Deforming osteoarthritis is a degenerative disease of the joints. Much remains unclear in the pathogenesis and etiology of deforming osteoarthritis. Normally, articular cartilage consists of chondrocytes (cartilage cells), collagen fibers and a ground substance, which consists of highly polymerized proteoglycans including protein, mucopolysaccharides and chondroitin sulfate. Chondroitin sulfate gives elasticity and firmness to the joint, distributing pressure under static load. Cartilage has no blood vessels and receives its nutrition from synovial fluid. It also lacks nerve endings. Cartilage has weak regenerative properties and the biological activity of cells is low. The pathological process as a result of this biological ability in cartilage does not develop quickly and proceeds without symptoms for a long time. Deforming osteoarthritis begins with metabolic cartilaginous disorders, but the root cause of such changes has not yet been established. Metabolic changes lead cartilage to aging and degeneration. Some internal and external factors play a certain role in the occurrence of deforming osteoarthritis.
Internal factors Internal factors contributing to the occurrence of deforming osteoarthritis include: disturbance of the pituitary-genital balance (menopause); genetic factor (heredity); the activity of lysosomal enzymes, which are involved in the processes of disorganization of the basic substance of cartilage, is exceeded (with deforming osteoarthritis, the activity of mainly cathepsin-D and neutral proteinase increases); immunobiological processes (entry of proteoglycan fractions from cartilage into the joint cavity), which have antigenic properties; violation of vascularization of joints (pathology of general and local circulation).
External factors: overload of joint functions; increased body weight; congenital anomalies; violation of statics; previous arthritis.
The extent to which each of these factors participates in the development of deforming osteoarthritis is unknown. If degeneration of previously modified cartilage occurs, then this condition is designated as secondary arthrosis. Its development can be facilitated by congenital static disorders (flat feet), arthritis, intra-articular fractures, injuries, and congenital joint dysplasia. In other cases, the disease is considered to be primary deforming osteoarthritis.
During metabolic disorders, depolymerization occurs in cartilage, as well as a loss of proteoglycans (chondroitin sulfate). This may be facilitated by increased activity of lysosomal enzymes, insufficient functional activity of chondrocytes producing proteoglycans in a defective form (in the form of small subunits), and changes in collagen fibers. A decrease in the amount of proteoglycans can lead to a decrease in the rate of diffusion.
Against the background of insufficient nutrition, the main substance of the cartilage degenerates, is replaced by connective tissue and disappears in some places. At the same time, some chondrocytes die and the remaining cells proliferate. The cartilage loses its elasticity, becomes dry, cloudy, and rough. Then it disintegrates and cracks appear, especially affecting the zone of maximum load (the middle of the articular surface). This process develops very slowly, usually not accompanied by changes in the bones and synovium. The disease remains clinically latent for a long time. Subsequent changes in bone tissue, synovial membrane and joint capsule are secondary.
Deprived of a shock absorber - cartilage, the articular surfaces of the bones are polished and compacted. Subchondral osteosclerosis appears. Sometimes areas of ischemia and necrosis (cysts) form. The periphery of the articular surfaces (nutrition of the cartilage) is less disturbed; its growth with further calcification is noted. Osteophytes are formed. Fibrous-sclerotic changes in the joint capsule lead to joint deformation. Irritation of the synovial membrane by cartilage breakdown products that have antigenic properties contributes to the development of synovitis.
Histological examination sometimes reveals fibrous tissue on the surface of the cartilage. Chondrocytes form large chondrons with light, chromatin-poor nuclei. Their cytoplasm is weakly pyroninophilic. Metachromatic material accumulates around the chondrocytes. Fibrils are located longitudinally throughout the articular cartilage to the subchondral bone.
The disease deforming osteoarthritis begins very gradually and imperceptibly. Osteoarthritis can develop in any joint, but the joints most often affected are those that are subject to heavy functional load: the hip, ankle, knee, and hand (distal interphalangeal) joints.
Patients complain of joint pain (sites of lesions), which intensifies with movement. By the end of the day, the pain intensifies. In the morning there is a noticeable relief of pain. With deforming osteoarthritis, “starting” pains are noted, their occurrence is associated with movement, with mechanical friction of the affected cartilage. With an increase in motor joint activity, the pain syndrome may decrease.
As the disease progresses, pain occurs when standing or walking for a long time, this is due to a decrease in the ability of the subchondral bone to withstand the load. It is very difficult for patients with deforming osteoarthritis to descend stairs. Pain may be associated with muscle contractures, spasms of muscle groups that are adjacent to the joints, as a result of irritation by osteophytes. Mild joint stiffness may often occur after resting (this stiffness is different from rheumatoid arthritis). Stiffness in osteoarthritis deformans is associated with muscle fatigue (regional) and can occur at any time (after movement, rest).
Deforming osteoarthritis is characterized by the joint symptom of “blockade” - severe pain suddenly appears while walking, which ultimately limits movement. Pain of this kind is provoked by the joint “mouse” (pieces of necrotic cartilage, fragments of osteophytes). Then, after a certain period of time, the pain syndrome decreases, which ultimately leads to the resumption of normal movement of the patient.
Women over 40 years of age, mainly those with excess body weight, are more likely to suffer from deforming osteoarthritis. On examination, joint deformities that are associated with bone growths may be noted. In the early period of the disease, external articular changes may be absent. Palpation reveals individual painful areas (medial side of the joint).
During the development of secondary synovitis, swelling of the joints may be observed, the temperature of the skin at the site of the affected joint may increase, and flexion contractures may be detected due to mechanical articular obstacles created by osteophytes and fibrosclerotic changes in the joint capsule. Clear atrophy of regional muscles is usually not observed. Varicose veins, cold extremities, and paresthesia may be observed. Deforming osteoarthritis can be combined with some degenerative lesions of the spine such as spondylosis and osteochondrosis.
Forms of deforming osteoarthritis
Clinical forms of the disease: gonarthrosis, coxarthrosis, arthrosis of the joints of the hands (distal interphalangeal). Coxarthrosis (deforming osteoarthritis of the hip joints) is a severe form of the disease. The background most often is congenital dysplasia of the heads of the hip bones, followed by the development of a pathological process of the hip joints. Pain appears in the buttocks, hip joints, and groin areas, which intensifies with movement in the joints. Joint function is noticeably affected, which leads to a change in gait. With bilateral lesions, a “duck gait” occurs. The disease can lead to shortening of the limbs due to flattening of the femoral head or deformation of the neck, subluxation. A progressive course is characteristic of secondary coxarthrosis. With gonarthrosis, there is a gradual onset of pain (knee joints), with intensification towards the end of the day, difficulty arises while going down the stairs, and reactive synovitis is possible. Further, limited extension and joint deformation may occur. The joint symptom of “blockade” periodically forms.
Arthrosis of the joints of the hands (distal interphalangeal) develops during menopause. Symmetrical, dense bone thickenings are noted; these are Heberden's nodes (the area of the distal interphalangeal joints), often sharply painful even at rest. In this case, the joints are deformed and their function suffers. Bone growths of Bouchard nodes (proximal joint area).
These laboratory parameters do not change with deforming osteoarthritis. Possible leukocytosis, a slight increase in ESR, also CRP, sialic acid (this is with reactive synovitis). There are no specific laboratory tests to diagnose deforming osteoarthritis. X-ray signs of deforming osteoarthritis are flattening of the articular surface, marginal growths (osteophytes), subchondral osteosclerosis (or subchondral compaction), narrowing of the joint space (medial side of the joint), cystic clearing.
The course of deforming osteoarthritis is long-term and progressive. Exacerbations of the disease can continue for years, then be replaced by more or less prolonged remissions. There are a compensated period and a decompensated period. During the compensated period, arthralgia periodically appears only after maximum and submaximal loads or with changes in meteorological factors. Pain during this period goes away on its own, without treatment. Progressive changes in cartilage lead to decompensated arthrosis.
During the long course of the disease and articular deformation, the functional properties of the joints are less affected than with rheumatoid arthritis. The exception is coxarthrosis. Ankyloses practically do not form in deforming osteoarthritis.
Based on all clinical data, radiological signs, functional state of the joints, and the course of deforming osteoarthritis, stages are distinguished: Stage 1 - pronounced limitation of joint mobility in one direction, initial osteophytes and some narrowing of the joint space. 2 tbsp. – moderate deformity with limited mobility (all directions), narrowing of the joint space, pronounced osteophytes. 3 tbsp. – severe deformation of the joints, limitation of movements, muscle atrophy, disappearance of the joint space, extensive osteosclerosis, joint “mice”.
The diagnosis of osteoarthritis deformans is based on radiological research data and does not cause difficulties. To establish the etiology of arthrosis, great importance is attached to the anamnesis (hereditary factor, trauma, working conditions, vibration). When diagnosing deforming osteoarthritis, the following signs are taken into account: the predominant articular localization of the process, which carries a large functional load; pain syndrome is “mechanical” in nature; changes in articular shape due to bone growths (Bouchard's, Heberden's nodes); there are no signs of an inflammatory reaction (only partial presence of moderate reactive synovitis); no significant impairment of joint function and absence of inflammatory activity in laboratory data; radiographic signs of deforming osteoarthritis; The course of the disease is slow and progressive. To clarify the diagnosis, joint puncture is performed (synovial fluid is examined).
For differential diagnosis of regenerative and inflammatory diseases of the joints with their atypical course, a puncture biopsy of the articular cartilage of the patella is performed. Histological examination can reveal a characteristic morphological picture of deforming osteoarthritis.
Differential diagnosis is carried out with various types of arthritis, often with rheumatoid arthritis, chondrocalcinosis, gout, various infectious arthritis and psoriatic arthropathy.
Unlike deforming osteoarthritis, rheumatoid arthritis usually begins with pronounced inflammatory phenomena (small joints) and laboratory data clearly changes with rheumatoid arthritis. A few months after the onset of the disease, muscle atrophy occurs around the affected joints, signs of osteoporosis (on x-ray), and isolated lesions. RF is detected in blood and synovial fluid.
Gout affects mostly males. It is characterized by acute paroxysmal joint attacks, which are manifested by high local activity of the process. In 80% of cases, the big toe (first metatarsophalangeal joint) is affected. Joint pain begins and noticeably intensifies at night, disturbing with complete rest. A sharp swelling of the periarticular tissues and hyperemia of the skin appear above the inflamed joint. There is persistent hyperuricemia in the blood serum. Characterized by the high effectiveness of colchicine, which can completely stop an attack of gouty arthritis within 24 to 48 hours.
Chondrocalcinosis, like deforming osteoarthritis, is manifested by damage mainly to large joints. Its distinctive features: acute paroxysmal nature of arthritis, calcification of articular cartilage, detected by X-ray, crystals of calcium pyrophosphate (synovial fluid).
Specific infectious arthritis is characterized by noticeable inflammatory manifestations in the joints, accompanied by fever and symptoms of general intoxication. They begin against the background of an infectious disease.
With psoriatic arthropathy, the pathological process involves mainly small joints of the hands, feet, and spine, and skin hyperemia above the inflammatory joints. Arthritis is usually preceded by skin manifestations of the joints of the hands; changes in the nails may be observed. X-ray picture: destruction of the heads of the middle phalanges, erosion of the interphalangeal joint of the first toe with bone proliferation of the base of the distal phalanx.
Treatment of deforming osteoarthritis is a difficult task, because... degenerative joint changes are almost irreversible. Basic principles of therapy: complex treatment procedures, systematic, long-term and persistent treatment.
Treatment should be aimed at eliminating external causes that may contribute to the progression of deforming osteoarthritis, restoring the functional properties of the affected joints, reducing and eliminating pain and inflammation. The effect on the metabolism of cartilage tissue is significant. The following types of therapy are indicated: regime measures, medications, physiotherapy, sanatorium-resort and sometimes surgical.
The articular load of the affected joints must be reduced in case of deforming osteoarthritis; it is important to follow these rules when taking analgesics, because pain syndrome (when taking analgesics) decreases and joint load may increase. Overloading the affected joints can lead to joint exacerbations. It is important to normalize body weight, which will reduce joint load (legs) and streamline the body’s metabolic processes. Patients are contraindicated: active physical activity, also work in one position (without movement); standing on your feet for a long time; labor or work with significant emotional stress, as well as unfavorable meteorological and climatic conditions (drafts, high humidity). Such people are shown easy and useful work.
Drug therapy for the treatment of deforming osteoarthritis includes non-steroidal anti-inflammatory drugs, which reduce pain and eliminate inflammatory processes - salicylates, pyrazolone derivatives, indomethacin, voltaren - (average therapeutic doses). Since osteoarthritis deformans often develops in older age groups, which often have concomitant lesions of the gastrointestinal tract, drugs with good tolerance are most indicated for them - naprosyn, brufen, voltaren. In addition, these drugs have a good analgesic effect. For reactive synovitis, intra-articular hydrocortisone is sometimes indicated (75 mg for large joints, 25 mg for medium joints at 7-day intervals). More frequent and repeated administration of corticosteroid hormones may worsen degenerative changes in cartilage. For clearly expressed symptoms of periarthritis, periarticular injection with a mixture of novocaine (0.5%) and lidocaine (2%) (2:1) is used.
In cases of deforming osteoarthritis with recurrent synovitis, aminoquinoline drugs (delagil, plaquenil, chloroquine, hingamine) are used for several years. To reduce pain caused by reflex spasm of the muscles adjacent to the joint, muscle relaxants are used - scutamil-C or mydocalm (3-week course). To influence vascular tone and improve blood circulation, injections of novocaine (2%) (10 days course), papaverine or no-shpa, and nicotinic acid are prescribed. Nicotinic acid affects the synthesis of proteoglycans and has some analgesic effect.
Pathogenetic therapy is aimed at improving processes in cartilage (metabolism) and the body as a whole. Rumalon has a stimulating effect on the synthesis of chondroitin sulfate by cartilage cells. The drug is used 1 ml intramuscularly (daily) (course of 25 injections). The first injection of rumalon is carried out at half the dose. After 3 months, it is recommended to repeat this course.
Subsequently, treatment is repeated after six months. In unadvanced cases of deforming osteoarthritis, after 1-2 courses of treatment with Rumalon, joint pain decreases, the development and progression of signs of arthrosis slows down. Instead of Rumalon, biostimulants (humisol 1 ml intramuscularly) (course of 30 injections) or aloe, peat, FiBS and others can be used. During treatment with drugs of this group, approximately 50% of patients feel worse. Temporary increased joint pain, fatigue, and increased drowsiness are possible. After 3 weeks of treatment, these subjective sensations disappear, and the general condition improves.
Local pathogenetic therapy is indicated: arteparone, trasylol, polyvinylpyrrolidone. Also, a mixture of sulfated acids mucopolysaccharides - due to the biochemical affinity with the substance of articular cartilage, easily penetrates the tissue, suppressing enzymatic processes, preventing the progression of degenerative changes.
Trasylol, contrical, gordox have anti-enzyme properties, inhibit proteases, lysosomal enzymes, thereby providing an anti-inflammatory effect. By suppressing the breakdown of cartilage proteoglycans by lysosomal enzymes, protease inhibitors have an inhibitory effect on degeneration processes. Trasylol is injected into the joint cavity at a dose of 20,000 units (once a week) (course of 2-3 injections). Also having a beneficial effect is the introduction of an artificial “lubricant” into the joint cavity - polyvinylpyrrolidone in combination with hyaluronic acid. The drug is used once a week (5-10 ml).
In the complex therapy of patients with deforming osteoarthritis, it is advisable to include courses of vitamins, as well as ATP, riboxin. In the absence of contraindications, anabolic steroids (methandrostenolone, retabolil, nerobolil) are used.
If deforming osteoarthritis occurs against the background of foci of chronic infection (tonsillitis, cholecystitis), the picture of the pain syndrome often changes noticeably. The pain becomes almost constant, disturbing even at rest. This is due to the addition of an infectious-allergic component. In these cases, complex therapy according to indications includes antimicrobial and antihistamine drugs. Physiotherapeutic procedures are also widely used in complex therapy: mud procedures, ozokerite, paraffin applications (articular area), electrophoresis of novocaine, ronidase, 10% sodium salicylate, ultrasound, diadynamic currents.
During the phenomena of reactive synovitis, hydrocortisone phonophoresis is indicated. Locally, rubbing with ointment, compresses with vipratox, ox bile, and virapin are used on the joint area (compensated stage).
Exercise therapy and massage help restore joint function. Exercise therapy is carried out without stress on the affected joints (sitting, lying down). Swimming in the pool is especially beneficial.
For deforming osteoarthritis, sanatorium treatment is effective. We recommend sanatoriums that have hydrogen sulfide, radon, iodine-bromine springs and various mud resorts.
Low-intensity laser radiation is increasingly being used to treat deforming osteoarthritis. The most effective laser radiation is helium-neon and helium-cadmium lasers) (15 sessions course). Laser therapy not only has a symptomatic analgesic effect, but also affects the pathogenetic mechanisms of the disease.
If complex therapy is ineffective, local radiotherapy of the most affected joints is resorted to.
Pronounced anatomical changes in the joints (surface with deformation) and a pronounced limitation of joint functions are an indication for surgical treatment - corrective operations or arthroplasty (endoprosthetics).
Prevention First of all, you need to avoid joint microtrauma and overload. Those. there must be suitable working conditions, rest, external conditions, climate; if possible, patients should receive annual sanatorium treatment.
Deforming osteoarthritis (DOA) is a degenerative-dystrophic disease of the joints, characterized by primary degeneration of articular cartilage with subsequent changes in the articular surfaces and the development of marginal osteophytes, which leads to joint deformation.
Epidemiology. DOA is one of the most ancient human diseases. Changes in the bone skeleton, such as osteoarthritis, have been found in the remains of Stone Age people. In 1802, Heberden first described arthrosis of the distal interphalangeal joints (Heberden’s nodes), but osteoarthritis was recognized as an independent nosological form only in 1911, when, according to Muller’s proposal, all arthropathy were divided into primary inflammatory and primary degenerative, and DOA was classified as the latter.
Nowadays, DOA is the most common reason for patients to present with joint complaints. According to rheumatologists in European countries and the USA, DOA accounts for up to 60-70% of all rheumatological diseases. It affects 10-12% of the population of developed countries, and among people over 50 years of age the incidence of the disease reaches 27%, and among people over 60 years of age - 97%. Although complete disability in patients with arthrosis is relatively rare, the disease often causes temporary disability and reduces the quality of life of patients.
Etiology. The main reason for the development of DOA is a mismatch between the mechanical load placed on the articular surface of the cartilage and its ability to resist this load , which ultimately leads to degeneration and destruction of the cartilage. A similar situation occurs when there is a mechanical overload of a certain joint or groups of joints (for example, arthrosis of the shoulder joint in a blacksmith, arthrosis of the wrist joint in a painter, arthrosis of the joints of the lower extremities with severe obesity).
Another etiological factor of DOA is a violation of the congruence of the articular surfaces , when the static load is distributed unevenly, and cartilage degeneration occurs at the site of maximum load (for example, with flat feet, congenital hip dysplasia, etc.).
In some cases, the load on the cartilage remains normal, but its physicochemical properties change , which makes the cartilage less resistant to normal load. This is facilitated by a variety of joint injuries, including minor, infectious or non-infectious arthritis, as well as metabolic damage to the joints, which occurs with gout, chondrocalcinosis, hemochromatosis, acromegaly, diabetes mellitus, etc.
The role of the hereditary factor in the formation of DOA is recognized only in cases of generalized primary osteoarthritis (polyosteoarthrosis) with multiple joint lesions and isolated lesions of the distal interphalangeal joints (Heberden's nodes).
Risk factors for developing DOA include:
age (its frequency increases like an avalanche in people over 45 years of age);
race (residents of China and South Africa are significantly less likely to suffer from DOA than whites, while in American Indians the disease is much more common);
previous joint injuries;
habitual overload due to professional or everyday stereotypical movements;
congenital joint pathology;
endocrine and metabolic disorders.
Of the totality of provoking factors, DOA is removable (modifiable), i.e. those for which preventive measures can be taken are only injuries and obesity.
Pathogenesis. In DOA, the articular cartilage is primarily affected. The main load on it is created by muscle contractions that provide movement in the joint. Cartilage is an excellent shock absorber, but its thickness of 1-2 mm is too small to protect the joint; subchondral bone and periarticular muscles act as additional shock absorbers.
Cartilage has two main functions:
1) ensures the sliding of articular surfaces during movement due to its extremely smooth surface (the coefficient of friction of two cartilaginous surfaces of a healthy joint is 15 times lower than the coefficient of friction of two ice cubes);
2) ensures uniform distribution of load over the articular surfaces and protects them from destruction.
For articular cartilage to perform its normal function, not only mechanical conditions , such as normal congruence of the articular surfaces and adequate static and dynamic loads. The biological properties of the cartilage itself must also be adequate , primarily its normal elasticity and strength.
Changes in the properties of cartilage may be due to disturbances in its metabolism. Among them, the main ones are qualitative and quantitative changes in glycoproteins , the main substance of cartilage. In the cartilage of a patient with DOA, instead of large-molecular agglomerates, glycoproteins are represented by small monomers that are not able to firmly retain water, and therefore its content in the cartilage increases. Excess water is absorbed by collagen, it swells, which leads to a decrease in cartilage resistance. Therefore, one of the earliest and most likely irreversible changes in cartilage is a violation of the orientation and size of collagen fibers and a disruption of the connection between them, leading to the destruction of the collagen network.
Degeneration of articular cartilage may also be associated with damage to the synovial membrane due to inflammatory processes, which leads to changes in the physicochemical properties of the synovial fluid and, consequently, to disruption of trophism, synthesis and differentiation of chondrocytes. In this case, a decrease in the synthesis of hyaluronic acid by synoviocytes and hyperproduction of prostaglandin E 2 , which stimulates the activity of osteoblasts and induces fibroplastic degeneration of cartilage.
Significant importance in the pathogenesis of DOA belongs to microcirculation disorders in articular tissues and, first of all, in the subchondral bone.
An immunological factor also plays a certain pathogenetic role . Cartilage proteoglycans have antigenic properties and can serve as a source of autoimmune reactions. Most likely, a secondary immune reaction plays a role in the development of reactive synovitis . Activation of matrix proteinases and overexpression of proinflammatory cytokines, primarily interleukin-1, are important in its pathogenesis.
It should be emphasized that modern concepts of the pathogenesis of DOA present this disease as multifactorial, realized through diverse pathogenetic mechanisms.
Pathological anatomy. Morphological changes in cartilage with DOA are similar to senile involutive changes, however, unlike them, with DOA, early and rapid development of degenerative changes in the cartilage, articular surfaces of the epiphyses of bones and the synovial-capsular apparatus .
The cartilage becomes dry, cloudy, rough, loses its firmness and elasticity, it becomes disintegrated, cracked and ulcerated with exposure of the bone and its fragmentation . The subchondral surface of the bone becomes compacted and polished under the influence of loads with the development of subchondral osteosclerosis and bone tissue defects in the form of cysts . These changes are most pronounced in the area of greatest load, i.e. in the center of the articular surface. Along the periphery, where the blood supply suffers less, compensatory growth of cartilage occurs with the formation of marginal osteophytes . In the later stages of the disease, secondary fibrosclerotic changes in the synovial membrane and capsule , often occurring with symptoms of reactive synovitis. Arthrosis of the knee and elbow joints is sometimes complicated by secondary osteochondromatosis due to the accumulation of osteochondral fragments in the articular cavity.
Classification. It is customary to subdivide DOA into primary (idiopathic) and secondary . Primary DOA is understood as a variant of the disease when the degenerative process develops in an initially healthy joint; in secondary arthrosis, degeneration affects a joint previously changed due to injury, inflammatory or metabolic lesions (Table 1).
In addition, mechanical , caused by the absolute overload of a healthy joint in the process of professional, household or sports activities, as well as structural , which is based on changes in the structure and trophism of the articular cartilage, as a result of which it ceases to cope with the usual physiological load and occurs relative overload of cartilage.
Taking into account the localization of the lesion, arthrosis of the hip joint ( coxarthrosis ), knee joint ( gonarthrosis ), interphalangeal joints of the hands ( Heberden and Busher's nodes ), generalized primary osteoarthritis (Kellgren's disease), osteoarthritis of the first metatarsophalangeal joint of the feet are also distinguished .
Of all joint diseases, this is the most common; according to statistics, osteoarthritis affects 10 to 16% of the world's population.
Osteoarthritis deformans is a chronic non-inflammatory disease of the joints (articular cartilage). It is based on premature aging and degeneration of articular cartilage, caused by the loss of the main component of the cartilage substance - proteoglycans.
Of all joint diseases, this is the most common; according to statistics, osteoarthritis affects 10 to 16% of the world's population. Most often, the disease affects women aged 45-55 years. And after 60 years, deforming osteoarthritis occurs in almost 100% of people.
The most common cause of osteoarthritis is a discrepancy between the load on the joints and their “margin of safety.” The culprits of this condition can be: excess weight, standing work, poor posture, playing sports (jumping, running or lifting weights). Presumably, the following are also important: metabolic and hormonal disorders, deterioration of blood supply to the joint, hereditary predisposition to diseases of cartilage tissue, old age, injuries, diseases such as rheumatoid arthritis and psoriasis.
With osteoarthritis, rapid aging of articular cartilage occurs. It loses its elasticity, the articular surfaces become rough, and cracks appear on them. In some places, the cartilage may wear away so much that the bone is exposed. With the loss of cartilage, bone tissue grows on the articular surfaces - a permanent deformation of the joint occurs.
With osteoarthritis, the hip (coxarthrosis) and knee (gonarthrosis) joints and interphalangeal joints of the hands are most often affected, although not a single joint is immune from this disease.
The onset of the disease looks like this: pain gradually appears in the joint when moving. With arthrosis of the hip joint, the pain comes from the upper part of the thigh and radiates to the knee, which is especially felt when walking. For those suffering from knee arthrosis, it is painful to go down the stairs; If the shoulder joint is affected, it is difficult to raise and lower the arm.
In general, the disease is characterized by the onset of pain under the influence of daytime physical activity and subsidence during the period of night rest. Short-term “starting” pain occurs after rest and soon disappears against the background of physical activity.
Gradually, the disease progresses: any movement begins to cause unbearable pain, and the joint becomes deformed and loses mobility. At this stage of the disease, it is only possible to remove the inflammation associated with arthrosis and reduce the pain, but it is no longer possible to restore the damaged cartilage.
Typically, osteoarthritis develops slowly and begins with damage to one joint, but after some time other joints are included in the process, primarily those that took on increased load in order to relieve the initially diseased joint.
If you experience joint pain and it does not go away within several months, immediately contact a rheumatologist or orthopedist.
After the examination, the doctor will prescribe additional tests:
Patients need to limit the mechanical load on the affected joint, therefore, during an exacerbation, semi-bed rest is recommended.
Anti-inflammatory drugs and chondroprotectors (drugs that protect cartilage) are most often used to treat osteoarthritis.
The use of physiotherapeutic methods leads to a reduction in pain. This uses ultraviolet light, electric currents, alternating magnetic fields, electrophoresis and phonophoresis of drugs on the joints. To strengthen muscles, the use of electrical myostimulation is recommended. Patients will benefit from therapeutic exercises for joints.
If a joint has irreversibly lost its function, the only treatment option is prosthetics.
Deforming osteoarthritis (DOA) is a disease associated with the destruction of articular tissues and deformation of adjacent bones. It is considered the most severe type of arthrosis of the joints and one of the main causes of disability among diseases of the musculoskeletal system.
Causes of deforming osteoarthritis
Osteoarthritis deformans affects almost any joint in the body, but the knee and hip joints are most commonly affected. Somewhat less commonly, osteoarthritis affects the joints of the spine, as well as the joints of the feet and hands.
Symptoms of deforming osteoarthritis are largely specific and determine the severity of the process:
Deforming osteoarthritis of the hands usually has the character of polyarthrosis, that is, it affects several joints, which leads to difficulty flexing and extending the fingers, pain and inflammation. Joint pain is accompanied by numbness, burning, and tingling. In the area of the affected joints, hard compactions form - Bouchard's and Heberden's nodes.
Treatment of arthrosis at the City Med Clinic Orenburg
Modern treatment of arthrosis includes a set of measures aimed not only at eliminating pain and inflammation in the joint, but also at slowing down the destruction of articular surfaces and restoring joint mobility.
Among the modern effective methods of treating arthrosis are:
Medicines relieve pain and inflammation. However, this therapy also has several serious side effects:
Call us at: 8 (3532) 607-500, we will tell you how to achieve a stable positive result in a few sessions, without chemicals or surgery, without allergies or side effects.
It develops slowly and usually does not cause serious disability, especially with appropriate management guidelines. Almost half of people over 60 years of age and virtually all over 80 years of age have osteoarthritis, but cases are now being reported in young people under 21 years of age.
Osteoarthritis occurs as a result of mechanical destruction of normal joint structures, changes in the capsule and damage to cartilage. Osteoarthritis most often affects the large joints of the knees, hips and spine. The process also often affects the joints of the hands.
A joint is a mechanism for the movable connection of bones, in which their ends converge in the articular capsule. The articular ends of the bones are covered by an elastic thin layer of hyaline cartilage, which does not contain nerve endings or blood vessels. During various movements, cartilage acts as a shock absorber, reducing pressure on the articulating surfaces of bones and ensuring their smooth sliding relative to each other.
The bones of the joints are held together by ligaments and tendons, which act like strong flexible cables and allow movement in the desired directions. They are completely surrounded by the joint capsule. The joint capsule is lined with a thin synovial membrane, which produces lubricating fluid into the joint space. The lubricating fluid provides nutrition to the hyaline cartilage and is a reliable lubricant of the articular ends of the bones. Inflammation of the synovial membrane (synovitis), hemorrhages into the joint cavity (hemarthrosis) contribute to the development of degenerative-dystrophic and inflammatory processes in the joint.
The first significant change in osteoarthritis is the softening and pitting of the smooth surface of the cartilage. As arthritis progresses, the layer of cartilage covering the joint surfaces becomes thinner until it completely collapses, leaving the ends of the bones exposed.
Without a normal gliding surface, it becomes painful and difficult to move the joint. As the cartilage continues to deteriorate, bone spurs form along the edges of the joint, as if compensating for the loss of cartilage by increasing the articular surfaces. This is the cause of joint deformities (the joint loses its shape) in arthritis. Popularly, this condition is called “salt deposition,” which is simply an illiterate name for arthrosis.
For many years, it was thought that osteoarthritis was the result of natural wear and tear on a joint throughout a person's life. But researchers now recognize that there are a number of factors leading to its development:
- age - with age, cartilage becomes less elastic and loses its resistance to stress;
- obesity - excess weight over a long period of time accelerates the process;
- damage (traumatization) of the joint - severe simultaneous injuries, accompanied by a bruise, fracture, dislocation, damage to the ligamentous apparatus of the joint, or repeated microtraumas of the joint, can contribute to the development of arthritis. Workers in a number of professions and professional athletes are exposed to microtrauma. An example is the development of arthritis of the knee joint in miners and football players; arthritis of the elbow and shoulder joints in those working with a jackhammer;
- family (hereditary) predisposition to osteoarthritis - some forms of osteoarthritis are indeed inherited in families, but heredity is not the main reason for the development of osteoarthritis.
The exact causes and mechanisms leading to osteoarthritis are still unknown.
Osteoarthritis often presents with few or no symptoms, even in cases where x-rays may show changes in the joint. You may have periods of instability and severe joint pain followed by long periods of stability.
Most older people experience some bouts of joint pain that soon go away or are relieved by rest and heat applied to the joint. Sometimes, however, symptoms are more severe and may include any of the following:
The first symptom that makes you see a doctor is pain in the joint. Patients often say that it is “aching” and poorly localized. The intensity of pain can vary depending on the stage of the disease - from severe, limiting joint mobility, to moderate, occurring only with certain movements. Joint pain tends to intensify with exercise and decrease after rest. As osteoarthritis progresses, pain begins to occur with minimal activity, and in advanced cases it can even wake the patient in the middle of the night.
Stiffness or “starting” pain usually occurs after a period of rest, especially in the morning, and after a period of low activity, when it is difficult to start moving, and soon disappears against the background of physical activity. Joint stiffness due to osteoarthritis is short-lived, usually lasting no longer than 15 minutes.
Increase in volume of the joint (swelling)
This occurs when irritation of the synovium causes extra lubricating fluid to leak into the joint, just as your eye produces tears in response to any irritation. But in a joint, the extra lubricating fluid cannot flow out as easily, and thus it causes swelling of the joint. This most often occurs in large joints: the hips, knees and spine.
A fairly common complication of osteoarthritis is the appearance of bone spurs (called nodules) in the joints of the hand. They usually occur in women and sometimes occur as early as the age of 40.
Although these knots can make the hand joints painful, most people continue to use their hands without restriction. Pain can be reduced with appropriate treatment in the early stages. Some people feel no pain with these joints, and many people with this type of osteoarthritis never have serious problems in other joints.
There are no specific laboratory tests to diagnose osteoarthritis, but tests may be done to rule out other forms of arthritis. With osteoarthritis, unlike other types of arthritis, there are no inflammatory changes in the clinical blood test; there is no rheumatoid factor characteristic of rheumatoid arthritis; There is no increase in serum uric acid levels, characteristic of gout. Your doctor will ask you to describe any physical stress or injury that may have led to your pain. The general examination will be carried out with close attention, especially to the joints that are bothering you.
X-ray examination helps to make a diagnosis, but does not predict the further development of symptoms of the disease. X-rays may show extensive changes, but this does not always mean in the clinic that the patient is in severe pain or is unable to work.
Among additional research methods, thermographic (thermal imaging) and ultrasound (ultrasound) examination of joints can help to detect inflammation in the joints or surrounding tissues, which cannot be seen on an x-ray.
Treatment cannot completely reverse changes that have already occurred in the joints, but treatment can slow the progression of the disease and control symptoms. As a rule, when you first consult a doctor, these changes are insignificant, and by following a certain motor regimen and rehabilitation recommendations, you can prevent further progression of arthritis. Neglect and procrastination are the worst enemies in the fight against osteoarthritis.
The doctor will likely recommend treatment that takes into account the stage of the disease and which joints are affected, the severity of symptoms, underlying chronic diseases, age, profession and daily activity.
- a certain rhythm of motor activity so that periods of load alternate with periods of rest, during which the joint must be unloaded;
- special physical exercises that allow you to form a good muscle corset around the joint, maintain normal mobility and sufficient blood circulation in the limb, strengthen the cartilage itself;
Controlling pain or using anti-inflammatory drugs or steroid injections into the joint to reduce inflammation or lubricant production. They are prescribed during an exacerbation of the disease and are aimed at relieving inflammation in the joint or tissues surrounding the joint. There is no need to try to relieve the aggravation on your own. Experience shows that better and faster results can be achieved by early consultation with a doctor, preferably a specialist (rheumatologist or arthrologist). Anti-inflammatory drugs have a huge number of unwanted side effects, so it is the doctor who will quickly select the most suitable one.
— in cases of severe long-term pain that does not go away with traditional remedies, as well as in cases of significant dysfunction of the joint, surgery of the hip or knee joints can bring real improvement and you should not be afraid of it.
It is important to first try to limit movements associated with increased stress on the articular cartilage. But at the same time, lead an active lifestyle by increasing physical activity, which does not have a negative effect on cartilage) in order to protect the joints (advice from a good doctor or physical therapy instructor can be very helpful).
Most disability in the early stages of osteoarthritis can be well corrected with a special exercise program and maintaining a normal body weight. Pain control and proper relaxation are also important to help you stay active.
Following all of the above recommendations will allow you to maintain satisfactory joint function throughout your life.
Due to the possibility of disability due to osteoarthritis, patients with osteoarthritis with damage to large joints, mainly knees and hips, are subject to observation, starting from the early stages of the disease.
Deforming osteoarthritis is a chronic degenerative disease of the joints, which is based on the degeneration of articular cartilage with subsequent changes in the bone articular surfaces, the development of marginal osteophytes, joint deformation, and the development of moderate synovitis.
There are primary and secondary deforming osteoarthritis. Primary deforming osteoarthritis develops in previously healthy cartilage under the influence of its excessive load. With secondary deforming osteoarthritis, degeneration of the already previously changed articular cartilage occurs.
The causes of primary osteoarthritis are not completely known. The main suspected factors for the development of primary osteoarthritis are:
The interaction of external and internal predisposing factors plays an important role in the development of primary osteoarthritis.
External factors contributing to the development of primary osteoarthritis: trauma and microtrauma of the joint; functional overload of the joint (professional, household, sports); joint hypermobility; unbalanced diet; intoxications and occupational hazards (nitrates, heavy metal salts, herbicides, etc.); alcohol abuse and intoxication; past viral infections.
Internal factors predisposing to the development of primary osteoarthritis: structural defects of the musculoskeletal system and static disorders leading to changes in the congruence of articular surfaces (flat feet, dysplasia, genu varum, genu valgum, spinal scoliosis); excess body weight; endocrine disorders; disorders of general and local circulation; concomitant chronic diseases, including previous arthritis.
The main causes of secondary osteoarthritis are: joint injuries, endocrine diseases (diabetes mellitus, acromegaly, etc.); metabolic disorders (hemochromatosis, ochronosis, gout), other diseases of the bones of the joints (rheumatoid arthritis, infectious arthritis and other inflammatory diseases of the joints, aseptic bone necrosis.
Under the influence of etiological factors, faster and earlier “aging” of articular cartilage occurs. Its metabolism is disrupted, first of all, depolymerization and loss of proteoglycans (primarily chondroitin sulfates) of the main substance and death of some chondrocytes occur. In osteoarthritis, the phenotype of chondrocytes changes and protein glycans and collagen, which are not characteristic of normal cartilage, are synthesized. The cartilage loses its elasticity, first of all in the center, becomes rough, fibers appear, cracks appear in it, the underlying bone is exposed, and later the cartilage may completely disappear. The lack of shock absorption under pressure on the articular surface of the bones leads to their compaction (subchondral osteosclerosis) with the formation of areas of ischemia, sclerosis, and cysts. At the same time, along the edges of the articular surfaces of the epiphyses, cartilage grows compensatoryly, and then ossification occurs - marginal osteophytes are formed. The presence of cartilage fragments in the articular cavity, phagocytosed by leukocytes with the release of lysosomal cytokine enzymes, leads to periodic synovitis, and with repeated relapses - to fibrotic changes in the synovium and capsule. Currently, the role of the immune system in the pathogenesis of osteoarthritis deformans has been shown: increased function of T-helpers, promoting the development of autoimmune processes - the appearance of specific autoantigens (altered proteoglycans) of cartilage, synovia, autoantibodies and immune complexes with subsequent damage to cartilage. An important role is played by the increase in the catabolic activity of various cytokines, as well as metalloproteinase enzymes of the cartilage itself.
About 10% of the population suffers from osteoarthritis, most often women aged 40-60 years; after 60 years, the disease occurs in almost 100% of people. The main and general signs for deforming osteoarthritis of any localization are the following:
Coxarthrosis is the most common and severe form of deforming osteoarthritis. Usually leads to loss of joint function and disability of the patient. In 60% of patients, coxarthrosis is secondary and develops as a result of osteonecrosis, malformations of the osteoarticular system (protrusion), injuries, functional overload (obesity, different lengths of limbs, etc.). Usually the patient begins to limp on the affected leg. Subsequently, pain in the groin area appears and gradually intensifies, radiating to the knee, lameness sets in, limitation of inward rotation of the hip and its abduction occurs, later external rotation and adduction of the hip, as well as its flexion and extension, are limited. Sometimes a “jamming” of the hip joint occurs. Atrophy of the muscles of the thigh and buttock develops quite quickly, later - flexion contracture, shortening of the limb, changes in gait, poor posture, severe lameness, and with bilateral damage - “duck gait”. Radiologically, the pathological process begins with a narrowing of the joint space and the appearance of bone growths, then the femoral head is flattened, which leads to shortening of the limb: calcifications can be observed in the soft tissues. The course of coxarthrosis is constantly progressive.
Gonarthrosis is often secondary, associated with injury to the knee joints or a static disorder; its course is more favorable than the course of coxarthrosis. The main symptoms are pain on the inside or front of the joint when walking, especially up stairs, which goes away with rest; pain is observed during the month preceding the time of diagnosis; instability of the joint, crunching during active movements in the knee joint, morning stiffness within 30 minutes. The radiograph reveals sharpening and elongation of the intercondylar eminence, narrowing of the joint space, and abundant osteophytes.