Rheumatoid arthritis is an autoimmune disease in which an inflammatory process occurs in the connective cartilage tissue and affects the joints.
Statistics say that 1% of the entire population suffers from the disease, and this is no less than 58 million people.
The pathogenesis of rheumatoid arthritis disease is worth considering in more detail.
Today, the etiology of rheumatoid arthritis is not yet fully understood. However, there are two options for the occurrence of the disease:
Hereditary causes are due to the patient’s genetic predisposition to damage the body’s immune system. A direct connection has been proven between the onset of the disease and the presence of special HLA antigens in the patient.
In addition to destroying the immune system, these antigens alter the body's normal response to infectious agents. HLAs block the body's defense system, its immune ability to resist, and allow the disease to “settle” in the body.
The hypothesis of a genetic predisposition to the development of pathology is confirmed by the fact that rheumatoid arthritis is often observed among close relatives and twins.
Infectious etiology. Modern medicine has data on several infectious agents that can trigger the appearance of rheumatoid arthritis. They are viruses:
And this list is not complete. Today, doctors are actively discussing the role of microbacteria in the development of pathology. Microbacteria are capable of expressing stress proteins that are causative agents of rheumatoid arthritis.
The following categories of people are at risk for arthritis:
The pathogenesis of rheumatoid arthritis is based on autoimmune processes that are disrupted at the genetic level. First, the articular membrane is damaged, then the disease becomes proliferative. Next, damage and deformation of cartilage and bone tissue begins.
In the synovial fluid, the concentration of collagen degradation products increases. The influence of these factors leads to the formation of immune complexes. After this, the mechanism of phagocytosis of immune complexes is triggered, which provokes the development of rheumatoid arthritis.
The appearance of immune complexes gives rise to platelet aggregation, promotes the formation of microthrombi, and causes pathological changes in the blood microcirculation system.
Immune complexes that damage joints cause inflammation. The pathogenesis of rheumatoid arthritis determines its clinical picture.
The main clinical manifestation of the disease is articular syndrome. Typically, with rheumatoid arthritis, joint damage occurs symmetrically on both sides.
The onset of the disease most often coincides with cold weather conditions and those periods when physiological changes occur in the patient's body. In addition, arthritis can begin after an injury, infection, stress or hypothermia.
Before the first signs of the disease appear, it is in a prodromal period, which can last several weeks or even months.
Main symptoms of arthritis:
Most often, the onset of the disease is characterized as subacute. But there is also an acute picture of the pathology: sharp pain appears in the joints and muscles, significant morning stiffness and fever are observed.
If rheumatoid arthritis develops gradually, the changes are subtle, and subsequent progression of joint damage does not impair their functionality.
The following symptoms are typical for the initial stage of the disease:
As the disease progresses, fibrotic changes are observed in the joint capsule, ligaments and tendons. These degenerative processes lead to deformities, contractures and dislocations of the joints.
There is limited mobility in the joints. Over time, the disease can lead to complete loss of their function. First of all, diarthrosis of the hand suffers: carpal, phalangeal and interphalangeal.
If the inflammatory process affects the interphalangeal joints, the patient’s fingers acquire a spindle-shaped shape. The hand of a person suffering from this type of arthrosis cannot bend into a fist. The interosseous spaces collapse, muscle atrophy develops. Eventually, the entire brush becomes deformed.
Next, damage occurs to the wrist joints. This is manifested by the appearance of pain in the wrist area, swelling, bone destruction, and the formation of ankylosis with adjacent joints.
Deformation of the hand can lead to the fingers becoming shorter, one phalanx growing into the other, and contracture developing in the joints.
The constant progression of the disease leads to impaired sensitivity and the occurrence of paresis of the fingers, as a result of which they lose mobility.
Damage to any joints is accompanied by stiffness in the morning and limited mobility. These factors lead to the fact that it becomes difficult for the patient to take care of himself; he cannot wash himself, comb his hair, get dressed, or hold cutlery in his hand.
Often people suffering from rheumatoid arthritis lose their ability to work and become disabled.
The course of rheumatoid arthritis can occur in one of the following ways:
Diagnosis of rheumatoid arthritis is currently carried out on the basis of a blood test, x-ray of the affected joints, and symptoms characteristic of this pathology. The blood is examined for ESR, platelet count, rheumatic factor.
The titer of antibodies to citrulline-containing cyclic peptide—ACCP—is considered the most effective.
Treatment of rheumatoid arthritis depends entirely on the symptoms of the disease.
Treatment of rheumatoid arthritis is a rather long process, which often takes years. It is very important to prevent osteoporosis in a timely manner. The patient's calcium balance in the body must be restored. To do this, the patient is prescribed a diet rich in this substance. The diet must include milk, cottage cheese, cheese, and walnuts.
The patient must perform daily therapeutic exercises. The selection of exercises is carried out so that muscle mass is preserved in the joint area, and the joints themselves do not lose their mobility.
Paraffin therapy, mud therapy, electrophoresis, and phonophoresis are prescribed as physiotherapeutic procedures. If the disease is in remission, sanatorium treatment is indicated.
Severe joint deformation requires surgical intervention, during which the joint is reconstructed and its functionality is restored.
Drug therapy consists of the use of the following groups of drugs:
Treatment with basic drugs slows the progression of the disease and brings about remission. Due to the fact that there are no significant joint deformities at the early stage of rheumatoid arthritis, basic therapy is most effective and plays an important role in the complex treatment of the pathology.
The most popular means of basic therapy are gold preparations, cyclosporine, methotrexate, and aminoquinoline drugs. If the prescriptions do not provide the expected effect, the doctor selects a combination of medications that should replace the previous therapy.
Nonsteroidal anti-inflammatory ointments and medications for rheumatoid arthritis are very effective. They provide antiviral and antibacterial effects.
Glucocorticosteroids should be prescribed in combination with slow-acting drugs. Current treatment methods involve the use of monoclonal antibodies, which slow the progression of the disease.
For each patient, treatment is prescribed individually. The duration of arthritis, the degree of joint damage, and the presence of concomitant diseases are taken into account. The patient must strictly follow all the doctor’s recommendations; only under this condition will the therapy bring results.
Arthritis, in contrast to dysfunctional conditions, is characterized by inflammatory processes (changes) in various tissue structures of the TMJ. which may be infectious-allergic. traumatic and less often - specific origin.
Infection of the joint occurs by contact with osteomyelitis of the branch and articular process of the lower jaw, purulent otitis. boils of the external auditory canal. by hemohepic route from the non-articular area for mumps, abscesses and phlegmon of the maxillofacial area and by metases from distant foci of infection. Inflammatory processes in the TMJ can be caused by common infectious diseases (influenza, tonsillitis, measles, scarlet fever, etc.). Lesions of this joint develop in rheumatic or rheumatoid polyarthritis.
By contact, infection of the joint is caused through the inner wall of the external auditory canal, to which the articular head is adjacent (N.M. Mikhelson, 1951; Herferd, 1962 and others).
With purulent otitis media, the periarticular area is first infected; then the infection penetrates through the Glaser fissure into the joint cavity (G.A. Vasiliev. 1950). In general infectious diseases, the inflammatory process can develop not only as a result of penetration of the infection itself into the joint cavity, but also through intoxication during anaphylaxis. associated with bacterial proteins (M.M. Diteriks. 1937; B.P. Kushelevsky, 1954;
Z.E. Bykovsky, 1949 etc.). When exposed to toxins, the body becomes sensitized. and at the same time, a wide variety of external factors (high temperature, hypothermia, trauma, hormones, toxins, fatigue, mental influences, etc.) can cause not only an exacerbation of existing hidden or fading processes, but can also create new foci of the infectious process .
A favorable condition for the development of the inflammatory process in the joint is the presence of many folds and convolutions, rich in small vascular branches of the capillaries. When exposed to infection or toxins, capillary thrombosis occurs, trophism is impaired and necrosis occurs in the tissues of the articular surfaces (Axhausen. 1928; Wassmund. 1952).
Acute and subacute inflammatory processes in the TMJ can arise as a result of one-stage macrotrauma (V.I. Korobkov, 1964; Yu.I. Vernadsky, 1966; Yu.A. Petrosov, 1982, 1996, etc.).
As a result of TMJ injury, there may be hemorrhages into the joint cavity with the formation of hematomas. After injury, the hematoma resolves very slowly, over several weeks. This has been confirmed by experimental studies
V.N. Pavlova (1954). An unresolved blood clot constantly irritates the proprioceptors of the joint capsule, which leads to increased production of synovial fluid and dysfunction in the joint. With traumatic damage to blood vessels, the vascularization of the joint is disrupted, in which even normal load leads to sudden degenerative changes in the bone structure of the articular surfaces. Vascular changes can manifest themselves in older people in the form of atherosclerosis, thrombophlebitis of some vessels (GJ Griffin, CJ Chap, 1961). When inflammation of a joint of a traumatic nature occurs in the initial stage, venous hyperemia, proliferation and expansion of the blood vessels of the epiphysis of the articular head are observed. In some areas, these vessels pierce the basal end plate, entering the cartilage and spreading towards the surface of the joint. These vascular and, together with them, connective tissue strands cause, during a long course of arthritis, the destruction of cartilage in the area where it is not calcified, form bone plates and, thus, lead to the development of intracartilaginous ossifications. In the peripheral part of the joint, where the articular capsule comes into contact with the periosteum, fibrocartilaginous growths first appear, in which vascularization and ossification occur. Marginal bone growths are so-called osteophytes. They are classified as arthrosis.
Arthritis in advanced cases is combined with arthrosis. A purulent infection causes an inflammatory process in the joint. After infection of the intra-articular synovial fluid, the process covers the joint capsule, then the purulent process melts the cartilaginous surfaces of the joint, including the meniscus, and gradually destroys the bone tissue of the joint elements, i.e. leads to arthrosis.
Traumatic injuries to joints, in addition to blows and bruises, can occur during childbirth when forceps are applied. We observed children with deforming arthrosis and ankylosis, the etiological factor of which was birth trauma.
Acute inflammatory processes in the TMJ can occur when exposed to a specific infection (tuberculosis, gonorrhea, actinomycosis, brucellosis, etc.).
Tuberculous arthritis is very rare, and more often in childhood and adolescence. The lesion covers one, two, less often three joints (P.F. Bogdanov). We encountered only two cases of tuberculous arthritis, which occurred with acute pain and limitation of movement in the joint. Isolated cases were observed by V.N. Konchalovsky, B. Lyakhovsky, A.M. Rashevsky, T.P. Vladychenkova and others).
Gonorrheal arthritis, according to Finger, accounts for 79 cases out of 559 patients (cited by A.E. Gelman). Goldin identified 9 cases of gonorrheal arthritis out of 65 patients with gonorrhea (but V.I. Korobkov).
There are isolated reports in the literature about syphilitic, actinomycotic acute arthritis (Yeissl, 1903).
Acute TMJ arthritis can occur with rheumatic and rheumatoid polyarthritis.
1. Arthritis caused by infection or parasitic infestation. These include:
— Arthritis that occurs after an acute respiratory infection, intestinal or urogenital infections. They appear after 4-6 weeks and belong to the group of reactive arthritis. This also includes arthritis, which develops as an immunopathological response to the introduction of an infectious agent.
— Arthritis in chronic infections (tuberculosis, leprosy, syphilis, viral hepatitis, infective endocarditis, HIV). They represent generalized inflammatory reactions.
— Arthritis caused by excessive growth of microflora in the blind intestinal pouch after surgical interventions.
— Arthritis due to helminthic and protozoal infections.
— Arthritis developing after vaccination.
B. Arthritis caused by direct damage to the synovial membrane of the joint by the causative agent of the disease. These are arthritis due to Lyme disease, syphilis, tuberculosis, atypical fungal or viral infection, and protozoal infestations.
— Artitis in malignant tumors (paraneoplastic). They develop either as an immunopathological response to a tumor or as a result of metastasis to the synovium of the joint.
— Arthritis in hematological diseases (hemorrhagic diathesis, hemolytic anemia).
— Arthritis, with acute pancreatitis and pancreatic cancer, as a result of cytosteatonecrosis.
— Arthritis due to decompression sickness, caused by improper decompression after a dive.
— Arthritis due to metabolic disorders (gout).
- Allergic arthritis. As a reaction to the administration of medications, serums, implantation of silicone prostheses, exposure to chemicals.
- Traumatic arthritis. They occur both with serious injuries and with light, but constantly repeated, monotonous load on the joint.
1. Pain in the affected joint. Occurs when moving or lifting heavy objects.
2. Feeling of stiffness.
3. In the joint area there is hyperemia, swelling, the skin over the joint is hot to the touch.
4. The joint has limited mobility.
It develops acutely, 1-3 weeks after the infection. There is swelling, hyperemia of the affected joint, the joint is painful, and movement is limited. Reactive arthritis most often affects asymmetrical joints; it is oligoarthritis. The joints of the toes are usually affected. Swelling quickly increases around the joint, and the skin becomes cyanotic in color. Often accompanied by inflammation of the tendons where they attach to the bones. Walking is difficult due to pain. Reactive arthritis lasts up to several weeks, but sometimes it can be prolonged. Extra-articular manifestations of the disease may be observed. This damages the skin, mucous membranes of the oral cavity, external genitalia, and conjunctiva. Possible development of myocarditis or pericarditis, damage to the renal collecting system (glomerulonephritis), and peripheral nervous system. With chlamydial infection, Reiter's syndrome occurs - a combined lesion of the urethra, conjunctiva and arthritis.
This is a rheumatic disease, the etiology of which is still unknown. There is information about a genetic predisposition to this disease. It develops more often in the autumn-winter period, during epidemics of respiratory diseases. In women, taking hormonal contraceptives and pregnancy reduce the risk of developing rheumatoid arthritis, while lactation, on the contrary, provokes it.
1. The initial stage, during which only osteoporosis around the joints is detected.
2. Osteoporosis and narrowing of the joint space.
3. Osteoporosis, narrowing of the joint space and bone erosion.
4. Joint ankylosis joins the above.
Local therapy - the use of non-steroidal anti-inflammatory drugs in the form of creams, gels, ointments. Intra-articular administration of glucocorticoids is also used. For moderate and severe pain, analgesics from the NSAID group are used. The use of chondroprotectors is relevant. These are drugs that slow down or stop the destruction of cartilage; their use reduces pain and partially restores joint function. For arthritis of infectious etiology, etiotropic therapy is prescribed.
Includes therapeutic exercises, reducing stress on joints, and selection of orthopedic shoes. Of the physiotherapeutic procedures, the most effective are massage, paraffin therapy, magnetic therapy, ultrasound, and acupuncture.
Indicated for severe forms of arthritis when joint function is lost.
c) biopsy of the synovial membrane (hypertrophy and increase in the number of villi, proliferation of integumentary synovial cells, fibrin deposition on the surface of the synovium, foci of necrosis)
d) study of synovial fluid (in RA – turbid, viscosity is reduced, the number of cells per μl is 5-25 thousand, neutrophils > 75%, mononuclear cells < 25%, ragocytes are present - neutrophils with inclusions in the cytoplasm of the Russian Federation, their shape resembles a mulberry, total protein 40-60 g/l, glucose 0.5-3.5 mmol/l, LDH > 300 units, RF detected)
Diagnostic criteria for RA:
To make a diagnosis of RA, at least 4 of the following criteria must be present:
1. morning stiffness for more than 1 hour
2. arthritis? 3 joints (polyarthritis)
3. arthritis of the joints of the hands
4. symmetrical arthritis
5. rheumatoid nodes
6. rheumatoid factor
7. characteristic radiographic changes
These symptoms must last for at least 6 weeks because... sometimes other arthritis can present the same way.
1. Treatment should be permanent (lifelong), complex (medication + physiotherapeutic + sanatorium-resort + surgical according to indications), individual, staged.
2. Drug therapy:
A. Basic therapy (slow-acting drugs):
— Arava (leflunamide) (1st place in effectiveness, used for > 5 years)
— methotrexate (2nd place in effectiveness, used for > 20 years)
- gold preparations (tauredon) (3rd place in effectiveness, used for > 60 years)
— sulfasalazine (4th place in effectiveness, used > 50 years)
— D-penicillamine (5th most effective, used > 40 years)
— azathioprine (6th place in effectiveness, used > 30 years)
— aminoquinoline drugs (plaquenil) (7th place in effectiveness, used for > 40 years);
All these drugs are effective in 40% of cases, in 30% there are side effects, in another 30% there is no effect; On average, the effect of basic therapy occurs after 2 months (Arava - 1 month). It is possible to combine basic drugs (methotrexate + sulfasalazine + plaquenil, etc.), but only if they are pathogenetic compatible.
B. Anti-inflammatory therapy:
1) NSAIDs: traditional, classic (indomethacin, diclofenac 75-150 mg/day in 2-3 doses, ibuprofen 1.2-3.2 g/day in 3-4 doses, etc.) and selective COX-2 inhibitors ( fewer side effects: meloxicam/movalis 7.5-15 mg/day, nimesulide/nimesil/nise 100 mg/day in 2 doses, celecoxib/celebrex)
— any drug can be prescribed, usually they start with the classic ones; if there are contraindications (gastric and duodenal ulcers, hypertension, kidney disease), selective COX-2 inhibitors are indicated (they are not started with them due to the higher cost of these drugs)
- if there is no effect, the drug is changed (effectiveness is assessed after 5-7 days of use)
- main side effect: damage to the gastrointestinal tract in the form of dyspepsia or ulcers (stomach, 12pcs, intestines); if ulcers are at risk, proton pump inhibitors (omeprazole) can be used
2) GKS – can be used
a) orally in small doses: 5-7.5 mg of prednisolone
b) IV in the form of pulse therapy - only in the presence of systemic manifestations (except for renal amyloidosis)
c) intra-articularly (not > 3 times/year) – for synovitis: diprospan (betamethasone), depo-medrol (methylprednisolone), kenalog (triamcinolone)
Each patient should be prescribed at least 2 drugs (1 from A, 1 from B), but there may be more. Only 20% of patients manage to achieve remission of the disease (on some basic drug); for the second time it is no longer effective. All RA patients have the right to free outpatient treatment, but not all drugs are included in the order (no arava: $100 a month or gold drugs: $70 a month).
Current trends in the treatment of RA - anti-TNF ? -therapy : Etanercept (Immunex, Enbrel) - a soluble dimer of the TNF?-receptor combined with IgG 1 (s.c. 2.5 mg 2 times a week), Infliximab (Remicade) - a monoclonal antibody against TNF? (iv drip after 8 weeks); the cost of a year's course of treatment is $10,000-12,000; these drugs are highly effective, because stop the progression of RA.
3. Physiotherapeutic treatment - should be aimed at reducing pain and inflammation, thermal procedures (mud, ozokerite, paraffin) are not allowed, electrotherapy, laser therapy, balneotherapy are allowed.
4. Sanatorium-resort treatment : the sanatoriums “Radon” (Dyatlovsky district of the Grodno region), “Pridneprovsky” (Rogachevsky district) are recommended; "Them. Lenin" (Bobruisk)
5. Surgical treatment:
a) synovectomy – causes attenuation of the process only for 2-3 years, i.e. temporarily; currently
not used, because causes secondary arthritis
b) joint replacement (hip, knee and smaller)
6. Rehabilitation : changing the stereotype of motor activity to prevent joint deformation; orthopedic aids that keep the joint in the correct position; physical therapy, physical therapy, sanatorium-resort treatment.
ARTHRITIES ( arthritis , singular; Greek arthron joint + -itis) are inflammatory diseases of the joints. The term “arthritis,” introduced by Hippocrates, was used in subsequent centuries to refer to any joint pathology. Starting from the 16th century, separate nosological forms of artitis began to be gradually identified.
Thus, Baillou (G. de Baillou) identified rheumatism among arthritis. In the 17th century, T. Sydenham described gout and rheumatoid arthritis as independent nosological forms. Several decades later, infectious specific arthritis was united by C. J. Bouchard under the general name “infectious pseudorheumatism.” In the 19th century, F. Muller, having made the first attempt to classify joint pathology, clearly distinguished inflammatory diseases of the joints (arthritis) from dystrophic ones (arthrosis). This division remains important to this day.
According to the domestic working classification, adopted by the first All-Union Congress of Rheumatologists in 1971, there are two main groups of arthritis: 1) arthritis - independent nosological forms; 2) arthritis associated with other diseases.
Independent nosological forms include: rheumatoid arthritis, rheumatic polyarthritis (Sokolsky-Buyo disease), ankylosing spondylitis (ankylosing spondylitis), infectious specific arthritis (gonorrheal, tuberculosis, dysenteric, viral, etc.), infectious-allergic polyarthritis (including palindromic rheumatism and intermittent hydrops of the joint), psoriatic polyarthritis, Reiter's disease.
Arthritis in other diseases includes: arthritis in allergic diseases, diffuse connective tissue diseases, metabolic disorders (gout, etc.), diseases of the lungs, blood, digestive tract, sarcoidosis, malignant tumors and some syndromic diseases.
In addition to the two main groups, traumatic arthritis is included in a separate group (due to the characteristics of their occurrence and treatment).
In recent years, the nosological affiliation of many forms of joint pathology has been clarified. In particular, it has been established that the so-called metabolic polyarthritis, climacteric and microtraumatic arthritis are in essence not inflammatory, but degenerative diseases of the joints and should be classified not as arthritis, but as deforming osteoarthritis (see Arthrosis).
The cause of the development of the inflammatory process in the joint can be a local or general infection, allergy, autoallergy, local trauma, etc. However, the etiology of some severe inflammatory joint diseases (for example, rheumatoid arthritis, ankylosing spondylitis, etc.) is still not clear enough. Factors contributing to the development of arthritis are hypothermia and physical overload of the joint.
Pathogenesis Arthritis is complex and diverse. The structural features of articular tissues - good vascularization of the synovial membrane and the presence of numerous nerve endings - determine the ability of joints to quickly respond with an inflammatory response to various direct and indirect influences.
In case of infectious specific arthritis, bacterial-metastatic and toxic-allergic paths of joint damage are possible. In the first case, the causative agent of the disease is introduced directly into the joint cavity by hematogenous or lymphatic route and can be detected in the synovial fluid. This is observed in tuberculosis, septic, gonorrheal and other specific arthritis. The damage to the joints in such cases is the most severe, with proliferative and destructive phenomena in the tissues. Sometimes there is a toxic-allergic mechanism for the development of infectious arthritis, when exposure to microbial toxins causes the development of allergic synovitis in the presence of increased sensitivity of articular tissues. The latter usually disappears under the influence of treatment without residual effects (synovitis in tuberculous arthritis, allergic form of gonorrhea, dysentery, brucellosis and other infectious arthritis).
Less studied is the pathogenesis of so-called nonspecific arthritis, which includes such widespread diseases as rheumatoid arthritis, ankylosing spondylitis, psoriatic polyarthritis, etc. The participation of infection in their origin remains unproven to this day.
According to modern concepts, the most important pathogenetic factor of these arthritis is a change in the general and tissue reactivity of the body, the development of allergies and auto-allergies.
It is assumed that under the influence of an as yet unknown primary allergen, possibly emanating from a focus of chronic infection, stimulation of immunocompetent lymphoid cells occurs. At subsequent stages, an altered 7S gamma globulin is formed, which has the properties of an autoantigen. In relation to it, autoantibodies are produced, which include the so-called rheumatoid factor (19S immunoglobulin, found in the blood of 80-90% of patients with rheumatoid arthritis). Subsequently, the autoantigen-autoantibody reaction is constantly reproduced. The formation of pathological immune complexes occurs mainly in the synovium.
This mechanism for the development of nonspecific arthritis is not fully proven and relates mainly to rheumatoid arthritis, but the presence of immune shifts in a number of nonspecific arthritis is currently beyond doubt. This is confirmed by the presence of autoantibodies to articular tissues and rheumatoid factor in the serum of patients with rheumatoid arthritis, as well as the detection of proliferation of lymphoid and plasma cells of the synovial membrane with the formation of multiple cellular infiltrates in patients with nonspecific arthritis.
In the mechanism of development of synovial inflammation in nonspecific arthritis, a large role is currently assigned to the phagocytosis of the formed immune complexes by leukocytes of the synovial fluid. It has been established that in this case damage to leukocytes occurs, accompanied by the release of proteolytic enzymes from their lysosomes, which support the inflammatory reaction in the joint.
In the clinical picture of arthritis, there are signs indicating that changes in the nervous system and especially its autonomic part play a role in the development of the disease (symmetry of joint damage, impaired trophism of muscles, bones, skin, impaired sweating, vascular tone, etc. ). However, the specific role of the nervous system in the pathogenesis of arthritis is not yet clear. The role of endocrine disorders is also not well understood. Selye's hypothesis (H. Selye), which attributes the main importance in the pathogenesis of a number of nonspecific arthritis to disruption of hormonal regulation of homeostasis, has not received direct confirmation. However, the role of endocrine disorders in the formation of the general pathological reactivity of the body, predisposing to joint disease, is beyond doubt. This is confirmed by the frequent development (or exacerbation) of nonspecific arthritis (for example, rheumatoid) in women during menopause.
Pathoanatomical changes in arthritis are determined by its nosological features and depend on the severity and duration of the process, as well as on the depth of the lesion. All elements that form the joint (bones, cartilage, synovial membranes, ligaments, joint fluid, etc.) can be involved in the inflammatory process, but in most cases the disease begins with exudative synovitis (synovioarthritis).
According to the nature of the exudate, serous, serous-fibrinous, purulent, putrefactive arthritis are distinguished. Serous and serous-fibrinous exudate is often observed in infectious specific arthritis, as well as in rheumatic and rheumatoid arthritis.
Clinically and morphologically, acute, subacute and chronic forms of serous and serous-fibrinous arthritis are distinguished, which at the same time can be successive phases of the development of the disease. Macroscopically, in the acute phase, swelling and hyperemia of the synovial membrane, capsule and periarticular tissues, an increase in the amount and turbidity of the joint fluid are found. Articular cartilage is usually not changed. Microscopically, fibrin clots, polynuclear cells and lymphoid elements are detected in the joint fluid. Bacteriological examination of the exudate usually shows its sterility, which gives grounds to talk about the toxic-allergic nature of serous arthritis.
In the synovial membrane, along with hyperemia and edema, proliferation and desquamation of integumentary synoviocytes, villous hypertrophy (Fig. 1), fibrin films on the surface, foci of fibrinoid swelling, diffuse infiltrates, mainly from lymphohistiocytic elements and single plasma cells, are microscopically detected. There is also disintegration and fibrinoid swelling of the walls of small arteries and veins, not only of the synovial membrane, but also of the joint capsule and periarticular tissues. Nerves and sensitive nerve endings are involved in the inflammatory process, which causes severe pain in the joint. The articular cartilage is microscopically unchanged. There may be osteoporosis of the epiphyseal bones.
In the subacute phase, alterative-exudative phenomena subside, and under microscopy, proliferation of connective tissue elements comes to the fore. On the inner surface of the synovial membrane, devoid of integumentary synoviocytes, peculiar “cellular cushions” are formed, represented by 10-20 layers of fibroblasts.
As the connective tissue matures, the process enters the chronic phase. Rough scars are formed, which lead to wrinkling of the capsule, ligaments and para-articular formations (tendons, fascia, aponeuroses), which significantly limits joint mobility.
The cellular composition of exudate in the subacute and chronic phases is represented by both neutrophilic and lymphoid elements.
Microscopy of articular cartilage reveals its fiber disintegration and foci of necrosis with the formation of defects in the cartilaginous covering and bone narrowing. Cartilage defects are replaced by granulation tissue, creeping onto the articular surface in the form of a film of varying thickness (pannus) - pannosic arthritis (Fig. 2 and 3).
However, such a sequence of development of cartilage changes does not always take place. It has been established that in rheumatoid arthritis, the phenomena of disorganization of the basic substance of cartilage with a decrease in the content of acidic mucopolysaccharides are observed already in the initial period of arthritis. Chondrocyte dystrophy develops gradually due to deterioration of trophism associated with compaction and disintegration of the main substance. Electron microscopy in chondrocytes shows a reduction in mitochondria and endoplasmic reticulum and an increase in the number of lysosomes. Apparently, in specific arthritis, articular cartilage, due to its lability in relation to metabolic disorders, is damaged at the onset of the disease.
With pannosic arthritis, a restructuring is observed in the subchondral parts of the bone, accompanied by the proliferation of endosteum and the formation of cysts. Further development of osteoporosis is noted. Less often, compaction (eburneation) of the subchondral parts is recorded; often there are marginal bone growths characteristic of deforming arthrosis (see). Endosteal growths penetrate into the joint cavity with the development of bone tissue in it. As a result of chronic forms of serous and serous-fibrinous arthritis, fibrous and bone ankylosis can form, which is facilitated by immobility of the joint due to severe pain.
With purulent inflammation of the joints, morphologically there can be: 1) purulent synovitis (see), or empyema; 2) phlegmon of the capsule; 3) purulent panarthritis (see). In the initial stages of purulent synovitis, the exudate may be transparent, but soon it becomes purulent or purulent-hemorrhagic. In the presence of anaerobic and putrefactive flora, gas bubbles may form in it (putrefactive arthritis). Microscopically, the synovial membrane shows leukocyte infiltration, foci of necrosis and the development of granulation tissue, creeping in the form of a pannus onto the articular cartilage (Fig. 4). In articular cartilage, areas of degeneration and necrosis are detected very early. Subsequently, necrosis and sequestration of significant areas of the cartilage develop, and in traumatic arthritis, even the entire osteochondral plate. Cartilaginous sequestra initially form in the area of contact with the inflamed synovial membrane and pannus, which is associated with the proteolytic action of leukocytes and the absorption properties of granulation tissue.
Capsular phlegmon is a consequence of the progression of purulent synovitis and is accompanied by sudden changes in the configuration of the joint due to swelling and purulent infiltration of tissues. As a result of further spread of inflammation to the tissues surrounding the joint, purulent panarthritis develops, accompanied by significant destruction of cartilage, intra-articular ligaments and bone epiphyses. Subsequently, paraarticular phlegmon, thrombophlebitis, and sepsis may develop. As a result of purulent arthritis, fibrous and bone ankylosis often occurs.
The course of arthritis can be acute, subacute and chronic. General clinical symptoms are joint pain, deformation, dysfunction, changes in temperature and color of their skin.
Pain in arthritis is spontaneous, most intense in the second half of the night and in the morning, and decreases after movement (the so-called inflammatory type of pain).
Joint deformation is a consequence of changes in soft tissues (exudative, proliferative and sclerotic processes), subluxations and contractures.
Joint dysfunction can be caused by both pain and morphological changes in articular tissues. It can be expressed in varying degrees - from mild, which does not deprive patients of their ability to work, to complete immobility of the joint due to fibrous or bone ankylosis. In acute arthritis, the limitation of mobility is usually reversible. Chronic forms are characterized by progressive limitation of mobility, first caused by pain, then by the development of proliferative and fibrotic processes. In rare cases, due to osteolytic processes or subluxations, on the contrary, the development of pathological joint mobility is noted.
Changes in the temperature of the skin of a joint are a fairly common symptom of arthritis. An increase in temperature can be observed with acute, subacute arthritis and exacerbation of chronic ones; concomitant skin hyperemia is possible. A decrease in temperature is observed in neurodystrophic arthritis, and in these cases the skin becomes cyanotic.
Patients usually complain of pain, changes in shape and limited joint mobility. The nature of the complaints may indicate the presence of an inflammatory process in the joint (severe spontaneous pain, progressive deterioration of joint function, rapidly occurring deformity, etc.).
In acute arthritis, the pain in the joint is usually very severe and constant. Characterized by significant pain restriction of joint function. On examination, hyperemia of the skin, an increase in the size of the joint and its defiguration may be observed. Palpation reveals diffuse sharp pain, fluctuation due to the presence of effusion in the articular cavity, and swelling of the periarticular tissues. Mobility is severely limited. Leukocytosis is detected in the blood (sometimes up to 25,000), a significant acceleration of ROE (up to 70 mm/hour), sharp changes in biochemical parameters, indicating the presence of an acute inflammatory process.
In subacute arthritis, all the above-described manifestations are less pronounced.
In chronic arthritis, pain occurs mainly when moving the joint. Upon examination, a change in the shape of the joints is detected, caused not so much by inflammatory edema of the periarticular tissues, but by proliferative fibrous changes, contractures, subluxations, and ankylosis. Palpation shows the presence of a dense, painful swelling of soft tissues. Laboratory indicators indicate a lesser severity of the inflammatory process.
The course of arthritis is highly variable. Acute, short-lived and completely reversible forms are observed (allergic, rheumatoid arthritis, etc.), as well as long-term, progressive chronic arthritis, the outcome of which can be a complete loss of joint function (bone or fibrous ankylosis in rheumatoid, septic arthritis, etc.). Chronic forms often lead to disability of patients.
The basic principle of diagnosing arthritis is a comprehensive examination of the patient using various methods.
The diagnosis is made based on:
1) anamnesis, which establishes a connection between joint damage and infectious diseases, focal infection, trauma, allergies or other pathological processes, and features of the onset of the joint process;
2) characteristic clinical data (“inflammatory” type of pain, swelling or deformation of joints due to exudative or proliferative phenomena in soft articular or periarticular tissues, progressive limitation of mobility in the joint);
3) the presence of laboratory indicators of the inflammatory process;
4) characteristic radiological data (epiphyseal osteoporosis, narrowing of the joint space, usuration of the articular surfaces of bones, ankylosis);
5) the results of a study of synovial fluid, a morphological study of the biopsied synovial membrane (the presence of proliferative type synovitis).
Anamnesis plays an important role in the diagnosis of arthritis. It helps to find out whether changes in the joint are inflammatory in nature and whether this arthritis is the underlying disease or is associated with the presence of another pathological process.
The inflammatory nature of the disease is determined by physical examination of the joint (local swelling, pain on palpation, changes in skin temperature, the presence of effusion, hardening of soft tissues).
One of the most important diagnostic methods that makes it possible to establish the presence and activity of a process in a joint is puncture of the joint with extraction and analysis of synovial fluid. Reduced viscosity, poor mucin clot, increased number of leukocytes (up to 50,000 per 1 mm3) indicate the inflammatory nature of the synovial fluid. Qualitative characteristics of cytosis (for example, the predominance of neutrophils in rheumatoid arthritis, lymphocytes in tuberculosis), the presence of crystals (for example, uric acid in gouty arthritis), sometimes the presence of infectious pathogens in the synovial fluid allow us to establish an accurate diagnosis of the disease.
Valuable information is provided by a morphological study of the biopsied (by puncture or excision) synovial membrane.
Recently, for more accurate diagnosis, arthroscopy has been used, which allows for visual inspection and photography of the synovial membrane.
Shifts in many laboratory parameters in arthritis are nonspecific and are characteristic of any inflammatory process (accelerated ROE, leukocytosis, increased DPA reaction, seromucoid, change in protein fractions towards an increase in the content of coarse proteins, detection of C-reactive protein).
Along with this, there are a number of serological tests that allow, in combination with the clinic, to establish a nosological diagnosis - Wasserman reaction (see Wasserman reaction), Wright reaction (see Wright reaction), Huddleson reaction (see Huddleson reaction), Bordet-Giangu reaction ( see Complement fixation reaction), determination of rheumatoid factor - Valera-Rose reaction, latex test (see Rheumatoid arthritis).
The main method of X-ray examination for arthritis is radiography in two standard projections with the use, if indicated, of additional projections demonstrating in more detail local changes in the articular surfaces of the affected joints (see Arthrography). For the same purpose, especially when studying small joints, radiography with direct image magnification is used (Fig. 5).
In some cases, to clarify the nature of changes in deep-lying areas of the epiphyses, invisible or not clearly visible with conventional radiography due to the superposition (overlay) of shadow elements, tomography is used (see). To detect inflammatory changes in the soft tissues of the joint, the so-called. soft contrast radiographs, sometimes without the use of intensifying screens.
Good results can be obtained with electroradiography (see) of the affected joints, which makes it possible to most clearly identify soft tissues and articular surfaces (Fig. 6).
The first and most constant radiological sign of arthritis, especially in the subacute stage, is osteoporosis (see). Therefore, it is very important to identify one or another type of osteoporosis (local, diffuse, uneven, spotty, etc.), and especially its dynamics, usually corresponding to the degree of neurotrophic and functional disorders in the affected joints.
At the same time, X-ray densitometry (see) provides significant assistance. Carrying out a cut is very advisable for a comparative dynamic study of joints of the same name, especially with unilateral damage. X-ray densitometry can be used not only for diagnostic purposes, but also to monitor the effectiveness of treatment, since it accurately reflects both the processes of bone demineralization during active arthritis (Fig. 7) and reparative processes during the reverse development of inflammatory changes.
The X-ray symptoms of arthritis are diverse and include the following signs: osteoporosis in all its varieties; sometimes widening of the joint space or more often its narrowing (total or partial) due to the presence of destructive changes in the osteochondral elements of the joint; marginal bone defects, so-called usurs, on the articular surfaces as a consequence of destructive processes; the presence of foci of destruction in the periarticular areas of bones; the formation of sequesters, often observed in specific arthritis, in particular tuberculous arthritis (Fig. 8); periosteal overlays in the area of the metaphyses of long tubular bones, as well as reactive osteosclerosis (see); changes in the relief of the articular surfaces of the bones and marginal bone growths on the bones forming the joint; dislocations and subluxations resulting from joint deformation in some forms of arthritis (Fig. 9).
Despite the fact that the x-ray picture observed in various forms of arthritis largely reflects the nature of the pathoanatomical changes in the osteochondral apparatus of the joint, differential diagnosis of all the various forms of arthritis and the stages of their development poses significant difficulties due to the frequent discrepancy between the clinical picture of arthritis and x-ray data research.
For example, in acute or subacute rheumatoid arthritis, when pathological changes develop in the synovium, X-ray data are usually negative, despite the stormy and characteristic clinical picture. The first radiological symptoms, in particular osteoporosis, are detected when the clinical diagnosis no longer poses any particular difficulties. Nevertheless, X-ray examination is also useful in these cases, since the discrepancy between clinical and radiological data can have a differential diagnostic value.
Of certain importance is not only the fact of the presence of osteoporosis, but also its qualitative characteristics.
In particular, diffuse osteoporosis is observed with a long, slow increase in clinical manifestations with neurotrophic changes and a sharp limitation of the function of the affected joint. Spotty osteoporosis usually occurs with rapidly progressive arthritis. Hypertrophic osteoporosis, even in the absence of destructive changes in the bones, indicates a long history of the onset of the inflammatory process, which had an acute clinical course in the past.
In infectious-allergic polyarthritis, characterized by an acute onset and rapid course, typical clinical manifestations are initially not confirmed by X-ray examination.
In case of infectious specific arthritis and polyarthritis, the X-ray picture can significantly contribute to both establishing the diagnosis of arthritis and determining the phase or stage of its development, and the dynamic assessment of X-ray data helps to correctly assess the effectiveness of the treatment and better determine the prognosis of the disease.
In the differential radiological diagnosis of arthritis and arthrosis (see), it is necessary to keep in mind the possibility of secondary arthrosis developing in arthritis.
Due to the high tendency to become chronic, arthritis often leads to disability. Thus, according to the World Health Organization, 3.1% of total disability is caused by chronic arthritis.
The use of etiotropic therapy is possible only for arthritis caused by a specific infection (tuberculosis, gonorrhea, brucellosis, etc.). In all other cases, complex pathogenetic therapy should be used, aimed at: a) changing the general and immunological reactivity of the patient (use of desensitizing, immunosuppressive drugs, influencing the focus of chronic infection, normalizing metabolism, vitamin balance, etc.), b) reducing general and local inflammatory reactions (use of medications, hormonal, physiotherapeutic agents, spa treatment), c) restoration of impaired joint function (therapeutic exercises, massage, physiobalneotherapy, occupational therapy), d) treatment of the underlying pathological process (for arthritis associated with other diseases).
The most important principle of the treatment of chronic arthritis is long-term staged treatment (hospital - clinic - resort), varying depending on the nature of the arthritis, its form, etc.
Physical therapy for arthritis is a mandatory component of complex treatment, but is contraindicated in the acute period.
In the subacute period, active, mainly lightweight, elementary exercises are used along the main axes of movement in the joints in combination with general strengthening and breathing exercises with gradually increasing load in a lying position, and then sitting and standing. Along with active exercises, careful passive movements are used to relax the limb being exercised as completely as possible, taking into account pain sensations (Fig. 10).
In the treatment of chronic arthritis, physical therapy occupies an important place in clinical, outpatient and sanatorium-resort practice. When the joints of the upper extremities are affected, exercises are performed mainly in sitting and standing positions (Fig. 11). In case of pathology of the joints of the lower extremities, the support function of the legs is trained in the lying, sitting and standing position (Fig. 12). For diseases of the spine, unloading positions for the spine are also recommended, for example, on all fours (Fig. 13). Active exercises are used: free, with effort, with the wide use of various apparatus, objects and special devices (especially for restoring hand function, for the purposes of domestic and work rehabilitation, etc.). Additionally, exercises on mechanotherapeutic devices are used. Patients are recommended to perform independent exercises with repetition of tasks during the day up to 4-6 times lasting 5-7 minutes in order to train the affected joints. In addition, morning hygienic exercises and walks are useful. It is advisable to carry out physical therapy in combination with massage, balneo- and mud therapy.
Good results are obtained from therapeutic exercises in water.
In the surgical treatment of rheumatoid arthritis, therapeutic exercises are used before surgery to increase the overall tone and resistance of the body. In the postoperative period, gymnastic exercises for non-operated joints are continued. Then, when the operated joint is freed from constant immobilization, passive movements are prescribed, gradually increasing their volume. Active exercises are first prescribed in light, free forms, and when a significant range of motion is achieved in the joint - with tension.
Orthopedic and surgical treatment of arthritis is carried out mainly when complex therapy is insufficiently effective. It is usually contraindicated in severe general condition of the patient, pronounced changes in internal organs and systems, during an exacerbation of a general or local pathological process, in early childhood (up to 5 years), etc.
Most often, the most functionally important joints are subjected to surgical treatment for rheumatoid arthritis: knee, hip-femoral, elbow, metacarpophalangeal and, less commonly, interphalangeal, radiocarpal, ankle and shoulder.
The nature of the surgical intervention is determined depending on the stage of the local pathological process and the function of the joint. In the initial stage, when there is pronounced synovitis, without destruction of cartilage and bone, preventive operations such as synovectomy are performed. The operation consists of maximum removal of the pathologically altered and hyperplastic synovial membrane, which has a beneficial effect not only on the operated joint, but often on the general course of the disease. In the future, when not only the synovial membrane is affected, but also the capsules of the ligamentous apparatus, destruction of cartilage and bone is noted, contractures develop, and a more radical intervention is indicated - extended synovcapsulectomy. In this case, simultaneously with the synovial membrane, the joint capsule, granulation tissue along the ligamentous apparatus, menisci, hypertrophied patellar fat body, fibrous adhesions, osteophytes around the condyles of the femur and tibia are excised; The patella is often resected, in the radiocarpal joint the head of the radius and the distal end of the ulna, etc.
In case of sudden destructive changes in the joint, persistent contractures and ankylosis, reconstructive operations are performed: subtrochanteric or supracondylar osteotomy of the femur to eliminate flexion contracture, total endoprosthetics using metal (hip, knee, elbow joints) or silicone (metacarpophalangeal and interphalangeal) endoprostheses , arthroplasty with interposition of homo- or autofascia, metal plates of various types (on the knee joint), etc.
Joint arthrodesis for rheumatoid arthritis is indicated in exceptional cases.
When many joints are affected, orthopedic surgical treatment begins with the leading joint (knee, hip-femoral).
For specific arthritis (tuberculous, gonorrheal, brucellosis, syphilitic, etc.), specific therapy is carried out, which is often, in particular for tuberculous arthritis, combined with surgical treatment (synovectomy, removal of necrotic foci and bone grafting, resection of articular ends and arthrodesis, arthroplasty and etc.). See also Arthrodesis, Arthroplasty, Bone grafting, Synovectomy.
Dropsy of the joints is intermittent - see Hydrarthrosis.
Specific infectious arthritis constitutes a group of joint lesions caused by bacterial, viral, fungal and parasitic diseases. Although the occurrence of these arthritis is associated with the presence of a general infectious process in the body, after the elimination of the latter they can continue for a long time as independent nosological forms. According to the mechanism of development, two forms of infectious specific arthritis are distinguished: bacterial-metastatic and toxic-allergic. The first form is characterized by severe damage to one or more joints with the presence of the pathogen in the synovial fluid. The second form is manifested by multiple synovitis or polyarthralgia without visible objective changes. There are also mixed forms of arthritis with damage to many joints and the presence of the pathogen in the synovial fluid.
Characteristic lesions of the musculoskeletal system in combination with clinical, bacteriological and serological data confirming the presence of an infectious disease make it possible to diagnose infectious specific arthritis. The study of synovial fluid (punctate) and biopsy material is of great differential diagnostic importance.
Brucellosis arthritis (arthritis brucellosa) is one of the common manifestations of brucellosis infection. In most cases, it is of a toxic-allergic and rarely of a bacterial-metastatic nature. Brucellosis lesions of the joints, more often than arthritis of other etiologies, are accompanied by periarthritis, tendovaginitis, bursitis, neuritis and other extra-articular lesions of the soft tissues of the musculoskeletal system. In the connective tissue of aponeuroses, joint capsules and muscles, cellulitis and fibrositis are formed in the form of connective tissue nodules and infiltrates. The typical location of brucellosis arthritis is the sacroiliac joints. Sacroiliitis (see) is often unilateral; it must be differentiated from sacroiliitis in ankylosing spondylitis (see Ankylosing spondylitis), psoriatic polyarthritis, dysenteric A. and Reiter's disease (see Reiter's disease). In addition, the knee, ankle, shoulder, elbow, radiocarpal joints, sternoclavicular joint and lumbar spine are affected. Particularly characteristic of brucellosis is the combination of spondylitis of the lumbar spine with sacroiliitis.
Of decisive importance in diagnosis is the detection of brucellosis in a given patient - according to anamnestic and clinical data, as well as based on the results of skin and serological reactions: Wright agglutination reaction (see Wright reaction), Huddleson reaction (see Huddleson reaction), Burnet skin test ( see Brucellosis), opson-phagocytic reaction.
The prognosis for the toxic-allergic form of brucellosis arthritis is favorable. Chronic brucellosis arthritis with presumed bacterial-metastatic genesis occurs as osteoarthritis with the development of persistent inflammatory changes in the joints and signs of osteochondral destruction, which leads to significant impairment of their function.
Treatment: in the acute period of the disease - antibacterial therapy; during the period of remission, exercise therapy, massage, paraffin, ozokerite and mud applications on the joints, spa treatment (radon and hydrogen sulfide baths, mud therapy) are indicated. See also Brucellosis.
Viral arthritis , sometimes accompanying viral diseases, can appear during any period of the disease. So, infectious hepatitis can begin as a kind of arthritis.
Arthritis with influenza is considered its rarest complication; arthralgia and myalgia associated with general intoxication are more typical, but influenza can activate latent coccal and other infections, which causes exacerbations of specific and nonspecific arthritis and rheumatism.
Arthritis (polyarthritis) can begin or be accompanied by diseases such as rubella, mumps, measles, and inguinal lymphogranulomatosis.
Treatment: the use of antibiotics or sulfonamides to treat the underlying disease, as well as anti-rheumatic drugs.
Gonorrheal arthritis , polyarthritis (arthritis gonorrhoica) develops in patients with acute and chronic gonorrhea, mainly in young people. It can be bacterial-metastatic and toxic-allergic. Most often, acute synovitis develops with serous, serous-fibrinous or (less often) purulent effusion, then the joint capsules, ligaments, and tendons are involved in the process. The onset is almost always acute, with exceptionally severe polyarthralgia. Subsequently, the process is localized in one joint, usually in the knee, ankle, or wrist.
The most typical is metastatic arthritis (monoarthritis with acute and subacute course). Morphologically, acute gonitis (see) can be serous or purulent, subacute - serous-fibrinous. In all forms, excruciating pain, high fever, and severe general condition of the patient are noted. The development of pathological changes in the joint is sharply expressed: deformation, flexion contractures (Fig. 14), muscle atrophy develop rapidly. Laboratory test indicators indicate the activity of the inflammatory process. Gonococci can be found in punctate. With improper or delayed treatment, severe destruction of articular elements and ankylosis quickly develops.
Currently, acute and chronic gonorrheal oligo- and polyarthritis of a toxic-allergic nature have become much more common. Acute polyarthritis can be provoked by injury or cooling. The process is quickly fixed in 2-3 large joints. With proper and timely treatment, in most cases the prognosis is favorable, but chronic gonococcal polyarthritis and spondyloarthritis can develop, very similar to rheumatoid arthritis and spondyloarthritis deformans.
A frequent and typical lesion of the musculoskeletal system during gonorrheal infection is damage to the foot - achillodynia (pain in the heel tendon) caused by achillobursitis, rapid development of "spurs", tendovaginitis, atrophy of the muscles of the foot and lower leg, followed by secondary flat feet.
Diagnosis of gonorrheal arthritis is very difficult due to the fact that patients hide or do not know about the disease, and the clinical picture may be similar to rheumatoid arthritis.
Anamnesis, the presence of a primary gonorrheal focus, a positive Bordet-Zhangu reaction, a positive skin test with gonovaccine, in some cases the presence of gonococci in the joint effusion, data from a general blood test, and x-ray examination are of diagnostic and differential diagnostic significance.
The prognosis in most cases is favorable, but acute purulent forms can lead to significant dysfunction of the joint, and subacute forms can take a chronic, relapsing course.
Treatment: in the acute stage of the disease, it is necessary to carry out a course of treatment with antibiotics; in severe cases, corticosteroids and autohemotherapy are used; in the chronic course of the disease during the period of remission, exercise therapy, massage, paraffin, ozokerite and mud applications on the joints, spa treatment (radon and hydrogen sulfide baths, mud therapy) are indicated. See also Gonorrhea.
Fungal arthritis can occur with actinomycosis, blastomycosis, coccidiosis and Madura foot. The process, as a rule, passes into the joint from the nearby bone affected by mycosis. In some cases, actinomycosis also spreads hematogenously, so bones and joints located far from the primary site, such as the foot, can be affected (Fig. 15). All fungal infections of the osteoarticular apparatus are characterized by the formation of fistulas and a long-term recurrent course. The diagnosis must always be confirmed by the detection of the corresponding fungus. Fungal arthritis should be differentiated from tuberculous and syphilitic lesions of the osteoarticular apparatus.
Treatment - antibiotics, sulfonamides, sometimes actinolysate, etc. - surgery (removal of the lesion).
Dysenteric arthritis (arthritis dysenterica) develops immediately or several weeks after dysentery. Currently rare. As a rule, these are toxic-allergic serous or serous-fibrinous synovitis, which occurs in the form of polyarthritis, and sometimes mono-arthritis of the knee or ankle joints. The joints are very painful, there is swelling and deformation. Joint effusion is rich in fibrin and polynuclear cells, but the pathogen is detected extremely rarely. The general condition of the patient changes slightly, despite long-term and persistent damage to the joints. The process often involves the sacroiliac joints, and moderate muscle atrophy is typical. Radiographs show the usual picture of arthritis (osteoporosis, changes in the joint space, unevenness of the articular surfaces).
The prognosis is favorable, but with a chronic recurrent course, contractures, persistent deformity and even fibrous ankylosis can develop.
Treatment: antirheumatic therapy is not effective. Complete rest, comfortable position of the joint, and dry heat are necessary. The use of antibiotics has a good effect. In severe cases, in addition to conventional desensitizing therapy, corticosteroids are used, and when the activity of the process decreases, exercise therapy, massage, paraffin, ozokerite or mud applications.
Parasitic arthritis (arthritis parasitaria) can develop with hydatid disease of the bones. Echinococcus is most often localized in the vertebrae, intervertebral discs, and less often in the pelvic bones and long tubular bones. Joint pain is usually associated with reactive synovitis caused by a process in nearby bone tissue.
Pneumococcal arthritis is observed very rarely, mainly in children and young people with lobar pneumonia. The bacterial-metastatic form most often affects one joint (knee, ankle) and proceeds as purulent arthritis (pneumococci are found in the joint puncture). In the toxic-allergic form, many joints are affected, but the process proceeds easily, with complete reversibility of all phenomena; no specific therapeutic measures are required.
Treatment of purulent forms - see below Acute purulent arthritis .
Septic arthritis ( arthritis septica ) develops against the background of general sepsis, most often caused by coccal microflora, Escherichia coli, etc. In most cases, arthritis is bacterial-metastatic (acute purulent arthritis), and sometimes toxic-allergic in origin. In the bacterial-metastatic form, acute purulent arthritis develops, most often of large joints, with a pronounced clinical picture - see below Acute purulent arthritis .
The toxic-allergic form of septic arthritis is acute and subacute migratory polyarthritis with a small effusion of a serous or serous-fibrinous nature. The process proceeds with the reversibility of all phenomena.
Treatment: antibacterial therapy for sepsis (see), anti-inflammatory drugs (salicylates, indomethacin), and, if necessary, glucocorticoid hormones are used.
Syphilitic arthritis ( arthritis syphilitica ) can appear in congenital and in all stages of acquired syphilis (see). Currently rare. With congenital syphilis, there can be several forms of arthritis: syphilitic Parrot osteochondritis, synovitis of the knee joints with a significant amount of effusion and a spherical shape of the knee joints - Clutton's joints, syphilitic dactylitis, etc. Arthritis in the first stage of syphilis can manifest itself as short-term polyarthralgia. In the second stage, pain in the joints, bones and muscles is also noted, worsening at night. Sometimes polyarthritis of a volatile nature is observed, in which salicylates do not help, but treatment with penicillin has a good effect. In the third stage there may be gummous arthritis of large joints, which is manifested by hydrarthrosis (see) with protrusion of the inversions of the synovial membrane (Fig. 16). Radiographs may show signs of arthrosis (secondary arthrosis). If the process is localized in one joint, it is externally difficult to distinguish it from osteoarticular tuberculosis. Syphilitic arthritis in the fourth stage is manifested by tabetic arthropathy, which most often affects the knee joint and is characterized by large structural changes with preserved function.
The diagnosis is made on the basis of the clinical picture, serological and radiological data (rounded bone defects in the epiphyses, periostitis). The Wassermann reaction with synovial fluid is often positive. Particular attention must be paid to the discrepancy between structural changes and joint function. The detection of syphilitic lesions of internal organs is of great diagnostic importance.
The prognosis depends on the severity of the underlying disease.
Tuberculous arthritis , osteoarthritis (arthritis, osteoarthritis tuberculosa) can be bacterial-metastatic and toxic-allergic. The first form is usually monoarthritis localized in the spine, knee, hip-femoral, elbow, wrist and other joints. The tuberculosis bacillus usually enters the synovial membrane of the joint or the part of the bone adjacent to the joint by hematogenous route from the primary foci of tuberculosis in the lungs, intestines or lymph nodes. Often the tuberculous process can spread from adjacent bones. Therefore, instead of the term “tuberculous arthritis,” the term “osteoarticular tuberculosis” is often used.
Tuberculous arthritis is a chronic disease that occurs with signs of general intoxication and local symptoms of synovitis. An X-ray examination in the epiphyseal part of the bone can reveal a limited focus of decalcification (Fig. 17), sometimes in the form of a bone defect, sequestration and narrowing of the joint space.
The final evidence of a tuberculosis process in a joint is the detection of tuberculosis bacilli in the joint fluid or changes characteristic of tuberculosis (tuberculosis tubercles) in the biopsy material of the synovium. Skin tests with tuberculin are of no small diagnostic importance. Untreated or poorly treated osteoarticular tuberculosis can be complicated by a leaky abscess that breaks out, leaving fistulas that do not heal for a long time and often reopen (see Tetechnik).
The toxic-allergic form of tuberculous arthritis, described by A. Poncet in 1902, is characterized by damage to many, mainly small joints of the extremities. According to the clinical picture, Ponce's polyarthritis resembles rheumatoid arthritis, so some authors dispute the existence of this form of tuberculous arthritis as an independent nosological entity and believe that in such cases we are talking about rheumatoid arthritis against the background of tuberculosis.
The described forms of tuberculous arthritis are currently less common than arthralgia and polyarthralgia in patients with tuberculosis. The cause of the latter must be considered both tuberculosis intoxication and sensitization of the body to drugs.
The diagnosis of tuberculous arthritis is made on the basis of clinical, radiological and bacteriological data, taking into account allergy skin tests.
Psoriatic polyarthritis (polyarthritis psoriatica) develops more often in patients who already have skin manifestations of psoriasis, on average 6 years after their onset, but sometimes it can precede them or appear simultaneously. Psoriatic polyarthritis is currently identified as an independent nosological form. Its clinical picture is extremely similar to rheumatoid arthritis, but has some features:
1. The distal interphalangeal joints of the fingers are almost always affected. At the same time, as a rule, the nails are affected (Fig. 18).
2. The process usually involves a small number of other peripheral joints (2-3, rarely more), and the damage is asymmetrical. In severe cases, the articular process can be generalized.
3. The intervertebral joints of the lumbar region and sacroiliac joints are affected, where ankylosis can develop, so psoriatic polyarthritis must be differentiated from ankylosing spondylitis.
4. The course is usually remitting, sharp exacerbations often alternate with partial remissions. In this case, there is a certain parallelism with the skin manifestations of psoriasis.
X-rays of the hands often reveal lysis of the distal phalanges of the fingers (arthritis mutilans), which is also typical for scleroderma (see). Otherwise, the X-ray picture differs little from that of rheumatoid arthritis.
The Valera-Rose reaction and a test with latex or dermatol (see Rheumatoid arthritis) are usually negative. Laboratory data show changes characteristic of the inflammatory process (acceleration of RER, leukocytosis, hypergammaglobulinemia).
Prognosis: As the process progresses, significant dysfunction of the joints develops.
Treatment: treatment of the underlying disease (see Psoriasis) and prescription of drugs used for rheumatoid arthritis. Gold preparations are contraindicated as they can cause exacerbation of skin symptoms. If the process is highly active, corticosteroids are indicated. A good effect is observed from the use of immunosuppressants, especially methotrexate.
Rheumatic polyarthritis - see Rheumatism.
In allergic and diffuse connective tissue diseases, metabolic disorders, diseases of the lungs, blood and digestive tract, sarcoidosis, intoxications, malignant tumors and vegetative-vascular dystonia, arthritis is a frequent but inconsistent manifestation. They are usually unstable and are based on exudative changes in the joints, which are clinically manifested by pain and more or less pronounced swelling of the joints. Treatment of these forms of arthritis should be aimed at eliminating the underlying disease. Analgesics are used as symptomatic drugs.
Arthritis is observed in the following allergic diseases : drug and serum sickness, capillary toxicosis and erythema nodosum. Long-term use of medications can lead to drug-induced illness and accompanying allergic arthritis. (multiple synovitis of a volatile nature). Volatile synovitis of an allergic nature is observed in joints and in serum sickness. In capillarotoxicosis, joint pain is caused by hemorrhagic vasculitis. Erythema nodosum, regardless of etiology, is manifested by pain in the joints, especially the knees, and sometimes by swelling. Joint symptoms usually disappear with erythema.
Arthritis with collagenosis is more persistent and is often difficult to distinguish from the initial forms of rheumatoid arthritis.
With systemic lupus erythematosus, joint damage is observed in almost all patients, often being the first symptom of the disease. Clinically, it is a subacute, protracted, but migratory arthritis, mainly of small joints, resembling rheumatoid arthritis. It is combined with damage to periarticular tissues (tenosynovitis, myositis, bursitis), which is the main cause of joint deformities (subluxations, contractures) that sometimes occur. A feature of this arthritis is the skin erythema sometimes observed over the affected joint, as well as the paucity of radiological changes compared to rheumatoid arthritis (slight narrowing of the joint space, isolated small erosions of the articular surfaces). When differential diagnosis with rheumatoid arthritis, it is important to take into account the data of laboratory (presence of LE cells, antinuclear factor) and morphological (poor cellular reactions, pronounced nuclear pathology in synovial tissue) studies.
Systemic scleroderma is characterized by two types of articular syndrome - true synovitis (rheumatoid-like arthritis) and periarthritis (pseudoarthritis), caused by a fibrous-sclerotic process in the skin, tendons and other soft periarticular tissues, leading to contractures and deformities of the joints. A feature of scleroderma joint syndrome is a significant predominance of fibrosclerotic phenomena over exudative ones, the presence of dense swelling of the skin covering the joint; Radiologically, slight bone destruction is determined (single small lesions with clear contours) and signs characteristic of scleroderma, such as osteolysis of the terminal phalanges and calcification of periarticular tissues. When examining a biopsied synovial membrane, pronounced sclerosis of the vessels and synovium is revealed.
With dermatomyositis, joint pain is usually caused by periarticular changes in the skin and muscles. Contractures of the joints, predominantly of the upper extremities, of myogenic origin are also often observed. As a rule, no changes are detected on radiographs of the joints.
With periarteritis nodosa , arthritis of an allergic nature can be observed, but more often the pain is not localized in the joint, but is diffuse in nature and associated with neurogenic and vascular disorders.
Arthritis can develop with pulmonary diseases : silicosis (see Kaplan syndrome), sarcoidosis, lung cancer. Kaplan syndrome was described in 1953 in miners suffering from anthracosilicosis. Joint changes in Kaplan syndrome are no different from rheumatoid arthritis (clinically, radiologically and serologically).
With sarcoidosis , which is a generalized granulomatosis that primarily affects the lymphatic system, lungs and skin, joint pain and sometimes spindle-shaped swelling are observed. In some cases, polyarthritis takes a chronic course. The diagnosis can be clarified during dynamic observation.
Paracarcinomatous arthritis in the form of persistent polyarthritis or polyarthralgia of toxic-allergic origin can occur in cancer of the stomach, lungs, and liver, remaining the only symptom of the disease for a long time.
This syndrome, described by French rheumatologists only in the 50s of this century, clinically manifests itself in the form of subacute arthritis with pain and slight swelling, mainly in the small joints of the arms and legs, which is accompanied by an acceleration of ROE, and can simulate the initial forms of many arthritis. It should be borne in mind that physiotherapy erroneously applied to these patients (if the underlying disease is not recognized in a timely manner) contributes to the rapid growth of the tumor.
Arthritis is one of the main manifestations of gout (see); also occur in acute and chronic leukemia (develop as a result of autoimmune processes or are associated with leukemic infiltrates in the synovium); with hemophilia (as a result of repeated hemorrhages in the joints).
Arthritis with ulcerative colitis and regional ileitis clinically resembles rheumatoid arthritis. However, in these cases there are also signs of ankylosing spondylitis and sacroiliitis, so they must be differentiated from ankylosing spondylitis.
Benign occupational polyarthritis currently belongs to the group of symptomatic joint lesions in general vegetative-vascular dystonia (see Vascular dystonia).
Acute purulent arthritis is an acute inflammatory process associated with the entry and development of a pyogenic infection (staphylococcal, streptococcal, pneumococcal, gonococcal, etc.) in the joint. Since acute purulent arthritis is very difficult, and the treatment has its own specifics, its description is highlighted in a separate section. Acute purulent arthritis is primary and secondary. In the case of primary infection of the joint, it is associated with its injury during an industrial or domestic injury, a gunshot wound, as well as after a puncture, surgery, etc. In secondary purulent arthritis, the microflora enters the joint per continuitatem from neighboring tissues (with phlegmon, an infected wound, etc.). etc.), from closely located purulent foci when they break through (with bursitis, paraosseous phlegmon, osteomyelitis, etc.), by hematogenous and lymphogenous routes (with sepsis, thrombophlebitis, osteomyelitis, tonsillitis, otitis, etc.).
An acute onset of the disease is characteristic. Complaints of severe pain and limited mobility in the affected joint, fever, and malaise.
Locally: the skin over the joint is tense, may be hyperemic, the configuration of the joint is changed due to inflammatory infiltration of tissues, accumulation of effusion and possible destructive changes in the epiphyses. The limb is in a forced, semi-bent position, in which the volume of the articular cavity increases, which leads to a decrease in pain. On palpation, pain, local hyperthermia is noted, and with a significant amount of effusion - fluctuation, in the knee joint - a symptom of patellar balling. The function of the affected joint is impaired - the volume of active and passive mobility decreases. When purulent inflammation spreads to the tissues surrounding the joint, symptoms characteristic of phlegmon are detected (see).
General clinical symptoms include manifestations of purulent intoxication: severe general condition, depression of consciousness, intermittent temperature, weakness, chills, progressive anemia, etc.
Laboratory examination: leukocytosis with a band shift, accelerated ROE, decreased albumin levels in the blood, increased levels of the globulin fraction, especially alpha-2 and gamma globulins. The study of the contents obtained during joint puncture allows us to determine the nature of inflammation, microflora and its sensitivity to antibiotics.
With acute purulent arthritis, complications are possible: para- and periarticular phlegmon, panarthritis, osteoarthritis, osteomyelitis, sepsis.
The diagnosis of acute purulent arthritis is made on the basis of anamnestic, clinical, radiological data and the results of bacteriological examination of punctate from the joint.
The prognosis depends on the extent and depth of pathological changes in the joint tissues; Possible adverse consequences - limited mobility in the joint up to ankylosis (see).
Treatment should be comprehensive, combining local and general, conservative and surgical treatment measures.
Local treatment: immobilization of the limb (plaster splints, splints, etc.), in the presence of a significant amount of purulent effusion, periodic puncture of the joint (Fig. 19) with evacuation of purulent exudate and washing of the joint cavity with antiseptic solutions. The first puncture of the joint ends with the introduction of broad-spectrum antibiotics; for all subsequent punctures, antibiotics are used, taking into account the sensitivity of the microflora to them; the frequency of such sanitation of the joint cavity depends on the rate of accumulation and the amount of newly formed effusion. Punctures are stopped when the effusion becomes serous and its amount becomes insignificant. Sometimes after the first puncture, nipple drainage is left in the joint cavity.
In acute purulent arthritis with severe complications (osteoarthritis, panarthritis, etc.), intra-arterial infusions of antibiotics, as well as intravenous and intraosseous administration of antibiotics are advisable. When the purulent process subsides, physiotherapy (UHF, ultraviolet radiation, ionogalvanization, etc.) is prescribed locally to resolve the inflammatory infiltrate, followed by massage and physical therapy, which helps restore joint function.
General treatment measures include the use of antibiotics, taking into account the sensitivity of the microflora, sulfonamide and nitrofuran drugs, as well as pyrimidine derivatives - methyluracil, pentoxyl; the use of immunobiological agents: therapeutic sera, staphylococcal toxoid, bacteriophages, vaccines and autovaccines, antiphagin, proteolytic enzymes, etc.; blood transfusion, plasma, infusion of protein hydrolysates, hemodez, glucose solutions, liquids with correction of electrolyte balance, etc. are necessary; It is important to provide the patient with vitamins and protein-rich foods.
Surgical interventions for acute purulent arthritis are resorted to when conservative treatment is unsuccessful. Arthrotomy (see) is best performed under anesthesia with mandatory drainage of the joint cavity and torsions. When periarticular phlegmons occur, they are opened and drained. Extensive surgical interventions (joint resection, amputation or disarticulation of a limb) are resorted to for complications of acute purulent arthritis: osteoarthritis, panarthritis, with steady progression of the purulent process with symptoms of severe intoxication that threatens the patient’s life.
Prevention of acute purulent arthritis consists of careful primary surgical treatment of various wounds of the joint, strict adherence to asepsis during planned operations on the joint, timely and correct treatment of general septic processes and purulent diseases in the tissues adjacent to the joint.
Arthritis in children most often has an infectious origin and is associated with a general or focal infection; less often, they can be caused by trauma or metabolic disorders. Features of the reactivity of the child's body determine some of the pathogenetic originality of arthritis at different age periods. At a younger age, arthritis of infectious origin develops, as a rule, through bacterial-metastatic pathways, and one or two, sometimes several, joints are affected. The course is often severe, and an unfavorable outcome is possible (for example, with septic arthritis in infants). In older age groups, arthritis of toxic-allergic origin most often occurs, occurring as synovitis, benign, cyclically with complete elimination of symptoms.
Infectious specific arthritis occurs in children somewhat differently than in adults.
In brucellosis, damage to the musculoskeletal system - one of the most frequent and striking manifestations of infection - is very diverse. Peri- and paraarthritis, synovitis, osteoarthritis may develop, but for children the most typical is arthralgia (68-80%), which, as a rule, is not accompanied by visible changes in the joints.
Acute brucellosis arthritis is observed in approximately 25% of all children, mainly of school age, who develop brucellosis. Develops as allergic synovitis. Large joints are involved in the process (knee, ankle, shoulder, elbow, wrist). Patients complain of pain and limited mobility in the affected joints, the joints swell, there is local hyperthermia, and sometimes hyperemia. Significant intra-articular effusion is very rare in children. X-ray changes in the joints are usually absent. The reverse development of the process begins after a few days - 1-3 weeks.
Chronic brucellosis arthritis in children is currently almost never encountered. Lesions of the sacroiliac joint, which are so typical for adults, are not observed in childhood.
As in adults, brucellosis infection in childhood is characterized by damage to the connective tissue of the joints in the form of bursitis, as well as fibrositis and cellulite. In this case, dense, painful nodules and cords or (less often) doughy infiltrates are palpated in the soft tissues of the joints. Tenosynovitis is relatively rare in children.
Differential diagnosis is carried out with rheumatic, rheumatoid, tuberculous, septic arthritis, etc. The diagnosis is made on the basis of a complex of epidemiological, clinical and laboratory data. The most reliable method is to use both the Wright and Huddleson serological reactions and the allergic intradermal Burnet test. The Huddleson reaction with joint effusion is not often used, since exudative phenomena in children are usually mild.
The prognosis is favorable. Treatment - see Brucellosis.
Arthritis and arthralgia due to viral infections are observed less frequently in children than in adults. With epidemic hepatitis, they can occur in the prodromal period, disappearing with the appearance of jaundice. As in adults, arthritis has been described in children as a rare manifestation of rubella, influenza, chicken pox, measles and other viral diseases.
Gonorrheal arthritis in childhood occurs as in adults, and is more common in girls. The principles of diagnosis and treatment are similar to those in adults. Prevention in children comes down to preventing infection with gonorrhea, primarily from a sick mother.
Fungal arthritis in children is rare and occurs only with systemic mycoses (actinomycosis, coccidiosis and some others) as a consequence of the generalization of the pathogen. It has no characteristic flow features. The diagnosis is made taking into account mycotic lesions of other organs and systems, data from microbiological, serological research methods and skin allergic tests. The study of biopsied pieces of tissue is important. The prognosis is serious. Antimycotic treatment.
Dysenteric arthritis practically does not occur in children at present.
Pneumococcal arthritis (purulent) develops with pneumonia and is of bacterial-metastatic origin. It proceeds in the same way as septic arthritis.
Septic arthritis , just like in adults, is one of the manifestations of general sepsis. Develops more often in early childhood, bacterial-metastatic genesis predominates. Against the background of a picture of severe sepsis, purulent arthritis of one or two joints occurs, usually the knee, hip-femoral, less often others, with its characteristic symptoms: acute pain, swelling, redness of the skin, increased temperature over the joint, forced position of the limb. In severely weakened patients, the symptoms of arthritis may be erased. The presence of pus during joint puncture confirms the diagnosis. Bacteriological examination of joint effusion and blood makes it possible to determine the pathogen in most patients.
The prognosis is serious, especially if the hip-femoral joint is affected. Treatment is carried out according to the general principles of therapy for sepsis (see) and purulent arthritis (see above Acute purulent arthritis ).
Syphilitic arthritis in children occurs primarily as a manifestation of late congenital syphilis in the form of synovitis of the knee joints, described by Clutton (HH Clutton, 1886). It develops more often at the age of 8-16 years, acutely or subacutely, sometimes after injury, and is characterized by mild or moderate inflammation, usually of both joints. The joints swell, exudate accumulates in them, mild pain, increased local temperature, and sometimes skin hyperemia and mild dysfunction are characteristic. In the blood - accelerated ROE, neutrophilic leukocytosis. X-rays of the joints usually do not reveal changes. The flow is protracted. If the disease begins acutely, with high fever, and there are no other signs of congenital syphilis and no indication of the mother’s illness, then the diagnosis is difficult. The combination of synovitis with symptoms of congenital syphilis is relatively rare. According to L. Borella et al (1962), of 8 children with syphilitic arthritis, only two had this combination (one with parenchymal keratitis, the other with labyrinthine deafness, Hutchinson’s teeth and nasal deformity). The positive Wassermann reaction with blood and synovial fluid is of decisive importance in diagnosis. Under the influence of specific treatment (see Syphilis), the arthritis goes away. Prevention of this form of arthritis is early preventative treatment for children born to affected mothers.
Tuberculous arthritis in most cases is bacterial-metastatic and occurs in the form of monoarticular osteoarthritis localized in the spine, hip-femoral and knee, and less often in other joints. Occurs more often in childhood and adolescence than in adults; proceeds the same way.
Much less common is the toxic-allergic form of tuberculous arthritis (Poncet's disease) with asymmetric damage to several joints, including small joints of the hands. According to the clinical picture, this arthritis, in its acute course, resembles rheumatic arthritis, and in its prolonged course, it resembles rheumatoid arthritis. In the differential diagnosis of Ponce's disease with rheumatism and rheumatoid arthritis, the presence of signs of tuberculosis infection and specific changes in the lungs helps. There are no changes in the heart or permanent deformation of the joints. Treatment is anti-tuberculosis.
Psoriatic polyarthritis in childhood is much less common than in adults. According to A. A. Studnitsyn et al. (1971), out of 350 children with psoriasis, arthritis was observed in one. The clinical picture of psoriatic arthritis is similar to that of rheumatoid arthritis with a subacute, slowly progressive course. There is asymmetrical damage to individual large joints; Unlike adults, the joints of the feet and the terminal interphalangeal joints of the hands are rarely involved in the process. X-ray reveals osteoporosis, rarely - signs of osteochondral destruction. An increase in ROE and slight neutrophilia may be observed; rheumatoid factor in the blood is not detected. The course is protracted, with periodic exacerbations.
The diagnosis is made taking into account the skin rashes characteristic of psoriasis, but it must be remembered that in children the skin rashes are scanty and their localization is atypical.
Treatment - treatment of the underlying disease (see Psoriasis) and the prescription of drugs used for rheumatoid arthritis, except for glucocorticoids and gold preparations.
In addition, pain in the joints and muscles can be observed with the so-called steroid pseudorheumatism, which is a consequence of exogenous hypercortisonism during long-term and high-dose treatment with glucocorticoids. Symptoms disappear when the dose of hormones is reduced or after their withdrawal.
When using certain medications, including antibiotics, sulfa drugs, bromides, iodides, thiouracil and others in children, as well as in adults, drug intolerance in the form of arthralgia or allergic drug arthritis is possible. With the cessation of the administration of these drugs, all phenomena usually disappear. With serum sickness, the development of allergic synovitis is possible.
From additional materials.
Reactive arthritis is an inflammatory disease of the joints that occurs as a result of an infection in genetically predisposed individuals; in this case, the causative agent of infection is not detected in the tissues of the affected joints.
Most often, reactive arthritis develops after infections caused by Yersinia, Chlamydia, Salmonella, Shigella, Klebsiella, and some other bacteria and viruses.
A typical example of reactive arthritis is arthritis due to acute rheumatism. Reactive arthritis has been described in various viral infections, in particular infectious hepatitis.
The pathogenesis of reactive arthritis has not been definitively established. It is assumed that reactive arthritis may be caused by the body’s immune response to an infectious agent or its antigens located outside the joint cavity (for example, in the intestine with yersiniosis), the formation of immune complexes and their deposition in joint tissues. The body’s immune response to its own tissue antigens is possible , released in the joint during initial short-term contact with the pathogen inf. diseases, or to antigens that cross-react with antigens of a microorganism, for example HLA-B27 (in particular, such cross-reactivity of the specified histocompatibility antigen and antigens of Yersinia and Klebsiella has been proven).
The clinical picture of reactive arthritis of any etiology is largely the same. Their common signs are: the development of the disease mainly in young people (up to 30-40 years), including children; chronological connection with the infection, that is, the occurrence of articular syndrome during the infection or, more often, 1-1.5 months after its acute manifestations subside (the severity of the infection itself may vary); as a rule, acute onset of arthritis: pronounced general (fever, leukocytosis, accelerated ROE) and local signs of inflammation; asymmetrical damage to the joints of mainly the lower extremities (knees, ankles, small joints of the toes), as well as inflammation of the tendons (especially Achilles) and synovial bursae (especially in the heel area); frequent involvement of the sacroiliac joints in the process with an x-ray picture of usually unilateral sacroiliitis; the presence in some cases of additional manifestations (conjunctivitis, keratoconjunctivitis, painless erosions of the mucous membranes of the mouth, genitals, keratoderma, etc.), forming a picture of Reiter's syndrome, or such as erythema nodosum, myocarditis, peripheral neuritis, etc.; absence of rheumatoid factor in the blood serum; frequent detection of the histocompatibility antigen HLA-B27. The number of affected joints varies (monoarthritis, oligoarthritis, less often polyarthritis). Severe periarticular edema may be observed, with the skin over the affected joint having a purplish-bluish coloration.
Diagnosis of reactive arthritis is based on identifying the connection between joint damage and the infectious process and the clinical features described above. The diagnosis must be confirmed by bacteriological (isolation of cultures of Yersinia, Shigella, Salmonella, etc.) or appropriate serological (determining the titer of antibodies to specific infectious agents over time) tests.
Differential diagnosis is carried out with rheumatoid arthritis (see) and the peripheral form of ankylosing spondylitis (see ankylosing spondylitis). The main criteria for differential diagnosis are given in the table.
In the early stages of the development of the disease, and especially with manifestations of intestinal or urogenic infection, broad-spectrum antibiotics (methacycline, erythromycin, vibromycin, etc.) are indicated for 2-4 weeks. For the treatment of arthritis, non-steroidal anti-inflammatory drugs (indomethacin, voltaren, butadione, etc.) and intra-articular administration of corticosteroids are mainly used. In particularly severe cases of the disease, it is necessary to resort to the prescription of corticosteroids. After acute manifestations subside, physiotherapy and balneotherapy, therapeutic exercises, and massage are indicated.
The prognosis is relatively favorable. In most cases, the disease ends with complete reverse development of the inflammatory process within 6-9 months. The symptoms of bursitis, tendonitis, and tendovaginitis may persist for a longer period of time. Reactive arthritis can recur in case of reinfection or become chronic, in which erosive changes in the joints (usually the feet) and progression of sacroiliitis up to complete ankylosis of the sacroiliac joints are possible.
Prevention is based on the prevention of infectious diseases and their timely treatment.
MAIN DIFFERENTIAL DIAGNOSTIC SIGNS OF REACTIVE ARTHRITIS, RHEUMATOID ARTHRITIS AND PERIPHERAL FORM OF ANKYLINED BECHTEROW'S DISEASE
Link to infection
As a rule, it is clearly visible
Typically absent
Primary location of arthritis
Joints of the lower extremities (knees, ankles, small joints of the feet), excluding hip joints
The wrist, metacarpophalangeal, proximal interphalangeal, and metatarsophalangeal joints are most often affected.
The joints of the lower extremities (knees, ankles, hips) are predominantly affected.
Symmetry of joint damage
Pain in the spine
It is observed extremely rarely, the lesion is unilateral
Observed constantly, the lesion is bilateral
erosive changes in joints
Rarely observed, asymmetrical
Often observed in the joints of the hands and feet, symmetrical
Extremely rare in the joints of the feet
calcification of the spinal ligaments
Extremely rare
Occurs often with long-term disease
Damage to the tendons and bursae of the heel area
Seen very often
Found in most patients
Histocompatibility antigen HLA B27
Detected in 50 - 80% of patients
Detected in 80-*90% of patients
Bibliography: Astapenko M. G. and Pihlak E. G. Diseases of the joints, M., 1966, bibliogr.; Beetham U. P. et al. Clinical study of joints, trans. from English, M., 1970; Bykhovsky 3. E. Rheumatic and non-rheumatic diseases of the joints and their sanatorium and resort treatment, M., 1962; Velyaminov HA Doctrine of joint diseases, L., 1924; Diterichs M. M. Introduction to the clinic of joint diseases, M. - L., 1937; Kagan E.M. Rheumatism of miners, Kharkov, 1934; Multi-volume guide to internal medicine, ed. E. M. Tareeva, t. 8, M., 1965; Multi-volume guide to surgery, ed. B.V. Petrovsky, vol. 2, M., 1964; Nesterov A.I. and Astapenko M.G. On the classification of joint diseases, Vopr. revm., no. 3, p. 47, 1971; Rheumatology, ed. V. T. Tsoncheva, trans. from Bulgarian, Sofia, 1965; Modern problems of rheumatology, ed. E. M. Tareeva, M., 1965; Sorkin A. 3. Diagnostic errors in pathology and malformations of the osteoarticular apparatus, M., 1969; Struchkov V.I. Purulent surgery, M., 1967; Tsarfis P. G. Treatment of rheumatism and joint diseases, M., 1969; Boyle JA a. Buchanan WW Clinical rheumatology, Oxford—Edinburgh, 1971; Cellary J., Horstowa H. and Nowak S. Atlas reumatologiczny, Warszawa, 1968, bibliogr.; Choroby narzfidu ruc-hu, pod red. W. Bruhla, Warszawa, 1969, bibliogr.; M ieh 1 ke K. Die Rheumafi-bel, B. ua, 1961; Rheumatoid arthritis, ed. by W. Muller ao, L.—NY, 1971, bibliogr.; Textbook of the rheumatic diseases, ed. by WSC Copeman, Edinburgh—L.. 1969, bibliogr.; Tichy H., Seidel K. u. Heideimann G. Lehrbuch der Rheumatologia, V., 1962; W right V. a. Moll JM Psoriatic arthritis, Bull, rheum. Dis., v. 21, p. 627, 1971.
Pathological anatomy A. —Multi-volume guide to pathological anatomy, ed. A. I. Strukova, vol. 6, p. 305, 311, M., 1962; Rusakova M.S., Grits-man N.N. and Pavlov V.P. On changes in articular cartilage in rheumatoid arthritis and the resorbing role of pannus, Arkh. pathol., t. 32, no. 7, p. 47, 1970, bibliogr.; Strukov A. I. and Beg-l and r I N A. G. Pathological anatomy and pathogenesis of collagen diseases, M., 1963; DettmerN. Einige Aspekte zum Problem der Arthrose, Z. Rheumaforsch., Bd 27, S. 356, 1968; Klinge F. Die rheumatischen Erkrankungen der Knochen und Gelenke und Rheumatismus, Handb. spez. path. Anat. Histol., hrsg. v. F. Henke u. O. Lubarsch, Bd 9, T. 2, S. 107, B., 1934; M ankin HJ The structure, chemistry and metabolism of articular cartilage, Bull, rheum. Dis., v. 17, p. 447, 1967; Phe-mister DB Changes in articular surfaces in tuberculous and in pyogenic infections of Joints, Amer. J. Roentgenol., V. 12, p. 1, 1924.
X-ray diagnostics A. - Ganchenko L. I. On the issue of X-ray symptoms of infectious nonspecific polyarthritis, Vestn. rentgenol, i radiol., No. 3, p. 18, 1967, bibliogr.; Grinberg A.V. X-ray diagnosis of occupational diseases of bones and joints, L., 1962; Dombrovsky A. I. and Masneva A. Ya. On the issue of silicoarthritis, Vestn. rentgenol. and radiol., No. 3, p. 79, 1970; 3 o-diev V.V. and Spasskaya P.A. X-ray changes in joints in collagen diseases, ibid., No. 3, p. 3, 1963, bibliogr.; Reinberg S. A. X-ray diagnosis of diseases of bones and joints, vol. 2, p. 535, M., 1964, bibliogr.; Romanova M. S. About the combination of infectious non-specific polyarthritis and Kashin-Beck disease, Vestn. rentgenol, i radiol., No. 3, p. 25, 1967, bibliogr.; Khomyakov Yu. S. Narrowing of joint spaces with infectious nonspecific polyarthritis, ibid., No. 2, p. 17, 1965, bibliogr.; S е z е S. etRyckewaert A. Maladies des os et des articulations, t. 1-2, P., 1970, bibliogr.
Therapeutic physical education for A. - Kaptelin A. F. Restorative treatment (therapeutic physical education, massage and occupational therapy) for injuries and deformations of the musculoskeletal system, M., 1969; Leporsky A. A. Therapeutic physical training for metabolic diseases and joint diseases, M., 1960; Therapeutic physical culture, ed. V. E. Vasilyeva, p. 233, M., 1970; M about sh-k about in V. N. Therapeutic physical culture at resorts and sanatoriums, p. 294, M., 1968; Fedorova G. S. Therapeutic physical education for polyarthritis, M., 1972.
Orthopedic and surgical treatment of A. - Vreden PP Practical Guide to Orthopedics, L., 1936; Panova M.I. et al. On surgical interventions on joints in the complex treatment of patients with infectious nonspecific polyarthritis, Ortop. and traumat., No. 9, p. 3, 1966; Sivash K. M. Alloplasty of the hip joint, M., 1967; S k l ya-renko E. T. Surgical treatment of infectious nonspecific polyarthritis, Kyiv, 1971, bibliogr.
A. in children - Bisyarina V.P. Brucellosis in children, M., 1971, bibliogr.; Bogomolova F.A. id. On joint damage and arthralgia in children, Vopr. ocher mat. and children, vol. 15, no. 9, p. 30, 1970; Dolgopolova A.V., Melikhova N.I. iKuzmina N. N. Clinical manifestations of infectious-allergic polyarthritis in childhood, Vopr. revm., no. 1, p. 35, 1970; Dyakonova N. I. Clinic of brucellosis in children, Tashkent, 1964, bibliogr.; Multi-volume guide to pediatrics, ed. Yu.F. Dombrovskoy, t. 6, M., 1964; N e-s t e r o v A. I. About a special clinical variant of infectious-allergic polyarthritis, Vopr. revm., no. 3, p. 3, 1965; Borella L., Go ob a g J. E. a. C 1 a g GM Synovitis of the knee Joints in late congenital syphilis, J. Amer. med. Ass., v. 180, p. 190, 1962; Borella L. ao Septic arthritis in childhood, J. Pediat., v. 62, p. 742, 1963, bibliogr.; Glutton HH Symmetrical synovitis of the knee in hereditary syphilis, Lancet, v. 1, p. 391, 1886; F ink GW Gonococcal arthritis in children, J. Amer. med. Ass., v. 194, p. 237, 1965; Madon E., Baroncelli PG et Ferrari G. La poliartrite cronica primaria, Minerva pediat., v. 21, p. 1461, 1969.
Agababova E. R. Reactive arthritis, Rheumatology, No. 1, p. 3, 1985; S i d e l n i k o v a S. M. et al. Yersinia arthropathy: some clinical and diagnostic aspects, Ter. arkh., t. 55, no. 7, p. 77, 1983; A hv o nen P., Si e vers K. a. A ho K. Arthritis associated with Yersinia enterocolitica infection, Acta rheum, scand., v. 15, p. 232, 1969.
M. G. Astapenko, G. Ya. Guobis, P. S. Eryalis; I. D. Kanorsky (sir.), M. D. Mikhelman (trauma), N. K. Permyakov (path. anat.), S. A. Sviridov, L. M. Freidin (rent.); G. S. Fedorova (medical physicist), A. A. Yakovleva (ped.), E. R. Agababova..