rheumatoid arthritis Flashcards
what is the rheumatologic (or rheumatoid) disease?
Rheumatologic (or rheumatoid) disease is much more than “arthritis” and encompasses a large group of dis- orders of the rheumatic diseases that affect bones, joints, and muscles.1
what is arthritis and other inflammatory conditions?
Often arthritis is used interchangeably with rheumatism or rheumatoid arthri- tis to denote aches, pains, and stiffness in the joints and muscles, but these terms are not synonymous. More than 100 rheumatologic (or rheumatoid) diseases affect various parts of the body. Some of the more common types include rheumatoid arthritis (RA), osteoarthritis (OA), systemic lupus erythematosus (SLE), juvenile rheu- matoid arthritis (jRA), scleroderma (SD), Sjögren syn- drome (SS), gout, ankylosing spondylitis, Lyme disease, giant cell arteritis (or temporal arteritis), bromyalgia syndrome (FMS), and psoriatic rheumatoid arthritis (pRA).1
What is the pathophysiology of musculoskeletal problems?
The cause of musculoskeletal problems is usually in am- matory, metabolic, degenerative, tumor, or some combi- nation thereof. Synovial in ammatory disorders, such as rheumatoid arthritis, begin in the synovium and second- arily damage the cartilage, joint capsule, and bone. In ammation at entheses, the insertion sites of tendons or ligaments on bone, is characteristic of the spondylo- arthropathies, such as ankylosing spondylitis. Crystal deposition disorders, such as gout or pseudogout, may also cause articular in ammation. Infections primarily involve the joint cavity (septic arthritis) or bone (osteo- myelitis). The nonin ammatory, degenerative disease osteoarthritis begins in the cartilage and leads to cartilage loss, subchondral new bone formation, and marginal bony overgrowth. Cartilage loss also may occur secondarily to synovial in ammation or trauma.1 Osteonecrosis of bone may be associated with secondary cartilage damage after collapse of the bony end plate. In ammatory diseases of the muscle usually manifest with painless proximal weakness. Periarticular in am- mation may involve tendons or bursae, and these struc- tures are common causes of pain and stiffness, often misinterpreted as arising from the joint itself. Finally, the common clinical problem of bromyalgia (widespread muscle pain) is characterized by soft tissue pain with local tenderness in speci c points but without abnormal blood studies.1
Although the rheumatologic diseases comprise a group of more than 100 important diseases, this chapter is limited to a discussion of eight: rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis (PsA), sys- temic lupus erythematosus (SLE), Lyme disease, bromy- algia (FMS), temporal arteritis, and Sjögren syndrome (SS), which are among the most common forms encoun- tered, are more dentally related conditions, and can serve as models for the dental management of other forms. Several important items regarding the dental manage- ment of patients with rheumatologic and connective tissue disorders, including effects on the temporoman- dibular joint (TMJ), salivary glands, and oral mucosal tissues, organ and system involvement, and drug therapy, are discussed here.
what is rheumatoid arthritis?
Rheumatoid arthritis (RA) is an autoimmune disease of unknown origin that is characterized by symmetric in ammation of joints, especially of the hands, feet, and knees. Severity of the disease varies widely from patient to patient and from time to time within the same patient.
pathophysiology of rhematoid arthritis?
With RA, the fundamental abnormality involves micro- vascular endothelial cell activation and injury.2-5 Primary changes occur within the synovium, which is the inner lining of the joint capsule (Figure 20-1). Edema of the synovium occurs, followed by thickening and folding. This excessive tissue, composed of proliferative and inva- sive granulation tissue, is referred to as pannus. In addi- tion, marked in ltration of lymphocytes and plasma cells into the capsule occurs. Eventually, granulation tissue covers the articular surfaces and destroys the cartilage and subchondral bone through enzymatic activity (Figure 20-2). This process also extends to the capsule and liga- ments, causing distention and rupture. New bone or brous tissue then is deposited, resulting in fusion or loss of mobility.2-5
A likely sequence of events begins with a synovitis that stimulates immunoglobulin G (IgG) antibodies. These antibodies form antigenic aggregates in the joint space, leading to the production of rheumatoid factor (autoantibodies). Rheumatoid factor then complexes with IgG complement, a process that produces an in am- matory reaction that injures the joint space.2-5
RA is a pleomorphic disease with variable expression. The most progressive period of the disease occurs during the earlier years; thereafter, it slows. Onset is gradual in more than 50% of patients, and as many as 20% follow a monocyclic course that abates within 2 years. Another 10% experience relentless crippling that leads to nearly complete disability. The remainder follows a polycyclic or progressive course.2-5 The long-term prognosis for people with abrupt onset of disease is similar to that for people with gradual disease onset. The course and sever- ity of RA are unpredictable, but the disorder is character- ized by remissions and exacerbations. For most patients, however, the disease is a sustained, lifelong problem that can be controlled or modi ed to allow a normal or nearly normal life.2-5
The life expectancy of persons with severe RA is shortened by 10 to 15 years. This increased mortality rate usually is attributed to infection, pulmonary and renal disease, and gastrointestinal bleeding.2-5
Many complications may accompany RA. Included among these are digital gangrene, skin ulcers, muscle atrophy, keratoconjunctivitis sicca (Sjögren syndrome), TMJ involvement, pulmonary interstitial brosis, peri- carditis, amyloidosis, anemia, thrombocytopenia, neu- tropenia, and splenomegaly (Felty syndrome).2-5
drug management of rheumatoid arthritis?
Symptoms of pain and swelling in RA are mediated, at least in part, by intense cytokine activity. NSAIDs inhibit proin ammatory pros- taglandins and are effective treatments for pain, swelling, and stiffness, but they have no effect on the disease course or on risk of joint damage. On the other hand, antiin am- matory properties have been noted for several disease- modifying antirheumatic drugs (DMARDs), which are used principally to control disease and to limit joint damage.2-5 These drugs include methotrexate and biologic response modi ers with actions targeted against speci c cytokines, such as tumor necrosis factor-α (TNF-α). Cor- ticosteroids are powerful, nonspeci c inhibitors of cyto- kines and, in some studies that compared them with placebo, are reported to effectively delay joint erosion.1-7
NSAIDs, especially aspirin, constitute the cornerstone of treatment. Aspirin may be prescribed in large doses on an individual basis. A common approach is to start a patient on three 5-grain tablets four times a day, then to adjust the dosage on the basis of patient response. The most common sign of aspirin toxicity is tinnitus. Should this occur, dosage is decreased. In addition to aspirin, many NSAIDs are available for use (see Table 20-3). Some of the more common NSAIDs include cyclooxy- genase (COX)-2 inhibitors, namely, celecoxib (Celebrex); ibuprofen (Motrin, Advil, Rufen, Nuprin); naproxen (Naprosyn, Aleve); sulindac (Clinoril); tolmetin (Tolec- tin); fenoprofen (Nalfon); piroxicam (Feldene); diclofe- nac (Voltaren); urbiprofen (Ansaid); di unisal (Dolobid); etodolac (Lodine), and nabumetone (Relafen).1-7
corticosteroids and RA
Corticosteroids (e.g., predni- sone, prednisolone) frequently are useful in controlling acute symptoms; however, because of multiple adverse effects, long-term usage is avoided if possible. One of the more potentially signi cant associated adverse effects is secondary adrenal suppression (see Chapter 15).1,3,7
