteoarthritis), which paradoxically are spared5. A representation of the mechanism of rheumatoid arthritis is shown in figure 4.Figure 4: Progression of rheumatoid arthritis in a joint. Bone:Eburnation in osteoarthritis is the gradual grinding of subchondral bone to form a dense, polished, marble like appearance12. In these areas, the bone is usually thickened or sclerotic12. Consequently there is the possibility that fractures can occur, allowing synovial fluid to be forced into the gaps formed, leading to the formation of fibrous walled cysts which are an important radiographic marker of osteoarthritis and degenerative changes6. Bone remodeling occurs in degenerative changes, forming shape change in the joint surface (e.g. flattening of the superior femoral head) and osteophytic molding at the joint margins9. (These processes are illustrated in figures 2 and 3.) Osteophyte growth leads to joint restriction and deformity such as Heberden s Nodes at the distal interphalangeal joints8,9. Ankylosis of the joint does not normally occur with simple degenerative change9.Figure 3: Advanced osteoarthritic changes in a joint. In rheumatoid arthritis, loss of overlying articular cartilage results in damage to the underlying bone5. Similarly to the erosion of cartilage, bone is eroded by enzymatic activity as well as osteoclastic activity stimulated by mediators released by pannus6. This has the effect of juxta-articular erosions, usually at joint margins, subchondral cysts and osteoporosis6. Fibrous Ankylosis of the bone may occur due to the fibrocellular pannus ossifying6.Muscle Bellies, Tendons and Tendon Sheaths:Change to the muscles and associated structures generally takes place more, if not exclusively in rheumatoid arthritis. Tendons in rheumatoid arthritic patients may undergo degradation within their substance resulting in lengthening without rupture and subsequent muscle dysfunction13. However, Tendonitis and tendon ruptures are not uncommon since any tendon in a synovial-lined sheath is subject to the inflammatory process13.Muscle bellies are subject to weakness due to atrophy secondary to joint inflammation although There may also be other secondary factors affecting muscle integrity such as nutrition and exercise 14. Alternatively, spread of the inflammation may affect muscles in close proximity to the joint6. With advancing age and osteoarthritis, muscles are prone to shorten due to lack of exercise and general degradation in the collagen repair and replacement processes. Muscle strengthening exercises can reduce pain suggesting that muscle weakness plays an important part in the cause of osteoarthritis15.Ligamentous Structures:Laxity of ligaments is a common complaint in rheumatoid arthritis13. This is due to degradation by inflammatory infiltrates and also due to cartilage loss effectively lengthening the functional ligament length6. The same loss of cartilage occurs in osteoarthritis although ligamentous injury may be primary to formation of the disease15.Neural Tissue:In rheumatoid arthritis, up to 42% of patients may have neurologic involvement. Potential causes include compression from rheumatoid nodules against a solid structure, proliferative synovitis or tenosynovitis in and enclosed space (e.g. carpal and tarsal tunnels) and neuropathy due to deformity13, 14. Spinal column involvement may take place in atlantoaxial disease13.In osteoarthritis however neural complications generally stem from osteophytic growth encroaching upon nerves as commonly occurs around the Inter Vertebral Foramina in the Lumbar and Cervical spine9. This can lead to pain radiation in the limbs or parasthesia9. Advancing age also bring about degeneration of the neural tissue directly. An aged brain for instance may be 100g lighter than a young one, with dementia and cerebellar signs affecting people with this shrinkage17. This is especially important with regard to osteoarthritis and the loss of motor neurones in the spinal cord17.Skin and Other Subcutaneous Tissues:Rheumatoid nodules are a common complication in around 20-30% of patients with rheumatoid arthritis13. They generally form granulomatous tissue within pressure subjected areas such as the extensor surface of the elbow, Achilles tendon, extensor surface of the fingers and less commonly over the metatarsal heads or toes13, 16. Presence of nodules may have consequences upon other tissues such as skin, bursae and so on13.Conclusion:Although rheumatoid arthritis and osteoarthritis have differing aetiology, clinical signs and outcomes. The two diseases do share several major similarities. Paramount of these is the massive source of disability, pain and suffering that both conditions have upon any affected population. Thus it is essential as primary care practitioners that we are able to find and prevent these diseases showing any clinical signs and symptoms and thus affecting patients.

ОТКРЫТЬ САМ ДОКУМЕНТ В НОВОМ ОКНЕ

ДОБАВИТЬ КОММЕНТАРИЙ  [можно без регистрации]

Ваше имя:

Комментарий

Другие видео на эту тему