20: Autoimmune Disorders

Autoimmune Disorders

Concepts of Immunity and Autoimmunity

The human body has the ability to resist almost all types of organisms or toxins that tend to damage the tissues and organs. This capacity is termed immunity. A specific type of immunity that arises from general processes, rather than from specific disease organisms is called innate immunity.

In addition, the human body has the capability to develop extremely powerful specific immunity against individual invading agents such as lethal bacteria, viruses, toxins, etc. This is called acquired immunity. Acquired immunity is caused by special immune system that forms antibodies and activated lymphocytes that attack and destroy specific organisms or toxins.

Two basic forms of acquired immunity occur in the body. In one of them the body develops circulating antibodies, which are globulin molecules in the blood that are capable of attacking the invading agent. This type of immunity is called humoral immunity or B-cell immunity (because B-lymphocytes produce the antibodies). The second type of acquired immunity is achieved through the formation of large umbers of activated lymphocytes that are specifically designed to destroy the foreign agent. This type of immunity is called cell mediated immunity or T-cell immunity (because the activated lymphocytes are T-lymphocytes).

Autoimmunity

Failure of the immune system to tolerate (antigen-specific immunological unresponsiveness) self-tissues. It is a condition in which structural or functional damage is caused by the action of immunologically competent cells or antibodies against normal components of the body.

When the concept of autoimmunity came to be accepted as a pathogenic mechanism, a large number of diseases were suggested to have an autoimmune etiology, based on the finding of autoantibodies in the patients. However, autoantibodies have also been found in the serum or tissues of otherwise normal and healthy elderly individuals. Autoantibodies are also formed following tissue injury and may serve a role in the removal of the products of tissue breakdown. This lead to the need to formulate criteria for diagnosing autoimmune diseases.

Diagnostic criteria for autoimmune disorders

The first criterion for recognizing autoimmune disease was given by Witebsky in 1957. This criterion was extended by many authors. Robert H Waldman documented the following criteria:

Classification of autoimmune diseases

Fergusson (1995) categorized autoimmune diseases as organ specific and non-organ specific.

Various classifications in literature do not necessarily group autoimmune diseases that specifically affect the orofacial region. Sumanth and Balaji Rao have proposed a simpler classification of autoimmune diseases that affect the orofacial region.

Giant Cell Arteritis

Giant cell arteritis is a relatively common form of large vessel vasculitis occurring predominantly in elderly individuals. The mean age of onset is 70 years with a 2:1 female-to-male ratio. Temporal artery is the common artery that is involved in cranial arteritis (Figure 1).

Muki proposed an autoimmune basis for giant cell arteritis because it occurred more frequently in patients with other autoimmune disorders such as thyroid disease or rheumatoid arthritis.

Periodontal Disease

For almost two decades the concept of autoimmune pathogenesis for periodontal disease was considered.

Alphonse et al (1981) have detected rheumatoid factor by latex slide agglutination in subgingival plaque, inflamed gingival tissue, stimulated pooled saliva and serum of patients suffering from chronic moderate periodontitis. They correlated the presence of rheumatoid factors to the periodontal disease and concluded an autoimmune origin of the disease.

Ftis et al (1986) found increased levels of antibodies to type I collagen in patients with periodontal disease than in control subjects.

Hirsch et al (1988) used enzyme-linked immuno spot test to enumerate antibody secreting cells to human collagen types I–IV by cells isolated from gingival and peripheral blood of individuals suffering from adult periodontitis. Analysis revealed the presence of high numbers of cells that secreted antibodies to type I collagen when compared to type III. They suggested that autoimmunity may contribute to the pathogenesis of this common disease.

Anusaksathien and Dolby (1991) postulated many possible explanations to explain the presence of autoantibodies in periodontal disease.

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder that may affect many tissues and organs—skin, blood vessels, heart, lungs and muscles—but principally attacks joints, producing a non-suppurative proliferative synovitis that often progresses to destruction of the articular cartilage and ankylosis of joints. Although the cause for RA remains unknown, there is convincing evidence that autoimmunity plays a pivotal role in its chronicity and progression, likening this condition to other so-called connective tissue diseases. RA can affect the TMJ.

Pathogenesis

It is currently believed that RA is triggered by the exposure of an immunogenetically susceptible host to an arth-ritogenic microbial antigen.

The involved mechanisms in the causation could be:

1. Genetic susceptibility: Rosenberg and Nuki have shown that 65–80% of the individuals suffering from RA have human leukocyte antigen (HLA)-DR4 and HLA-DR1 or both. Other haplotypes like DW4, DW10, DW13, DW14 and DW15 have also been implicated.

2. Primary exogenous arthritogen: Roudier et al proposed Epstein–Barr virus as the primary microbial agent for the causation of RA. Other microbial agents like retroviruses, parvoviruses, mycobacteria, borrelia and mycoplasma could also initiate the disease.

3. Autoimmune reaction: Warder in 1940 proposed the presence of rheumatoid factor, which was the first human autoantibody described in association with RA.

    Although T cells played a primary role in the pathogenesis of RA, B cells were also involved. In 1993, Panayi reported that approximately 80% of patients have rheumatoid factors which were directed against Fc portion of IgG, present in serum and synovial fluid. The presence of rheumatoid factors in the joints is believed to contribute to the inflammatory reaction. Williams in 1996 observed that rheumatoid factors showed principal specificity for structures on C3 and C2 (Fc) domains of IgG, which thus defined rheumatoid factor as an autoantibody associated with RA.

4. Mediators of tissue damage: Panaji in 1993 reported that the rheumatoid synovium was heavily infiltrated with lymphocytes, most of which were CD4+ helper T cells. They generate cytokines, which in turn could activate other immune cells and macrophages.

Joint manifestations

Katz classified the joint manifestations as:

The changes of RA most useful for diagnosis are noted in the hands and wrists. They include swan neck deformity, ulnar deviation, dorsal interosseous muscle atrophy and swelling of wrist.

Temporomandibular joint manifestations

It is believed that TMJ symptoms develop in more than one-third of the patients during the first year of RA.

According to Tegellerg and Kopp (1987) and Votalia (1964), the most characteristic clinical signs of RA affecting the TMJ were palpatory tenderness of the joint, crepitus from the joint and swelling in relation to the TMJ region.

Almost 60% of the individuals present with bilateral involvement of joints.

Severe RA involving the TMJ can result in a progressive anterior open bite due to bilateral destruction of mandibular condyles.

Hugh Ogus described a possible course of rheumatoid involvement of the TMJ. He proposed that the TMJ involvement progresses through three phases:

Radiographic features of rheumatoid arthritis affecting the TMJ

1. Formation of new bone (marginal proliferation) was described in 1975 by Hugh Ogus. It is reported that the erosions of the articular surface were the most important diagnostic finding of RA in other joints and not the TMJ.

2. Subcondylar cystic destruction and severe destruction of bone eventually lead to complete loss of condyle. Such destruction will give the remaining condylar bone the shape of the mouth piece of a flute.

3. Anterior open bite and reduced joint space (due to destruction of articular cartilage).

4. The most characteristic radiographic signs of RA in the TMJ are erosions of cortical outline and reduced joint space (Figure 2) as proposed by Akerman et al in 1988.

Kopps in 1995 stated that the radiographic diagnosis of RA in TMJ was difficult. However, absence of radiographic changes in the TMJ will not exclude the possibility of early RA in TMJ.

Extra-articular manifestations of rheumatoid disease

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Jan 12, 2015 | Posted by in Oral and Maxillofacial Radiology | Comments Off on 20: Autoimmune Disorders

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