Rheumatoid arthritis

Rheumatoid arthritis (chronic polyarthritis) is the most common inflammatory disease of the joints. The onset is often sudden with pains in the little finger or toe joints. It can affect other joints, particularly the hands, knees, shoulders, ankles and hips. Typically it prefers to attack the carpal bones, the phalangeal joints (Metacarpophalangealgelenk) and the proximal interphalangeal (PIP).

The fingers and Zehenendgelenke (distal interphalangeal, DIP) are, in contrast to gout, not affected. The affected joints become swollen. Reddening of the affected joints may be added. A symmetrical (occurring on both sides) stammfernen synovitis of joints is typical but not mandatory. These symptoms are usually most pronounced. As the illness progresses more and more joints are affected.

In most cases the disease progresses in waves, a surge typically lasts between a few weeks and months. Between the individual episodes, the symptoms diminish. Treatment is difficult because an improvement in health is not necessarily due to the therapy.

Abbreviated with RA is rheumatoid disease (arthritis), PCP (primary chronic polyarthritis) or cP (chronic polyarthritis). Special forms of rheumatoid arthritis are the Felty syndrome, Caplan syndrome and Juvenile idiopathic arthritis.

Epidemiology (incidence, gender and age distribution)

Apart from the activated inflammatory arthritis, rheumatoid arthritis is the most common inflammatory joint disease. Worldwide 0.5-1% of the population is affected. In Germany it is estimated the number of illnesses per 800,000 women is about three times as often as that of men.

Rheumatoid arthritis is susceptible to people of all ages. It frequently occurs between 35 and 45 years of age. It may also affect children and this is what we call juvenile idiopathic arthritis. Prevalence increases with age. The peak incidence is in females between the ages of 55 and 64 and in men between the ages of 65 and 75.

Cause

The causes of this disease have so far been largely unexplained. It is assumed autoimmunity is the cause of the attacked endogenous substances, such as articular cartilage and the cells of the immune system. Recently the link between periodontal disease and the occurrence of rheumatoid arthritis has been discussed. A genetic influence, including through studies of twins has repeatedly been demonstrated with certain MHC alleles and HLA-associates.

Pathogenesis
Changes in the articular
Invading cell groups
Degradation of cartilage and bone by proteolytic enzymes
Necrosis in the heart

Typical x-ray
The clinical picture of rheumatoid arthritis is the result of structural processes that take place in the joint and joint-related tissues. As a full disease appears complex and will be presented in the following paragraph, but is not supported by recent research findings:

It is described that misguided immune cells migrate into the affected joint, and then produce inflammatory mediators – cytokines – to help immune cells communicate with each other. The cell membrane of target cells is a receptor for the key-lock principle and induces the corresponding reactions.

Interleukin-1 (IL 1) and tumor necrosis factor alfa (TNF-α) were too available and accessible to the destructive inflammatory process in the cartilage tissue and the activation of bone-degrading cells. Arising by the action of cytokines in the synovial membrane (synovium), a tumor tissue (the pannus) destroys after a certain period, the cartilage, bone and other structures of the affected joint.

Meanwhile, it has been shown in mice that have emigrated to the typical RA that synovial fibroblasts from affected joints via the bloodstream into previously healthy joints. This could explain the typical growth pattern of the disease.

The inflammatory process is limited however, estimated according to investigations conducted by the Center for Rheumatology, Pathology, Mainz, as compared to others that have been immunologically induced with inflammatory joint diseases. Although this is seen in most cases the reason for the severe joint destruction never provided evidence of the destruction of bone and cartilage by an immunological inflammation.

The joint destruction in rheumatoid arthritis is the work of a specific oncological process, which is developed in phases from the pluripotent cell synovial matrix. The aggressive homogeneous cell penetrates cartilage and bone of densely packed large polygonal cells. The big bright nucleus contains 1 to 2 nucleoli.

These cells express a number of highly potent proteolytic enzymes that they use for the rapid destruction of joint cartilage and bone degradation through empowerment. Aggressive cell groups collapse within a few days and are absorbed by inflamed cells and macrophages. Inflammatory factors are involved in the destruction process. The process, however, leaves behind the familiar, and is often wrongly attributed to the inflammatory pannus.

This aggressive phase may be repeated on the same joint and the process of destruction is continued. This rheumatoid arthritis-specific process is classified by the German Cancer Research Center as a “tumor-like proliferation”. Another potentially fatal inflammatory component of rheumatoid arthritis without interference is the acute death of tissues due to a local release of collagens.

They destroy poor vascularized collagenous structures. It would lead to tendon ruptures in tendons in the eye and attacks on the sclera which could lead to the loss of the eye. They can destroy the walls of arteries and thus lead to dieback of limbs. These are processes that are beyond clinical observations, and are therefore often largely attributed to other diseases (for example) myocardial infarction.

Diagnostics

The diagnosis is done by the laboratory, clinic and imaging procedures. Laboratory: A search for rheumatoid factors (RF antibodies in the blood), test the blood sedimentation rate (ESR) and C-reactive protein (CRP). Rheumatoid factors (RF) here are not conclusive, only indicative and can be demonstrated in other diseases with rheumatoid factors.

The most prominent representation of the ACPA test systems are the CCP assay and the detection of auto antibodies against mutated citrullinated vimentin (anti-MCV ELISA). Clinic: Enumeration and localization of painful and swollen joints and patient self-assessment. Imaging techniques:

At the start and over the course of X-rays or MRI examinations necessary to assess damage to the bone (erosions). Typical radiographic findings include subchondral osteoporosis, destruction of adjacent bone, ankylosis and joint deformities and ulnar deviation.

With the soft tissue and bone scan the pattern of distribution of inflammatory activity of various joints are represented quite well. These are usually for the diagnosis. The following criteria of the American College of Rheumatology (ACR) taken from 1987:

Morning stiffness in at least one joint for at least one hour
At least three different regions of the joint
Arthritis in hand or finger joints
The same joints of both halves of the body
Rheumatoid nodules
Detection of rheumatoid factors
Radiological changes in the joints
The first four criteria must be available over a minimum period of six weeks and be met at least four of these seven criteria.
Disease activity at diagnosis and to guide therapy is often determined by the DAS28.

Therapy
Drug treatment

In the drug therapy of rheumatic diseases there are traditionally four main groups of drugs that can be distinguished:
Analgesics (painkillers)
non-steroidal anti-inflammatory drugs NSAIDs
Glucocorticoids
Antirheumatic drugs (Long-acting anti-rheumatic drugs (LWAR) krankheitskontrollierende medications (disease-modifying anti-rheumatic drugs, DMARDs)

The various classes of drugs have different effects and therapeutic targets. Their application is therefore often simultaneously, for instance, often in addition to DMARDs in addition to cortisone or anti-inflammatories. Modern concepts of treating rheumatism are characterized by the fact that different methods are combined.

The success of treatment depends largely on the different diseases and situations of each individual and the right combination of treatments. Very often this is used alone or in combination, SAARD MTX (methotrexate), the basis of efficacy and tolerability of the quasi-”gold standard” of therapy it is based on.

Newer therapeutics are antibodies, soluble receptors or antagonists, which are directed against pro-inflammatory cytokines such as IL-1 or TNF-alpha and are also called “biologics”. A new treatment option offers the B-cell therapy with rituximab (CD20 monoclonal antibody), which has been approved in Europe since July 2006. Rituximab is currently used after failure of the first TNF-alpha antibody.

Surgical treatment of rheumatoid arthritis

As a branch of orthopedic surgery, the rheumatoid was established. The doctors specialize in applying them to the serious and sometimes severe joint changes that may arise during the course of rheumatic disease and treat them surgically.

Synovectomy

The synovial membrane – the inner layer of joint capsule – is the actual location of the disease process. In the early stages it may very well affect the entire course and thus they need to be removed surgically. Depending on the anatomical conditions of the affected joint, it is often a failure to complete, but a significant reduction of the diseased tissue usually has a soothing effect.

Synovial tissue is also present in the tendon sheaths. Normally, it ensures there is food for and lubrication of, the tendon. In rheumatic diseases, particularly in the back of the hand with the extensor tendon compartments, there can be severe swelling, so-called synovitische cushion.

The diseased synovium attacks these tendons and the tendons can tear. Early Synovectomy has a restraining effect on the disease process. Later when it came to the destruction of joints, such a rich, relatively small intervention was no longer used. Depending on the location, the type and function of the joint there are different methods that are used.

Joint resection

The damaged joint replacement will be removed. Further treatment with plaster and splints have enabled the goal of a functionally satisfactory scar formation. Often these procedures are used at the metatarsophalangeal joints.

Arthrodesis (stiff joints)

The diseased joint is removed and the bone stumps are fixed in a favorable position for the function of each other. After healing one is mostly pain free. In rheumatoid patients fusions are preferable in the thumb, the carpal joint, digital distal (to the so-called DIP joints), upper and lower ankle joints and the midfoot.

Arthroplasty

A portion of the joint is resected, filling the resulting defect with autologous tissue. Mostly a rolled-up tendon is used. This approach makes sense in the area of the wrist.

Endoprostheses

Early detection and consequent stage-drug therapy (see basic therapy) is a very important role. With increasing joint cartilage destruction, movement, and rest pain, also in rheumatic diseases, the decision has been made for a joint prosthesis.

The aim of this approach lies in a reduction of pain; improving joint mobility and joint stability. A special feature of prosthetic surgery in rheumatic patients is consistent with inner rheumatic inflamed synovial membranes (synovium).

Typical areas that can be replaced with an artificial joint for rheumatic patients are the major joints (shoulder, hip, knee, ankle, and elbow) and a few small joints (metacarpophalangeal and finger joint). Particularly in rheumatic patients, they should not wait too long to get the inflammatory destruction of stabilizing capsular ligament structures or the development of bone defects prior to the so-called Endoprothesenoperation.

In arthroplasty (installation of artificial joints) there is a distinction of cemented joints. At the knee, it also delineates in ascending order according to the degree of enforced joint leadership “uncoupled” from “partially coupled” and “fully coupled”prostheses.

The used prosthetic materials and designs are different from such as those used in conventional osteoarthritis. A peculiarity, however, is the artificial replacement of MCP joints and PIP joints. Generally speaking, the operational implementation of an artificial joint in rheumatic arthritis is not by the patient.

Immuno-modulating drugs (e.g. cortisone, biologics, etc.) reduce the body defenses through chronic illness and other factors after surgery and the prosthetic loosening rate compared to other arthritis sufferers. Nevertheless, the artificial joint replacement in rheumatic patients is a very great enrichment of the treatment options with a significant increase in quality of life.

Radiosynoviorthesis

An alternative to surgical treatment is the radiosynoviorthesis (RSO). Efficacy in rheumatoid arthritis is confirmed by studies with a high level of evidence. The indication is given to the RSO after six months of basic therapy by intra-articular injection of cortisone solutions of the disease process. The successes of the RSO are better the sooner it is used in the disease process.

As absolute contraindications are pregnancy and lactation, as a relative contraindication to treatment in children and adolescents. The nuclides used (especially 90Y, 186 Re and 169Er) are determined by the size of the treated joint. It is pure or at least main beta-emitters.