ARTHROSES (arthrosis, singular; grech, arthron a joint + - ösis; synonym: the osteoarthroses deforming the arthroses deforming osteoarthroses) — degenerative and dystrophic diseases of joints.
And. are the most widespread diseases of joints and therefore have exclusively great practical value, their frequency increases with age. According to Kellgren, Laurence (J. Kellgren, J. Lawrence) and others, radiological symptoms And. are observed at 87% of women and at 83% of men at the age of 55 — 64 years. At 22% of women and at 15% of men 50 years are more senior there are not only radiological, but also clinical signs And. Considerable part A. proceeds asymptomatically.
Depending on absence or existence of the previous pathology of joints And. share on primary and secondary. The forms beginning without the noticeable reason (40 years are aged more senior) in the joint cartilage which is not changed until then belong to primary. They usually affect many joints at the same time, i.e. are polyarticulary. Secondary And. anomalies of a statics, arthritis, an aseptic necrosis of a bone, an inborn dysplasia develop at any age owing to an injury, vascular disorders, and affect only one or several joints.
Etiology and pathogeny
Aetiology and pathogeny primary And. completely are not found out. Among the etiological factors promoting development of local displays of a disease, first place is won by the static load exceeding functionality of a joint, and mechanical microtraumatization. With age there occur changes of vessels of a synovial membrane. The important part is assigned also a nek-eye to endocrine frustration, especially increase in activity of somatotropic hormone of a hypophysis, depression of function thyroid and gonads, etc. At obesity there is not only an increase in mechanical load of joints of the lower extremities, but also the general impact of metabolic disturbances on function of a musculoskeletal system is noted. Besides, value of infectious, allergic and toxic factors is not excluded. A certain role of pathology of veins of a shin in development is noted And. knee joints. There are also data indicating a role of heredity in an etiology And.
In the light of modern representations pathological process in joints at arthrosis develops as follows. As a result of long raised and even normal load of joints at simultaneous changes in vessels of a synovial membrane and deterioration in conditions of food of a cartilage lysosomes of cells of a cartilage collapse and proteolytic enzymes which cause a depolymerization of proteino-polisakharidny complexes become more active. Such activation of lizosomalny enzymes causes death of cells, especially in a surface layer of a cartilage owing to what the cartilage loses the elasticity, on its surface small cracks are formed, the strengthened penetration of enzymes of a synovial membrane, especially hyaluronidases, cathepsines, plasminogen, etc., in a cartilage begins.
During the aging of a cartilage in it anaerobic glycolysis therefore the maintenance of a lactate increases dominates and pH decreases. It increases activity of the specified enzymes since their optimal effect happens in acid medium, and degradation of components of intercellular substance of a cartilage is even more aggravated.
In response to the increased depolymerization of proteino-polisakharidny complexes and reduction of components of a cartilage there occurs proliferation of chondrocytes and strengthening of synthesis of a hondroitinsulfat. Thus, dystrophy of a cartilage gradually progresses, the surface layer gets it klochkovidny structure. Besides, at And. properties of synovial fluid change, edges is good lubrication agent, especially at the expense of hyaluronic to - you. It promotes development too And.
The synovial membrane rich with connective tissue elements, circulatory and limf, vessels, nerves, takes part in development too And., especially at emergence of reactive inflammatory reactions. At elektronnomikroskopichesky studying of a synovial membrane two types of cells are allocated: type A and type B. Cells of type A are preferential absorbtivny and have ability to englobe, and cells of type B generally develop complexes hyaluronic to - you and proteins. At And. activity of these cells amplifies in the beginning, and in process of progressing of process weakens. The reasons causing launch of this mechanism are unknown. Believe that the genetic predisposition caused by defect in synthesis of polysaccharides and enzymes of a cartilage can matter.
In an etiology and a pathogeny secondary And. the major role is played by the injuries breaking an integrity or congruence (compliance) of joint surfaces.
Other reasons secondary And. also the acquired disturbances of a statics, the postponed arthritises, diseases of an epiphysis of bones, diseases of a metabolism (e.g., gout, an ochronosis, Kashin's disease — Beck), endocrine diseases are inborn a dysplasia (a hypothyroidism, a diabetes mellitus, etc.).
The inborn and acquired defects of a cartilage and other elements of the bone and joint device in combination with proceeding or even the increasing load of joints can lead through a certain span to A. Uchityvaya's development that circumstance that injuries and microtraumatization, anomalies of a statics (varus or valgus position of hips, shins and stop, flat-footedness, congenital dislocation or a dysplasia of a hip, a kyphosis, a lordosis, scoliosis, etc.) » the postponed diseases of bones (aseptic necroses) and joints (arthritises) and some other states very often are the reason of development of arthrosis, Hakkenbrokh (M. of Hackenbroch, 1968) suggested to call them preartroza and to take preventive measures for the prevention And.
A pathogeny (addition)
Distinguish primary, or genuinical, deforming osteoarthrosis (DOA) when dystrophy of a joint cartilage begins in the joint which is not changed before, and the secondary osteoarthrosis which is an outcome of the previous arthritis, an osteochondropathy, an injury of a joint, the inborn or acquired disturbances of a statics. In the first case develops And. all or many joints (system And., or the polyosteoarthrosis), in the second case is observed damage most often of only one-two joints.
To primary And. also age changes of joint fabrics appearing later 50 — 60 years can be referred (involute, or senile, an osteoarthrosis). However in this case dystrophic changes of a cartilage develop extremely slowly without the expressed changes of a bone and a synovial membrane and, as a rule, are not shown clinically. It gives the grounds to consider senile And. as independent nozol, form.
Mechanisms of development of dystrophy of a joint cartilage at primary DOA are identical to those which take place at senile arthrosis: disturbance of metabolism of the main substance of a cartilage with loss of its main component — the proteoglycans providing hydrophily of a cartilage, its elasticity and elasticity. The decrease of proteoglycans leads to disturbance of processes of diffusion in a cartilage, to its dryness, a razvolokneniye, fragmentation and its gradual disappearance. Uniformity of changes of a joint cartilage at DOA and senile And. allows to connect DOA with early aging of a joint cartilage. More bystry, than at senile And., development of this process at DOA leads to secondary changes of surrounding fabrics: to consolidation and sclerosis of joint surfaces of an epiphysis, development of multiple regional osteophytes (see), to the phenomena of a secondary reactive synovitis owing to antigenic properties of decomposition products of a cartilage and to secondary fibrous and sclerous changes of a synovial membrane and the joint capsule. All these changes lead to emergence of pains and others a wedge, signs of DOA.
Early wear of a joint cartilage can be a consequence: a) the long raised load of it exceeding physiological — an absolute giperpressiya on Fick and Arles (P. Ficat, J. Arlet, 1977); b) decrease in tolerance of a cartilage to a daily fiziol, loading — a relative giperpressiya. To an absolute giperpressiya most often conduct the unfavorable conditions of work and life causing long microtraumatizations) a cartilage and disturbance of his metabolism (a decrease of proteoglycans). However as DOA develops not at all persons subjecting the joints to overloads, this factor can be considered as only one of elements of a pathogeny of DOA. Also the role of the increased load of a cartilage at obesity is similar. Major importance in disturbance of metabolism and destruction of a joint cartilage has decrease in resistance of a cartilage to a daily fiziol, loading and microtraumatization. In this plan the genetic factor has an essential role, the proof of what is the fact that in families of patients with system DOA this disease, according to G. Lawrence et al. (1977), meets twice more often than in population. The mechanism of implementation of a genetic factor at DOA is completely not deciphered, but most of authors believes that it takes place funkts, insufficiency of cartilaginous cells — the chondrocytes synthesizing proteoglycans or in insufficient quantity, or in a defective form (not in the form of large units, and in the form of small subunits) owing to what they easily leave a cartilage.
The great value in a depolymerization of proteoglycans and their decrease from a cartilage is given to a superactivity of lizosomalny proteolytic enzymes — cathepsine-D and neutral metaldependent proteinase which quantity in an artrozny cartilage, according to A. I. Sapolsky et al. (1974), is increased by 2 — 3 times. The rupture of lizosomalny membranes and exit of proteolytic enzymes in a cartilage can occur under the influence of supertension on a cartilage, a hypervitaminosis, a hyper sensitization, disturbances of microcirculation in joint fabrics and other reasons suppressing oxidizing enzymes and thus the proteases stimulating an exit.
The role of primary defeat of a synovial membrane (its fibrosis and a zapustevaniye of capillaries) as the reasons of deterioration in food of a cartilage and disturbance of his metabolism at genuinical DOA is not supported by most of researchers. However in the 70th disturbance of microcirculation in a subchondral bone is proved, also the venous hyperemia develops in a cut at DOA staz. At the same time it is not excluded that these disturbances are secondary.
Influence of an endocrine factor, namely disturbance of pituitary and genital balance, the great value was attached to Krom in the past, called in question as in many cases it is impossible to explain development of DOA at rather young age and in the absence of endocrine disturbances.
It is proved that the joint cartilage has antigenic properties [Herman (J. The N of Herman), 1976], and at his dystrophy develops hypersensitivity of the slowed-down type. It gives the chance to consider an immune factor as an origin at DOA of the secondary inflammatory reactions in a joint supporting a continuous current patol, process.
Thus, disturbance of metabolism of a cartilage at primary DOA, apparently, can be a consequence of a complex of various reasons which specific weight in different cases And. it is various. However thin mechanisms of metabolic disturbances in a joint cartilage remain still not clear.
The secondary deforming osteoarthrosis is a consequence various patol, processes in a joint from which disturbance of full coincidence (congruence) of joint surfaces results. At the same time loading is distributed not evenly, and concentrates on the limited site of a cartilage, as leads to bystry development of dystrophic process in this place, to considerable deformation of joint surfaces and progressing of process.
At the heart of pathoanatomical changes at And. the progressing dystrophic and necrobiotic processes in a joint cartilage which are followed by deformation of sochlenovny surfaces of bones (fig. 1) lie. From here the most widespread term — deforming And. As a rule, an epiphysis of bones is involved in process that gives the grounds to call a disease also an osteoarthrosis. Deforming And. most often develops in joints of extremities. However also intervertebral disks can be surprised (see. Diskartroz ).
A gross appearance deforming And. depends on a stage of a disease. In an early stage the razvolokneniye, a roughness, first of all at the edges of a joint cartilage is noted. Further its thinning, an uzurirovaniye and formation of hillocks of various sizes is observed. In far come cases at the edges of a cartilaginous covering bone growths are formed — osteophytes (see).
In the sites perceiving pressure, the surface deprived of a cartilage under the influence of continuous friction as if otshlifovyvatsya. Bone «shlifa» have an appearance of zheloboobrazny dents.
All these changes cause deformation of a joint. The head of a hip, e.g., can get a fungoid, cylindrical form or be flattened. It is deformed as well a joint hollow (fig. 2). Considerable changes are undergone by sheaves, a synovial membrane, the capsule. Intra joint sheaves become reinforced, loosened. At a sharp disfiguration of a joint they can undergo a necrosis, an atrophy or to grow together with a joint bag. Nipples of a synovial membrane increase in sizes, sometimes gain treelike character. In their stroma development of fatty tissue, a cartilage and bone is observed. Such nipples can otshnurovatsya and turn into free intra joint bodies (see. Joint mouse ).
The amount of synovial fluid is, as a rule, sharply reduced that was an occasion to characterize a disease as «a dry inflammation of joints».
Microscopic picture deforming And. it consists of the dystrophic changes of a joint cartilage (fig. 3) which are followed by its vascularization and ossification from subchondral departments of a bone. In regional departments excess proliferation of chondroblasts can be observed, edges are compensated not so much by a decrease of cartilaginous tissue how many promotes a disfiguration of a joint owing to formation of an ecchondrosis. An ecchondrosis is exposed to calcification and substitution by a bone tissue with formation so typical over time for And. osteophytes.
In a cartilage the razvolokneniye, and also mucous and fatty dystrophy of the main substance, decrease in content of acid mucopolysaccharides is defined. These changes are followed by formation of numerous gaps and cracks. At the same time on borders with a synovial membrane and marrowy spaces the phenomena of a chondrolysis and a rassasyvaniye of cartilaginous substance therefore the collagenic fibers passing here are unmasked are noted. In late phases the necrosis of chondrocytes and disappearance of fibrous structures is possible. The large centers of a necrosis of a cartilage meet only in hard cases of a disease. In basal departments of a cartilage there are marrowy cavities surrounded with thin bone beams.
In subchondral departments the phenomena of a lacunary resorption and a new growth of a bone are noted, and in zones of bone «shlif» the osteosclerosis develops. In deeper departments of an epiphysis osteoporosis with formation of the cysts surrounded with a belt of the sclerosed bone prevails. Here islands of cartilaginous tissue which, according to some authors, represent growths of the cartilaginous callosity extending from deep departments of not calciphied zone of a joint cartilage meet. In rare instances islands of cartilaginous tissue in the form of peculiar «hernias» eminate over a surface of bone shlif (fig. 4).
False and bone ankyloses at deforming And., unlike arthritises, do not develop.
The clinical and X-ray pattern
Liouba A. develops and proceeds very slowly and never leads to heavy dysfunctions of joints and especially to a false and bone ankylosis. An exception is the hip joint differing in the anatomic features (the deep joint hole containing apprx. 2/3 heads of a femur, and rather narrow joint crack which is quickly decreasing at any pathological process). In this joint restriction of mobility and involvement in process of myshechnosvyazochny elements very much is early observed that in far come cases quite often is the reason of an invalidism of patients. However the anchylosis also in this case does not come if to And. inflammatory process does not join.
Any form A. proceeds without the general signs of an inflammation (acceleration of ROE, a disproteinemia, temperature increase, emaciation, etc.). Primary And. often is followed by disturbance of a lipometabolism, arterial hypertension, atherosclerosis and other diseases. Very important line And. discrepancy between the morphological changes in joints observed on roentgenograms and clinical displays of a disease is. Sometimes at minor radiological changes severe pains and restriction of mobility are noted. In other cases at considerable radiological changes clinical symptoms are very moderate. It depends on several reasons. First, the joint cartilage is completely deprived of vessels and nerves. Therefore its defeat does not give symptoms until pathological process does not go beyond the cartilage. Secondly, the synovial membrane, the joint capsule, sinews and muscles having the numerous nervous receptors perceiving pain not in all joints are surprised at the same time and in the same degree. Thirdly, not at all patients And. develops equally quickly: the more slowly it begins and proceeds, the clinical symptoms since the organism manages to use all compensatory adaptations are less expressed.
Joint symptoms And. there are of pains, feelings of constraint, bystry exhaustion, rigidity, deformations, a crunch, etc. Pains are usually stupid. They are changeable, amplify during cold and wet weather, after long loading (e.g., by the evening) and at intention movements after a condition of rest («starting pains»), In hip joints of pain irradiate to the inguinal or sciatic area (at the same time tension of abductors and sgibatel of a hip is noted). Very often, especially at senile And., instead of pains only the ache and feeling of weight in bones and joints is noted. This feeling is very close to feeling of constraint at a pseudorheumatism, but differs in short duration and small intensity. True restriction of mobility at And. it is observed seldom, it is about rigidity and bystry fatigue of joints more often. All these symptoms are caused by disturbance of congruence of joint surfaces, changes (a thickening, calcification, a sclerosis) in the joint capsule, sinews and other soft tissues and a spasm of muscles. Deformations of joints are best of all noticeable in distal interphalangeal joints of hands (geberdenovsky small knots), in a hip joint (a condition of an inflection, adduction and external rotation of a hip), in knee joints (a thickening of a bone tissue at the expense of regional osteophytes) and are caused by bone growths, but not swelling of soft tissues, as at arthritises (see). Roughnesses of joint surfaces, limy deposits and a sclerosis of soft tissues are the reason of a crunch of joints (most often knee). Unlike a small, crepitant crunch at synovites, for And. the rough crunch is characteristic.
X-ray inspection allows to diagnose And., to establish a stage of process, to carry out differential diagnosis. By the main method of a research at And. the X-ray analysis is (see. Artrografiya ). In addition to a standard X-ray analysis, in the presence of indications apply tomography (see), and also functional X-ray analysis and X-ray cinematography (see) which allow to determine amplitude of movements, relationship between joint departments of bones at various provisions of a joint etc. At X-ray inspection comes to light that defeat usually begins as monoarticulary process, and at multiple defeat of change in one joint prevail over changes in others. Pathological process progresses and gradually becomes polyarticulary.
It is clinicoradiologically possible to allocate three stages during And. First stage it is characterized by minor changes. There is a scarcely noticeable narrowing of a joint crack, especially in places of the greatest functional load (e.g., in lateral department of a crack of a hip joint and in medial department of a crack of a knee joint), and insignificant bone growths, preferential at the edges of a hollow of a joint (fig. 5) appear.
Second stage differs in more expressed changes (fig. 6). Narrowing of a joint crack becomes well visible. Reorganization of joint surfaces decides on changes of a joint crack. Surfaces of an epiphysis of bones are deformed, flattened and become uneven; bone growths reach the considerable sizes and lead to deformation of the joint ends of bones. Especially sharply it is expressed in a hip joint: the head of a hip is flattened, considerably increases in the diameter and gets a fungoid form. The nature of deformation of the joint ends of bones also the statiko-functional load influences a certain segment of an extremity therefore the configuration not only heads, but also hollows of a joint changes (e.g., a pseudo-protrusion of an acetabular hollow, flattening of a joint surface of a shovel, tibial bone etc.). Deformation of joint surfaces is followed by disturbance of congruence, up to development of incomplete dislocations and dislocations in a joint. Disturbance of relationship between joint departments of bones involves redistribution of lines of statiko-functional loads that the plow of vara, humerus varus, to the arc-shaped curvature of bones etc. in turn leads to development of deformation in type.
In third stage development of process occurs the changes in deeper sites of bones which are followed by a sclerosis of a subchondral bone tissue. Besides, the centers of cystous reorganization which at an arrangement in regional subchondral departments of bones form the uzura reminding tubercular defeat come to light various size.
Quite often in the second and especially in the third stage And. the intra joint bodies which are formed as a result of a separation of bone growths and calcification of a nekrotizirovanny cartilage (fig. 7) come to light. Intra joint bodies have irregular shape, the size and quantity them are variable. The true atrophy and regional osteoporosis are not characteristic for And.; the exception is made And., proceeding with sharply expressed morbidity and dysfunction of a joint.
Secondary And. are characterized by development of changes in joint departments of bones against the background of primary process which radiological can be shown in the form of deformation of a bone and change of its structure. As a result of basic process one of the bones participating in formation of a joint most sharply changes. Other bones usually (in the absence of inflammatory process) suffer much less. The joint end of a bone is deformed, flattened and quite often collapses (fig. 8). The structure of spongy substance of a bone is exposed to reorganization that is shown by osteolytic and osteosclerotic changes. Further morbid conditions of the bones forming a joint come to an end with development secondary And., degree of manifestation to-rogo depends on the nature of basic process. At secondary And. narrowing of a joint crack, a thickening of surfaces of bones due to regional bone growths and formation of the centers of cystous reorganization is defined.
Except the listed general clinical and radiological symptoms, And. separate joints have some additional features.
Arthrosis of distal interphalangeal joints of fingers of hands (geberdenovsky small knots, geberdenoartroz) represents one of the most frequent localizations primary And., usually strikes women, especially in the climacteric and postclimacteric periods. Geberdenovsky small knots (fig. 9, 10) are considered as early display of primary genetically caused polyarthrosis which is at the same time connected with an overload of distal interphalangeal joints small and hard work. Geberdenovsky small knots develop very slowly, asymptomatically, often imperceptibly for the most sick. Only in late terms small pains develop, usually during the change of weather, small morbidity at a palpation and noticeable eminences on both parties of a dorsum of distal interphalangeal joints are formed. On the roentgenogram narrowing of joint cracks, roughness of joint surfaces, a subcartilaginous sclerosis and side osteophytes is noted.
Arthrosis of proximal interphalangeal joints of fingers of hands (busharovsky small knots) meets considerably less than geberdenovsky small knots, but on the clinical and X-ray pattern almost does not differ from the last. As a rule, busharovsky small knots appear at the persons having geberdenovsky small knots (fig. 9). It helps to distinguish them from a pseudorheumatism, at Krom proximal interphalangeal and metacarpophalangeal joints separately or jointly very often are surprised. Besides, deformation of a joint at busharovsky small knots is caused not by a thickening of soft tissues (as at arthritises), and firm bone growths.
Arthrosis of a carpal and metacarpal joint of the I finger (rizartroz a thumb) meets approximately also often, as well as geberdenovsky small knots. At the same time both defeats can be at the same time. Frequent microtraumatization is the reason of a rizartroz.
Clinical and X-ray pattern (fig. 11) — same, as well as at And. two previous localizations.
Arthrosis of an elbow joint it is observed less often in connection with the loading reduced by it. However at some types of work, especially with vibrotools, conditions for long microtraumatization of these joints and for development professional are created sometimes And. (at miners, smiths, founders, bricklayers, etc.) which is shown by the sharp pains amplifying after full bending and extension in a joint. Soon there comes a nek-swarm restriction of its mobility. The rough crunch in a joint at the movements is often noted. Except narrowing of the Joint crack (fig. 12), subcartilaginous) an osteosclerosis and regional osteophytes, the joint mice representing or pieces come off and then a calciphied cartilage (e.g. are often observed, at the stratified osteochondritis), or manifestation of a joint chondromatosis.
Arthrosis of hip joints (coxarthrosis) is one of the most frequent and severe forms of degenerative diseases of joints. Early dysfunction of these joints as it was already specified, is caused them by special anatomical structure. Specific weight of secondary forms of the coxarthroses caused by the inborn displaziya, dislocations and incomplete dislocations of a hip postponed diseases and injuries of a head of a hip (Pertes's disease, Pedzhet's disease, bone and joint tuberculosis) and other reasons is especially big. So, according to S. Seze et al. (1956), secondary coxarthroses make 58% of all coxarthroses, 40% from them make the coxarthroses caused by an inborn incomplete dislocation. According to Malvin (M. of D. Malvin, 1971) inspecting 200 patients with a coxarthrosis, inborn dismorfoza of a hip joint are revealed at 65% of patients And.
Secondary coxarthroses more often unequally affect both joints or happen unilateral. Primary are usually symmetric. Unlike other localizations And., at coxarthroses accurate correlation between clinical symptoms and radiological changes is observed, and sometimes even clinical symptoms appear first of all. Pains during the walking and lameness develop only by the end of the working day in the beginning, later keep all day, and in hard cases are so intensive that prevent the patient to fall asleep, irradiate in a knee joint, to the sciatic and inguinal area. Restriction of mobility comes early. The patient by force keeps a leg in the provision of an inflection, adduction and external rotation. The attempt to unbend, take away or turn a hip of a knutra causes severe pain. For compensation of a flexion contracture the lumbar lordosis develops. As a result of the specified deformations the leg seems shortened. On the roentgenogram (fig. 13) all are visible characteristic for And. changes: narrowing of a joint crack (on all joint or only in its upper part), a subcartilaginous sclerosis (both from a head of a femur, and from an acetabular hollow), regional osteophytes (also in the field of both joint surfaces) and bone cysts (both in an epiphyseal part of a head of a hip, and in haunch bones).
Arthrosis of knee joints (gonartroz) meets as often as the coxarthrosis, but usually proceeds asymptomatically. Damage of these joints is connected with the following circumstances: first, the knee joint has a large number of cartilaginous educations (except the big area of a joint cartilage, there are intra joint meniscuses which level insufficiently congruent joint surfaces of bones and serve as peculiar shock-absorbers); secondly, knee joints are under a continuous load of body weight, especially at corpulent people; thirdly, knee joints are very often injured.
The last circumstance causes frequent emergence of a so-called chondromalacia of a patella at persons of young and middle age then develops gonartroz. The large role in development of a gonartroz is played by obesity: first, load of knee joints significantly increases; secondly, increase in intra joint adjournment of fatty tissue complicates already difficult conditions of food of a joint cartilage.
Clinical symptoms of a gonartroz are very various. In an initial stage pains at ascension are noted, it is even more — during descent on a ladder, at a rising after rest, and also in wet and cold weather and after long stay standing. Sometimes pains acute that can be caused by irritation of a synovial membrane pieces of the come-off cartilage and development of a reactive synovitis. At the same time accumulation of a large amount of exudate and protrusion of a suprapatellar bag and pockets of the joint capsule is possible. The rough crunch in an initial stage of a disease is defined at a palpation, and in far come cases is listened at distance. Morbidity below a patella, on its edges is noted and at the shift of a patella in the medial and lateral direction. At a research of synovial fluid find moderate increase in concentration of protein and increase in viscosity (unlike a pseudorheumatism, at Krom viscosity is reduced). The number of leukocytes in it does not exceed 3000 in 1 mm 3 , among them only a quarter make polinukleara (at a pseudorheumatism a cytosis to 20 000 leukocytes in 1 mm 3 , 3/4 make polinukleara of them). Important value in differential diagnosis of a gonartroz with a pseudorheumatism of knee joints has a morphological research of the material of synovia received at a biopsy.
On roentgenograms of knee joints (fig. 14 and 15) characteristic for And. changes: narrowing of a joint crack, subcartilaginous sclerosis, regional osteophytes and cystic reorganization of adjacent parts of bones.
Points of intercondyloid hillocks of a tibial bone are among precursory radiological symptoms of a gonartroz. Also small erosion in the lower third of a back surface of a patella, narrowing of a crack between a patella and a femur and osteophytes on top and bottom edges of a patella are observed. At a gonartroza joint meniscuses, especially medial often are surprised. It leads to sharp narrowing of a joint crack or to Au-shaped or H-shaped deformations.
Gonartroz can be secondary (as a result of injuries, the postponed arthritises, injuries of meniscuses, the stratified osteochondritis, a chondromatosis, etc.) or primary (arising without the noticeable reason, perhaps, as a result of aging of a cartilage or a long professional overload). More often than And. other localization, gonartroz is complicated by a synovitis. In this case speak about a gonartroza with a reactive synovitis.
Arthrosis of the I metatarsophalangeal joint is the most frequent And. in the field of foot (fig. 16). It is caused by valgus deformation of a thumb of a leg or its long traumatization.
And. can affect also other joints, napr, temporal and maxillary, humeral, radiocarpal, talocrural and costovertebral joints (see. Spondylarthrosis ). All of them are shown by similar clinical and radiological symptoms.
Polyarthrosis the dystrophic disease of many joints at the same time is called. As a rule, it is primary form of a disease. Develops usually at advanced or senile age as a result of endocrine and metabolic, climacteric frustration, toxic influences and other reasons. Meets also at younger age. The combination of damages of joints of extremities and a backbone is characteristic of polyarthrosis. At the same time also geberdenovsky small knots are almost always observed.
Diagnosis of any And. put on the basis of clinical, radiological and datas of laboratory. Asymptomatic and latent forms A. can be diagnosed only by a X-ray analysis. In diagnosis of clinically expressed forms also other diagnostic criteria are used. According to an artrotsentr of Institute of rheumatism of the USSR Academy of Medical Sciences, the diagnosis deforming And. usually put on the basis of the following signs:
1. Preferential localization of process in the joints bearing the greatest exercise stress.
2. The joint pain appears at the movements and an exercise stress. Sometimes in the most expressed cases there are constant pains of inflammatory character that is connected with development of a secondary reactive synovitis.
3. Change of a shape of joints due to bone growths. The similar phenomena are found most often in small joints of brushes, feet, in knee joints.
4. Restriction of functions of joints usually moderate, caused by pain or (more rare) bone growths; false and bone ankyloses never happen.
5. Lack of signs of a local inflammation. Seldom there is a moderate reactive synovitis with an exudate in a cavity of a joint.
6. Lack of shifts of the laboratory indicators testimonial of existence of inflammatory process.
7. Slow progressing of a disease.
The anamnesis and comprehensive inspection of the patient help to define a form A., the reason of its development, prescription and disease severity accompanying a disease, etc.
The differential diagnosis is carried out with arthritises (see). At arthritises of pain of inflammatory type, deformation of joints at the expense of the exudative and proliferative phenomena in soft circumarticular tissues, but not due to bone growths, the movements in joints are limited considerably. Shifts of laboratory indicators demonstrate existence of inflammatory process. Differential diagnosis is helped by results of a research of synovial fluid and a morphological research of a biopsirovanny synovial membrane.
At X-ray inspection the general for both processes is narrowing of a joint crack, however at arthritises it is narrowed more and unevenly in different departments. At arthritises, especially tubercular and rhematoid nature, along the joint surface of bones at various levels from it the centers of destruction are defined various form and size. Besides, in initial stages of arthritises, and also during the progressing of inflammatory process there are regional uzura having uneven and indistinct outlines. At stabilization of process or development of reparative changes the centers and uzura get more accurate and equal outlines. At And. there are centers of cystous reorganization surrounded with a sclerous zone; a certain localization, as a rule, connected with the place of the gross statikofunktsionalny capacities is characteristic of these centers. For arthritises, unlike And., is more characteristic osteoporosis (see), they can end with formation of bone anchylosis (see) or secondary deforming And. For primary And. the bone anchylosis is not typical.
Forecast And. depends on a form and localization of a disease, age and the general condition of the patient. Primary And. usually proceed more favorably and with less expressed clinical signs, than secondary. Weight of the last is aggravated with the previous diseases or injuries. Most hard coxarthroses which often result in disability proceed. And. at elderly and old people usually proceed more hard, than at young faces. Concerning complete elimination of morphological changes the forecast of all forms A. adverse since the complete recovery of a cartilage at the adult is impossible. However at many forms A. the pain syndrome can be eliminated and function of a joint is almost completely recovered.
Treatment And. also depends on a form and localization of defeat, the general condition of the patient. Treatment shares on etiotropic, pathogenetic and symptomatic. Etiotropic treatment is possible only at secondary And., which etiology is known. It generally comes down to orthopedic correction of a statics of joints, reduction of load of the joints which were injured in the past, sanatorium treatment.
To actions of pathogenetic treatment And. it is necessary to refer use of stimulators of formation of chondroid fabric for substitution of defects of a joint cartilage (Rumalonum and other biological stimulators); the muscle relaxants eliminating reflex spasms of muscles (Mydocalmum, Seduxenum, scutamil, etc.); the vasodilators improving food of a cartilage (nicotinic to - that, thermal procedures, massage, etc.); sex and anabolic hormones (hexestrol, Nerobolum), and also intra joint administration of inhibitor of proteases of Trasylolum.
The important place in treatment And. borrow symptomatic actions. Conservative therapy first of all is directed to elimination of pains. For this purpose use salicylates, drugs of a pyrazolon row (Butadionum, Rheopyrinum, pyramidon, analginum), drugs from group of indometacin (indometacin, Indocidum, a metindol). It is very important to provide rest to the affected joint periodically (several times a day). Anesthetics are warmly on area of the affected joint and surrounding soft tissues (the paraffin, a diathermy warming compresses, hot bathtubs, etc.), infiltration of periartikulyarny fabrics solution of novocaine, Bernard's currents, ultrasound, a roentgenotherapy. Corticosteroids inside or are vnutrisustavno used only in exceptional cases, in the presence of a persistent reactive synovitis, by a small course since their prolonged use even more aggravates pathological process in a joint.
The good effect gives sanatorium treatment using mud applications, hydrosulphuric and radonic bathtubs, massage and remedial gymnastics.
In cases of a heavy current And., especially knee and coxofemoral joints, sometimes it is necessary to resort to surgical intervention.
In the second stage palliative operations, napr, Foss's operation (department of muscles which are attached to proximal department of a hip) are shown at And. hip joint. Such method of treatment as valgiziruyushchy, variziruyushchy or cross belongs to pathogenetic therapy in this stage osteotomy (see). The similar osteotomies made at And., call osteotomia medicata since after them inflow of blood to a joint increases, its food improves. At arthrosis of a hip joint make an osteotomy with shift according to Mac-Marri for transferring of load of other site of a cartilage (see the Hip joint). In the third stage more radical operative measures are shown: if there are no multiple bone cysts — an arthroplasty (see); in the presence of cysts and at mobile other pair joint — artificial ankylosis (see); at bilateral deforming And. — an arthroplasty on the «best» joint and an artificial ankylosis on other party in an advantageous position for a support. At an artificial ankylosis use distraktsionno-compression devices (see). In certain cases apply Endoprosthesis replacement of a hip joint across Sivash (see. Arthroplasty ).
Prevention primary And., caused preferential by age and a professional overload, consists in fight against a senilism of an organism by means of a balanced diet, sufficient physical activity and a hardening of an organism, on the one hand, and elimination of professional vrednost, with another. Prevention secondary And. — treatment of a basic disease.
Astapenko M. G. Dystrophic arthritises, Mnogotomn. the management on vnutren. to diseases, under the editorship of E. M. Tareev, t. 8, page 301, M., 1965, bibliogr.; Astapenko M. G. and Pikhlak E. G. Diseases of joints, M., 1966, bibliogr.; Glauber A. The deforming arthrosis, Mnogotomn. the management on the orthopedist, and travmat., under the editorship of Η. P. Novachenko, t. 2, page 137, M., 1968, bibliogr.; Klioner I. L. Senile and degenerative changes in joints and backbone, page 9, 50, etc., M., 1962, bibliogr.; Kosinskaya N. S. Degenerative and dystrophic defeats of the bone and joint device, page 15, etc., L., 1961, bibliogr.; Rheumatology, under the editorship of V. T. Tsonchev, the lane with bolg., page 473, Sofia, 1965, bibliogr.; Tsarfis P. G. Treatment of rheumatism and diseases of joints, page 236, etc., M., 1969, bibliogr.; Arthritis · Arthrose, hrsg. v. J. Lindner u. a., Bern u. a. 1971;;; Boyle J. A. a. Buchanan W. W. Clinical rheumatology, Oxford — Edinburgh, 1971; Choroby narz3.au ruchu, pod red. W. Brühla, s. 413, Warszawa, 1969, bibliogr.
Astapenko M. G., etc. About some mechanisms of development of a degeneration of a joint cartilage at the deforming osteoarthrosis, Rubbed. arkh., t. 49, No. I, page 9, 1977; Brandt K.D., Palmo ski M. J. a. Perricone E. Aggregation of cartilage proteoglycans, Arthr, and Rheum., v. 19, p. 1308, 1976; Cooke T.D. o. Identification of immunoglobulins and complement in rheumatoid articular collagenous tissues, ibid., v. 18, p. 541, 1975; FassbenderH. G. Pathologie der chronischen Polyarthritis, Med. Welt, Bd 26, S. 2033, 1975; F i with a t P. et Arlet J. 35tio-pathog£nie de l’arth-rose, Rev. Rhum., t. 44, p. 627, 1977; Herman J. H. a. Carpenter B. A. Immunobiology of cartilage, Semin. Arthr. Rheum., v. 5, p. 1, 1976, bibliogr.; Man-kin J. H. a. o. Biochemical and metabolic abnormalities in articular cartilage from osteoarthritic human hips, J. Bone Jt Surg., v. 53-A, p. 523, 1971; Sapolsky A. I., H o w e 1 1 D. S. a. W o e s s-n e r J. F. Neutral proteases and cathepsin D in human articular cartilage, J. clin. Invest., v. 53, p. 1044, 1974; S w e e t M. B. a. o. Biochemical changes in progressive osteoarthrosis, Ann. rheum. Dis., v. 36, p. 387, 1977.
Pathological anatomy of A.
The multivolume guide to pathological anatomy, under the editorship of A. I. Strukov, t. 6, page 320, 329, etc., M., 1962; In a t of and N. S. of ampere-second of h and η 1 e at J. Existence and incidence of osteoid in osteoarthritic femoral heads, J. Bone Jt Surg., v. 51-B, p. 366, 1969; Heine * J. Über die Arthritis deformans, Virchows Arch. path. Anat., Bd 260, S. 521, 1926, Bibliogr.; H u 1 t h A., L indberg L. a. T e 1-h g H. Mitosis in human osteoarthritic cartilage, Clin, ortop. related Res., v. 84, p. 197, 1972; Jeffery A. K. Osteogenesis in the osteoarthritic femoral head, J. Bone Jt Surg., v. 55-B, p. 262, 1973; Lang E. J. Arthritis deformans und Spondylitis deformans, Handb. spez. path. Anat., Histol., hrsg. v. F. Henke u. O. Lubarsch, Bd 9, T. 2, S. 252, B., 1934, Bibliogr.; Pommer G. Von den Frühstadien und den Rückbildungsbefunden der gichtischen Harnsalzablagerungen, Beitr. path. Anat., Bd 90, S. 513, 1933; R a-d i n E. L., Paul I. L. a. R about s e R. M. Pathogenesis of primary osteoarthritis, Lancet, v. 1, p. 1395, 1972; Roth-well A. G. a. In e n t 1 e at G. Chondrocyte multiplication in osteoarthritic articular cartilage, J. Bone Jt Surg., v. 55-B, p. 588, 1973.
Radiodiagnosis of A.
Maykova-Stroganov V. S. and Rokhlin D. G. Bones and joints in the x-ray image, the Extremity, L., 1957, bibliogr.; Reynberg S.A. Radiodiagnosis of diseases of bones and joints, t. 2, M., 1964; Rokhlin D. G. Radiodiagnosis of diseases of joints, p. 2, L., 1940; Rubasheva A. E. Private radiodiagnosis of diseases of bones and joints, Kiev, 1967; Hagi-dekov G., etc. Radiodiagnosis, the lane with bolg., Sofia, 1962; In 1 ä h a R. Rentgenologie kosti and kloubu, v. 1 — 2, Praha, 1963; D eäk P. Diagnostik derKnochen-und Gelenkkrankheiten nach führenden Röntgensymptomen, Budapest, 1966, Bibliogr.; About r e n d i C. Knochen-, Gelenk-und Weichteilerkrankungen im Röntgen*-bild, Jena, 1968, Bibliogr.
Orthopedic treatment of A.
Mikhelman M. D. Treatment of the deforming arthrosis of a hip joint, Works 1st Vsesoyuz. congress travmatol. - the orthopedist., page 124, M., 1965; Languages D. K. The deforming (disfiguring) osteoarthrosis, Ortop. and travmat., No. 6, page 7, 1960, bibliogr.; E.E Rienzo C's Barbie-ri. Trattamento chi-rurgico della coxartrosi, Arch. Ortop. (Milano), v. 79, p. 113, 1966, bibliogr.
A. A. Matulis (artr.), H. K. Residents of Perm (stalemate. An.), M. K. Klimova (rents.), F. R. Bogdanov (ORT.); M. G. Astapenko.