Osteoarthritis of the knee joint: degrees, treatment, diet

Osteoarthritis of the knee joint is a consequence of chronic inflammation, which causes degenerative changes in tissues. The reasons for this phenomenon are numerous and varied, but they all have the same effect - an inflammatory process affecting cartilage tissue, ligaments, meniscus, etc. As a result, the cartilage becomes thinner, and the bones begin to rub against each other as they move, simultaneously irritating the nearby nerve fibers. Severe swelling and noticeable pain occur, the joint loses mobility and becomes stiffer. Gradually, ossification of cartilaginous tissue occurs with the formation of osteophytes. Modern medicine knows how to deal with this and guarantees patients relief from unpleasant and dangerous symptoms while maintaining knee mobility.

Causes

Most cases of the disease occur after 45 years of age, but recently the pathology has become steadily “younger” and is often diagnosed in younger people, mainly women. Among the reasons that cause inflammation and osteoarthritis of the knee joint are:

age, which causes a whole bunch of degenerative changes in the tissues of the body;
excess weight, as a result of which the load on the lower limbs and joints increases sharply, and the tissues wear out faster under intense mechanical stress;
atherosclerosis;
diabetes mellitus, which causes complications in the form of inflammatory joint diseases;
hormonal disorders;
genetic predisposition, which is associated with a special shape of the lower extremities or disorders in the structure of joint tissues;
consequences of injuries and regular overload;
professional sports activities that increase the patient's exposure to microtrauma and damage;
rheumatoid arthritis;
metabolic disorders, etc.

Therapeutic exercise for osteoarthritis

Therapeutic exercise is your best friend in the treatment of osteoarthritis in the early stages. Sports are excluded during illness.

In the exercise therapy room, the patient is introduced to special means of knee protection - fixing bandages. They contribute to uniform load on the joint. Be sure to wear bandages on both knees, even if only one hurts!

Effective exercises for knee osteoarthritis that you can do at home.

Initial position	Actions (perform smoothly, without straining the joints)	Quantity
Stand vertically with your back to the wall, arms down.	Touch the wall with your palms, shoulder blades and buttocks. Slowly rise onto your toes. Descend.	5-7 seconds, 15-20 times.
Lying down, feet rest on the floor, legs bent.	Raise your right leg to knee height, straighten, hold, and lower smoothly. Repeat with your left leg.	7 seconds, 10 times on each knee.

Symptoms

Manifestations of the disease depend on the gender and age of the patient, his level of physical activity and other symptoms of osteoarthritis of the knee joint. Typically complaints are received about:

severe pain in the knee joint during activity, which gradually subsides after a long rest;
swelling of the knee;
a feeling of warmth inside the joint, which can be caused by an inflammatory process and heating of bone tissue during friction;
noticeable stiffness of the knee joint after a long immobile position;
reduction in the range of motion of a joint, which makes it difficult to perform normal movements: climbing stairs, getting out of a car, getting up from a chair, etc.
extraneous sounds in the knee joint: creaks, crunches and crackles;
reaction of the joint to weather conditions.

Classification

Deforming osteoarthritis has several degrees of severity, determined by the characteristics of the disease and on the basis of a medical examination.

The scientific community distinguishes three stages of this disease:

the first degree is set when there is a slight decrease in the level of joint mobility, its edges are very slightly deformed, the joint space has narrowed only slightly, and the growths are at the initial level;
the second degree is marked by a decrease in the mobility of the cartilage, the appearance of crunches during movements, mild muscle atrophy, a more obvious narrowing of the gap and the appearance of significant bone growths;
third degree is the most serious. The joint is severely deformed and severely limited in its movements, the joint space is completely absent, the bone is clearly changed. There are many growths and cysts.

Some experts also distinguish another stage - the initial stage of development of the disease. It is difficult to detect because it does not appear on x-rays.

Diagnostic methods

A quick and accurate diagnosis can be made by studying the medical history and analyzing complaints about well-being, as well as clarifying the presence of the same disease in the family and the list of factors influencing the development of pain and its extinction. In addition, to clarify the nature of the pathology, an orthopedic surgeon can write a referral to:

radiography to assess the condition and severity of bone tissue damage: the presence of osteophytes, abnormal limb axis, sclerosis, reduction of cartilage tissue;
ultrasound examination to assess the structure of the joint;
magnetic resonance imaging, which allows you to accurately indicate the causes of pain in the joint;
a blood test, which is prescribed as part of differentiated diagnostics to exclude rheumatoid diseases, boreliosis, etc.

Additional diagnostic methods are prescribed according to the doctor’s decision in order to clarify the nuances of the development of grade 1, 2 or 3 osteoarthritis of the knee joint and evaluate the disease over time.

Introduction. General information about osteoarthritis

Osteoarthritis (OA) is one of the most common human diseases, known since ancient times. Signs of O.A. found in the remains of primitive people, Egyptian pharaohs. The 20th century was marked by many technical innovations that greatly changed people's lives. On the one hand, the relief of physical labor has reduced the load on human joints, on the other hand, it was the emergence of many technical devices that led to an increase in the development of arthrosis in people of certain professions: drillers, miners, workers in vibration installations, etc. The development of vehicles led to a decrease in motor activity of a significant part of the population, increasing material well-being leads to an increase in body weight above the norm in more than half of the world's population. Currently, the prevalence of OA is steadily increasing, as is the proportion of elderly people [37].

In 1986, the Osteoarthritis Subcommittee of the American College of Rheumatology (ACR) Committee on Diagnostic and Therapeutic Criteria proposed the following definition of OA: “Osteoarthritis is a heterogeneous group of diseases that lead to joint symptoms due to deterioration of the integrity of articular cartilage and changes in the underlying bone" [13].

In 2003 V.A. Nasonova in her book “Rational Pharmacotherapy of Rheumatic Diseases” gave a more complete definition of this disease. OA is a heterogeneous group of diseases of various etiologies, but with similar biological, morphological, clinical manifestations and outcome, which are based on damage to all components of the joint, primarily cartilage, as well as subchondral bone, synovium, ligaments, capsule and periarticular muscles [23 ].

High functional demands placed on the knee joint, the unique anatomical structure and biomechanics - all these factors determine the high frequency of its damage throughout a person’s life [19].

Epidemiology of osteoarthritis

Of all the diseases of the musculoskeletal system, OA (according to the international classification - osteoarthritis) (M15-M19 according to ICD-10) represents the most complex socio-economic and medical problem [30]. According to official statistics of Russia, in 2004 the total number of registered patients with lesions of the musculoskeletal system was more than 14 million people [8].

According to the International Decade on Osteoarticular Disorders, more than 42 million people in the United States suffer from arthritis, and more than 7 million people have limited mobility. Disability due to arthritis is accompanied by great economic losses for the patients themselves, their families and society. In the United States, every year 39 million arthritis patients visit a doctor for help, more than 500 thousand of them are hospitalized. At the same time, the cost of medical care amounted to 15 billion dollars, and the total economic losses - 65 billion. Predictive statistics show that if you do not intervene in the situation, then by 2021 60 million people, i.e. almost 20%, may develop arthritis population, and 11 million of them may become disabled. Do diseases of the musculoskeletal system matter for Russian society and Russian healthcare? Of course, the overall prevalence of musculoskeletal diseases over 10 years (1988–1997) increased from 7.5 million to 11.2 million, an increase of more than 49% [21, 22].

According to numerous authors (N.I. Korshunov, V.V. Marasaeva, E.Ya. Baranova, E.S. Tsvetkova, E.R. Agababova, N.A. Bogomolova, R.M. Tikhilova, 2006; K Blanc, 2004; E. Roos, 2007), the socio-economic significance of the problem is determined by the predominant (up to 60-82.5%), damage to people of middle, most working age and a high proportion (up to 35%) of patients who received disability due to about this disease. The socio-economic significance of the problem is given by the fact that pathology is widespread in middle-aged patients among the entire population [15].

The prevalence of OA in the population (6.43%) increases with age and reaches maximum values (13.9%) in people over 45 years of age [32]. According to German scientists who published statistics on OA of the knee and hip joints, the incidence of OA is 10 out of 2230 people and the prevalence of the disease is from 0.5 to 36%, depending on age. The results were assessed in 29 studies based on the example of 14 countries of the Eurasian continent [53].

According to WHO, more than 12% of the world's population (700 million people) suffer from deforming arthrosis of the joints; it causes disability and deterioration in the quality of life of patients. According to expert estimates by O.M. Folomeeva et al. (2006), N. Bellamy et al. (2006), from 1990 to 2021, due to increasing life expectancy and the aging of the population, the number of patients with OA may double. In people under 45 years of age, the prevalence of OA increases by 57%, and in people over 65 years of age it reaches 90%. According to O.M. Folomeeva et al. (2003), L.I. Alekseeva (2003), V.V. Povoroznyuk (2004), J. Pelletier et al. (2006), rates of temporary and permanent disability in OA are comparable to those in cardiovascular pathology.

Pathogenetic aspects

For many years, the development of OA was considered a consequence of the aging process. Currently, views on the pathogenesis of OA have changed significantly. It is assumed that the pathogenesis of OA consists of 2 components: “pathological stress”, i.e. pathological load on the joint, which can also be associated with injury and dysplasia, and “pathological cartilage”, in the formation of which the main role belongs to metabolic disorders, in a significant number of cases due to aging [18, 52].

The basis of the disease is a violation of the adaptation of articular cartilage to mechanical load, primarily a shift in the balance of cartilage tissue metabolism towards catabolic processes. Normally, the synthesis and degradation of cartilage elements are in a balanced state. Changes in articular cartilage in OA can be caused by both genetic and various environmental factors, i.e. OA is a multifactorial disease [36].

It is currently believed that the progression of the degenerative-destructive process in the joints is based on many complex reasons and mechanisms interacting with each other, only partially related to age-related changes. In recent years, evidence has been obtained of the influence of genetic predisposition, biomechanical and metabolic changes, local inflammation, etc. on the development of OA [35].

The main etiological factors in the development of gonarthrosis are macro- and microtraumas of the knee joint caused by intense physical activity: sports, professional, and excess body weight [31].

In this case, the load is unevenly distributed over the surface of the articular cartilage, and the maximum pressure is concentrated in a small area, in the place of greatest convergence of the articular surfaces, leading to dystrophy and degeneration of the cartilage.

The basis of these degenerative changes is a violation of cartilage metabolism, accompanied by a decrease in the content of proteoglycans and rupture of collagen fibers. In general, the content of proteoglycans in the cartilage matrix reaches 3-10%. The main proteoglycan of cartilage tissue is aggrecan, which assembles into aggregates with hyaluronic acid [7]. Large aggregates of proteoglycans are extremely hydrophilic and bind most of the water contained in cartilage. Water accounts for approximately 70% of the total mass of articular cartilage. In normal, undamaged cartilage, large hydrophilic aggregates of proteoglycans are intertwined with each other and pulled together by a network of collagen fibers, giving the cartilage elasticity [11].

In normal adult human cartilage, matrix components are synthesized by chondrocytes at a low rate. There is strict regulation of the rate of matrix renewal - a delicate balance between synthesis and destruction. With O.A. the most pronounced pathomorphological changes occur in the cartilaginous matrix. Functionally, chondrocytes, regulating metabolism, carry out, on the one hand, the synthesis of cartilage tissue (anabolism), and on the other, degradation processes, i.e., disintegration (catabolism) of aggrecans (large proteoglycan) and other components of cartilage tissue. With O.A. the balance is disrupted, both synthesis and breakdown of the matrix are enhanced, with catabolic processes predominant [33].

OA is characterized by two parallel processes: degradation and synthesis of the extracellular matrix of articular cartilage and subchondral bone; the main role in the regulation of these processes belongs to the cytokine system [28].

The most pronounced pathomorphological changes in arthrosis occur in the cartilage matrix. They lead to the development of progressive erosion of cartilage and destruction of type II collagen fibers, as well as degradation of proteoglycan macromolecules. Disorders of cartilage metabolism are based on quantitative and qualitative changes in proteoglycans—protein-polysaccharide complexes that ensure the stability of the structure of the collagen network, which is the basis of the cartilage matrix. Cartilage damage in arthrosis occurs as a result of increased synthesis and release of collagenase and stromelysin (metalloproteinases) from chondrocytes, which destroy proteoglycans and the collagen network (Fig. 1). An increase in the synthesis of collagenase and stromelysin in the affected cartilage may be genetically determined; it is under the control of cytokines released from the synovial membrane and leads to further degradation of the cartilage matrix [39].

Rice. 1. Morphological changes in cartilage in osteoarthritis.

Normally, articular cartilage is elastic and compressible; under high pressure loads, the surfaces of the articular cartilage are coated with a special lubricant, which ensures smooth movement with almost no friction. Collagen, proteoglycans and hyaluronic acid are mainly responsible for these properties of cartilage. The shape and tensile strength of cartilage is provided by type II collagen, which is unique to joints. Another important component of cartilage is proteoglycan (macromolecules in which a core protein is associated with one or more glycosaminoglycan (GAG) chains). GAGs are divided into two groups: non-sulfated (hyaluronic acid, chondroitin) and sulfated (chondroitin sulfate, keratan sulfate). Together with collagen fibers, GAGs provide cartilage resistance to external influences (Fig. 2). With O.A. GAG synthesis by chondrocytes decreases. The synthesis of collagen type II also decreases with an increase in the synthesis of collagen types I, III, and X. In the early stages of OA, chondrocytes are activated, which produce a number of cytokines (interleukin-1β, tumor necrosis factor α) and enzymes (metalloproteinases, inducible nitric oxide synthetase, cyclooxygenase-2), which contribute to the destruction of cartilage and the development of inflammatory changes in the affected joint [29] .

Rice. 2. Proteoglycan aggregate of the cartilage matrix.

Recent studies indicate the role of pro-inflammatory cytokines IL-1β, TNF-α in the pathogenesis of OA and the immune nature of inflammation. Both cytokines were detected in increased quantities in the synovium, synovial fluid and cartilage in patients with OA. In chondrocytes, these cytokines increase the synthesis of proteases, especially metalloproteinases, reduce the synthesis of collagen types II and IX, proteoglycans, tissue inhibitor of metalloproteinases, stimulate the production of oxygen radicals, nitric oxide, which contributes to the progression of catabolic processes in cartilage [6].

Inflammation plays a certain role in the pathogenesis of OA, although the cause of its development is not always clear. Inflammation is involved in the degradation of cartilage through the production of proinflammatory cytokines (interleukins-1β and -6, tumor necrosis factor, etc.), which promote the release of enzymes that damage collagen and proteoglycans, collagenases, stromelysin, as well as prostaglandins and plasminogen activator inhibitor-1 ( Fig. 3) [16].

Rice. 3. The role of IL-1 in the pathogenesis of osteoarthritis (iNOS - inducible synthetase; NO - nitric oxide; MMP - matrix metalloproteinase).

These factors play an important role in modeling inflammation and pain. The onset of release of biologically active substances supports inflammation in the joint tissues in OA, resulting in subsequent damage to the synovial membrane of the joint with the development of reactive synovitis and increased production of proinflammatory cytokines.

Released proteoglycans, breakdown products of chondrocytes and collagen, being antigens, can induce the formation of autoantibodies with the formation of a local inflammatory process [20]. The resulting antigen-antibody complex acts on macrophages in the synovial membrane. This promotes the release of a large number of inflammatory mediators: oxygen radicals, prostaglandins, leukotrienes and interleukins. Inflammatory mediators, having a damaging effect, destroy chondrocytes. As a result, reactive synovitis occurs. The inflamed synovium, in turn, releases biological inflammatory mediators, which maintains synovitis and promotes cartilage destruction. This creates a vicious circle of inflammatory response [4].

As a result of the described processes, the formation of synovial fluid and endogenous hyaluronic acid is affected. The situation is aggravated by inflammatory mediators, which contribute to increased vascular permeability and increased plasma transfusion into the synovial fluid, which leads to a decrease in the concentration of hyaluronic acid and a decrease in the viscoelastic and lubricant properties of the synovial fluid and, as a consequence, its protective capabilities [1]. A decrease in the viscoelastic properties of synovial fluid increases the sensitivity of cartilage to damage and other influences. It is obvious that the viscoelastic properties of synovial fluid, which depend on hyaluronic acid, play an important role in the functioning of the joint, both normally and in pathology [43].

Analyzing the data of many authors, V.N. Pavlova (1980), T.N. Brylenkova et al. (2000), S.F. Ermakov (2002) and others, with osteoarthritis, the concentration of hyaluronic acid in the synovial fluid decreases, and the content of proteoglycans in the extracellular matrix of articular hyaline cartilage increases, which leads to deterioration of the properties and accelerated destruction of the cartilage surface [46].

In OA, hyaluronic acid in the synovial fluid of the knee joint has a molecular weight less than normal. A decrease in the concentration of hyaluronic acid, a violation of the synthesis of this substance and free radical degradation are accompanied by a decrease in the elastoviscose protective effect - this requires studying the possibility of supplementing the synovial fluid with exogenous hyaluronate [51].

Clinical manifestations of osteoarthritis

Since articular cartilage does not contain nerve endings, changes in it may remain asymptomatic for a long time [25]. According to numerous authors (V.I. Mazurov (2005), N.G. Kashevarova, L.I. Alekseev (2006), N.A. Khitrov (2009), Yu.A. Olyunin (2012)), the first and the leading symptom of the disease is pain. It usually increases under the influence of physical activity and decreases after rest.

Currently, ideas about the clinical picture of O.A. have been significantly expanded and clarified. Naturally, pain in the affected joints is the leading sign of the disease, but it is important to pay attention to the symptoms preceding pain: stiffness in the affected joint after rest for no more than 30 minutes, varying degrees of impaired joint mobility when performing individual movements, a feeling of instability in the affected joint and functional restrictions, pain points around the joint, increased volume of the joint, crepitus during movement, stiffness [21].

Assessing the intensity of pain in OA is mandatory, since pain is the leading complaint in most patients. The intensity of pain can be determined using a 4-point verbal rating scale (VRS): 0 points - no pain, 1 point - mild, insignificant pain, 2 points - moderate pain, 3 points - severe pain, 4 points - very severe pain. The assessment of pain according to the SVR is carried out by the patient himself and is subjective. A visual analogue scale (VAS) provides a more accurate idea of pain intensity. The VAS pain assessment is carried out using a 100 mm ruler, which has no divisions on one side and a graduated millimeter scale on the other side. A double-sided slider - a pointer - moves along this ruler. O means absence of pain, o means maximum, unbearable pain.

Also, among subjective questionnaires filled out by patients themselves, the most common are scales for assessing disorders in OA: hip joint - Hip disability and Osteoarthritis Outcome (HOOS), knee joint - Knee Injury and Osteoarthritis Outcome (KOOS), as well as WOMAK - for hip and knee joints, OXFORD - for the hip, knee, shoulder and elbow joints. Most scales, which include an objective assessment of joint function by a physician, are used in the post-traumatic and postoperative periods, but can also be used for OA [9].

The main symptoms and signs of osteoarthritis according to P. Dieppe (1995):

Symptoms:

— “mechanical” nature of the pain (occurs and intensifies with load on the joint in the evening);

- subsides at rest at night;

— morning stiffness (<30 min);

- limitation of range of motion;

- decreased functional ability (difficulty putting on socks, etc.).

Signs:

- painful points along the edge of the joint space (during palpation of periarticular tissues);

- dense thickenings along the edge of the joint space;

- rough crepitations - clicking or jamming;

- moderate signs of inflammation (“cold effusion”);

- limited painful movements;

- feeling of “tension” in the joint;

- instability (signs of severe destruction of bone tissue of the joint).

The appearance of cartilaginous detritus and inflammatory mediators in the joint cavity induces inflammatory changes in the synovial membrane, which are accompanied by pain and swelling of the joint. A decrease in the elasticity of articular cartilage is accompanied by a change in the load on the subchondral bone, which causes the occurrence of osteosclerosis and the formation of osteophytes.

Over a long period, the condition of patients can remain relatively stable. However, over time, OA progresses, leading to the development of deformity (varus or valgus) of the joints and serious functional impairment.

In many patients, OA is accompanied by stiffness in the joints, which occurs after resting in the morning or evening. Unlike the long-lasting stiffness characteristic of rheumatoid arthritis, stiffness in patients with OA disappears within a few minutes of starting to move.

Another typical manifestation of OA is joint dysfunction. The patient begins to experience difficulty walking and performing daily activities. Crepitation is one of the differential diagnostic signs of OA.

OA primarily affects the joints of the hands, knees, and hips. Development of O.A. KS is accompanied by degradation of articular cartilage, remodeling of the subchondral bone, and decreased strength of the periarticular muscles. Some patients experience synovitis, ligamentous incompetence, and signs of bone marrow damage. Changes by K.S. heterogeneous and focal in nature. The formation of limited areas of cartilage destruction leads to load redistribution and overload of individual areas of the joint, which contributes to the progressive loss of cartilage [25].

Normally, pain endings are present in all joint structures, with the exception of cartilage. With O.A. partial vascularization and innervation of the cartilage occurs. Due to its thinning and damage, shock-absorbing properties decrease, the load on the subchondral bone increases with the development of edema and pain. In addition, cartilage fibrillation also induces pain and inflammation [38].

Instrumental methods for diagnosing osteoarthritis

Of the instrumental non-invasive methods for diagnosing OA, the most commonly used are radiography of joints, MRI, ultrasound, and CT.

1. X-ray of joints

Radiological signs of OA are found in 50% of people aged 55 years and in 80% of people over 75 years of age [24]. Radiological stages of OA are described and proposed by Kellgren and Lawrence (1957), approved by WHO (1961), improved by Lequesne (1982).

Stages of osteoarthritis according to Kellgren and Lawrence:

Rice. 4. Stages of osteoarthritis of the knee joint.

0—no radiological signs;

I - cyst-like restructuring of the bone structure, linear osteosclerosis in the subchondral parts, the appearance of small marginal osteophytes;

II - stage I symptoms + more pronounced osteosclerosis - narrowing of the joint space;

III - pronounced subchondral osteosclerosis, large marginal osteophytes, significant narrowing of the joint space;

IV - coarse massive osteophytes, the joint space is difficult to trace, the epiphyses of the bones forming the joint are deformed and sharply compacted.

Among the instrumental methods for diagnosing joints, the most common is radiography. A comprehensive examination of the patient requires the mandatory use of this method. Typical radiological signs of OA are narrowing of the joint space, the presence of secondary bone changes with subchondral sclerosis, osteophytes and the formation of subchondral cysts [5].

Radiography is used as the primary method for identifying and monitoring OA of all joints. An imbalance between the formation of building material for cartilage restoration and its destruction leads to thinning of the cartilage and the appearance of ulcers on it (usually only in the loaded part of the joint) [34].

The X-ray method is highly sensitive in detecting subchondral sclerosis, but its capabilities are limited when the process is localized in the patellofemoral region of the knee joint. The formation of subchondral cysts, most often in the medial part of the joint, is sometimes accompanied by thinning of the cartilage. They may be missed due to local osteopenia or sparse trabeculae [3].

The total thickness of the articular cartilage on radiographs is determined by the width of the X-ray joint space between the articular surfaces of the epiphyses of the bones. This indicator is still used as the main one in the radiographic diagnosis of OA, and standard radiography of the knee joints in frontal and lateral projections is recommended by WHO and ILAR as the method of choice for assessing the dynamics of changes in articular cartilage during clinical trials of drugs.

Radiography remains the simplest and most widely available method for examining joints to assess anatomical changes in bone structure in OA. From the point of view of diagnostic efficiency, simplicity and ease of use, especially interesting are mobile X-ray diagnostic devices with a multi-position stand of the “C-arm” type, which are widely used in world practice. Devices of this class make it possible to conduct studies in any projection without changing the patient’s position. The characteristic radiographic manifestations of OA are usually easily identified on standard radiographs, with a narrowing of the radiographic joint space corresponding to a volumetric reduction in articular cartilage. Subchondral osteosclerosis and osteophytes at the edges of the articular surfaces are a response of bone tissue to an increase in mechanical load in the joint, which indicates degenerative changes and a decrease in the volume of articular cartilage. These radiological symptoms are considered as specific for OA, are used to diagnose OA and are included in the radiological criteria (in combination with clinical ones) for diagnosing OA [26].

2. Magnetic resonance imaging of joints

Magnetic resonance imaging (MRI) is used in various fields of medicine and in almost all cases provides valuable information. The advantages of the method include high soft tissue contrast, free choice of image plane, three-dimensionality of the information obtained, the absence of radiation exposure and artifacts from bone structures and air.

Due to its ability to directly visualize articular cartilage, accuracy and reproducibility, increasing as technology improves and new protocols are created, MRI has become a standard method over the past 20 years for the assessment of cartilage and osteochondral damage, as well as the process of restoration of the articular surface after injury and reconstructive plastic surgery. .

Although various methods for obtaining images of articular cartilage (sonography, contrast arthrography) are currently known, MRI is considered the method of choice. In addition, MRI allows one to obtain information about the condition of the subchondral cancellous bone (Fig. 5) [12, 17].

Rice. 5. MRI picture of osteoarthritis of the knee joint.

Due to the cutting in any plane, good visualization of vascular structures and high contrast of soft tissues, MRI is used in diagnostically difficult cases, for example, when it is necessary to assess the involvement of vascular structures, when differentiating benign and malignant formations [18], as well as to evaluate pathological changes in articular cartilage , meniscus and ligaments of the knee joint [5].

Disadvantages of MRI include sensitivity to motion artifacts; lower spatial resolution than with KT; duration of the study; poor visualization of bone structures, stones and calcifications.

Modern approaches to the treatment of OA

For almost 250 years, doctors and scientists have been searching for surgical ways to restore articular surfaces of joints after cartilage damage. Back in 1743 W. Hunter o [49].

Numerous experimental and clinical studies have shown the possibility of treating cartilage with stopping its further destruction and even restoration, although the pathogenesis of changes in isolated damage to articular cartilage has not yet been sufficiently studied. Clinical experience has shown that if the lesion is left untreated, the lesions are difficult to heal and involve the rest of the articular surface in the degenerative process. Therefore, treatment of an isolated defect may delay or even prevent the development of generalized OA [40].

Modern treatment of OA should be aimed at the main links in the pathogenesis of the disease, not only to help reduce the severity of pain, but also to restrain the progression of structural changes in the affected joint. Modern approaches to the treatment of OA are reducing pathological symptoms and improving the quality of life of patients using various treatment methods [2].

Treatment of OA is carried out using conservative, surgical and combined methods.

Towards conservative treatment

include: drug therapy (non-steroidal anti-inflammatory drugs, dietary supplements, hyaluronic acid preparations, chondroprotectors, antioxidants); administration of platelet rich plasma (PRP).

Surgical methods

include: arthroscopic debridement, ultrasonic cold ablation, microfracture of cartilage defects, autologous osteochondroplasty and three-dimensional autologous chondrocyte culture transplantation, arthroscopic laser reconstruction.

A complex approach

combines conservative and surgical methods with an evidence-based level of effectiveness, which can significantly curb the progression of the pathological process [27].

In the last 30 years, there has been some progress in research devoted to the development of methods for surgical restoration of articular cartilage in case of its damage and diseases. The main task is to provide optimal conditions for the regeneration or repair of cartilage tissue. Repair involves restoring the damaged articular surface by replacing the cartilage defect with new tissue, which is fibrocartilage, which is not capable of completely restoring the structure and function of normal hyaline articular cartilage. During regeneration, a new articular surface is formed, identical to the original hyaline cartilage [45].

“Mosaic chondroplasty”, or osteochondral autoplasty, is one of the most popular methods of plastic surgery of local cartilaginous or osteochondral defects of the femoral condyles. The technique is based on plastic surgery of the defect with cylindrical osteochondral grafts with hyaline cartilage at the end, taken from non-contact areas of the femoral condyles. Osteochondral autotransplantation as a method of surgical treatment of local cartilage defects of the knee joint was first described in 1908 by N. Judet.

In 1963, C. Campbell showed the survival of osteochondral grafts without changes in the structure of the cartilage for periods of more than 1 year. A. McDermott et al. in 1985 reported positive long-term outcomes of osteochondral transplantations in 100 patients. In 1992, the Hungarian orthopedist L. Hangodi described the technique of autoplasty of osteochondral defects of the femoral condyles with cylindrical osteochondral grafts with a diameter of 4.5 mm and a length of 15-20 mm, taken from non-contact areas of the femoral condyles. This technique gained wide popularity under the name “mosaic chondroplasty” and for a long time took a leading position in world orthopedic practice [10, 47].

From the above it follows that surgical treatment is an integral part of modern complex therapy for damage to articular cartilage. The operations can be independent, but more often they accompany surgical interventions on other damaged elements of the knee joint, which have caused secondary trauma to the cartilage tissue. At the same time, surgical operations directly on damaged cartilage tissue require systematization and clarification of the indications for their selection, study of the effectiveness and sustainability of results in the long term [41, 42, 44].

According to European authors M. Marcacci, E. Kon (2006); B. Clair, A. Johnson (2009), Tom Minas (2010), nowadays one of the most pressing and insufficiently studied problems in modern arthrology is the treatment of local defects and diseases of the articular cartilage of the knee joint [50]. The introduction of minimally invasive endoscopic methods of surgical treatment of this pathology is currently the defining direction of world medicine. Therefore, arthroscopy of the knee joint (as well as any other) is currently the main method of surgical treatment for the early stages of OA [14].

Based on the analysis of literature data on the structural features and function of hyaline cartilage, the etiopathogenesis of its destructive-dystrophic destruction and the treatment of damage to the articular surface of the knee joint, we highlight the following main points. Hyaline cartilage ensures the functional usefulness of the knee joint as an organ of support and movement. In deforming osteoarthritis of the knee joint, damage to the hyaline articular cartilage is considered a polyetiological pathology with a very complex, differently interpreted pathogenesis. The most severe form of its damage is full-thickness defects of a destructive-dystrophic nature. Treatment of patients with damage to articular cartilage is an urgent problem in modern orthopedics and transplantology, requiring further study of the etiopathogenesis of the disease within the framework of experimental and clinical medicine [48]. The best treatment for OA is provided by complex treatment - a combination of surgical and conservative approaches.

Promising areas in modern medicine are tissue engineering and cell therapy. These areas have been introduced into many areas of medicine; Traumatology and orthopedics are no exception. A special place in cell therapy is occupied by autoplasma enriched with platelets, which, according to world literature, has shown fairly good regeneration of various types of tissue, including in the treatment of knee OA.

On the pages of the journal “Endoscopic Surgery” we will present several works devoted to the treatment of deforming osteoarthritis.
We invite our colleagues to join in the discussion and discussion of methods of treating this serious and complex disease of the 20th
-
21st centuries.

Treatment options

Until recently, endoprosthetics was considered the optimal way to treat the disease. Today, modern medicine is ready to offer effective courses of conservative treatment that allow:

cope with pain;
restore mobility to the joint;
reduce the risk of disease progression and complications.

As part of conservative treatment, the patient is shown:

measures to reduce body weight;
daily exercise;
taking general and local drugs;
special diet for osteoarthritis of the knee joint.

The list of medications for regular use includes:

analgesics and non-steroidal anti-inflammatory drugs;
corticosteroid injections;
ultrasound-guided drug injections;
injections of hyaluronic acid, which softens bone movements and reduces their mutual friction;
anti-inflammatory ointments to relieve discomfort and temporarily restore mobility of a swollen joint;
knee stabilizers and braces;
Physiotherapy methods – massage, manual therapy, iontophoresis, ultrasound.

Surgical treatment of grade 1-3 osteoarthritis

If conservative methods are ineffective, the patient is referred for surgical treatment. Several types of operations are practiced, which are selected taking into account the complexity of the pathology and the possibilities of its mechanical correction:

arthroscopy is a minimally invasive intervention that allows you to restore the damaged joint structure, relieve discomfort and even avoid endoprosthetics for a long period of time;
osteotomy – partial excision of bone tissue with significant damage, after which the patient undergoes a long rehabilitation period;
endoprosthetics - installation of part or the entire joint in the knee in place of damaged tissue. A relatively complex operation, the results of which largely depend on the skill of the surgeon.

With early diagnosis and timely treatment, the problem can be dealt with without serious consequences for the joint and its mobility.

Course of the disease

Osteoarthritis begins with changes in the synovial fluid, which fills the joint and allows it to perform its functions. Normally, this fluid is thick and plays the role of a lubricant that nourishes cartilage tissue. When this fluid loses its properties, the cartilage surrounding the bone softens. It becomes thinner, more vulnerable and less elastic. The liquid penetrates into the cracks of the cartilage and begins to affect the bone tissue itself. As a result of these structural lesions, the joint loses its mobility.

The first signs of this degenerative process in the knee are a decrease in the functionality of the joint. When exercising, a person experiences discomfort that turns into pain if the movement is not stopped. Discomfort occurs with any tension - it is difficult to bend the leg, straighten it, or step on it. At first, discomfort appears during physical activity, but later it becomes difficult to even walk. If no measures are taken, the disease will progress and redness will appear around the knee joint and the knee will swell slightly. And after rest, the joint recovers quickly.

Grade 1 knee osteoarthritis is not usually considered a cause for concern. This is due to the fact that the discomfort quickly passes. It is difficult to even diagnose the lesion, because with rest the symptoms disappear, and the knee looks and feels completely healthy.

But it is important to understand that there should not be discomfort in the knees. It is wrong to attribute joint stiffness to age, because first-degree osteoarthritis is, in principle, considered an age-related disease. The older a person is, the more attention should be paid to the condition of the skeletal system, and in case of any difficulties, still consult a doctor. At this stage the disease is easier to stop than at later stages (2nd, 3rd degree).

A rheumatologist treats bone and joint diseases. He will conduct an examination, interview and, based on the characteristic symptoms, will suspect osteoarthritis in the initial stage. After confirming the diagnosis, simple and affordable medications are prescribed in small quantities, and the main emphasis in treatment is on proper physical activity (physical therapy), massage, diet and physical therapy.

Noltrex injections:

effective at any stage of knee arthrosis;
give a long-lasting effect - from nine months to two years;
do not cause allergies due to their synthetic origin;
absolutely safe due to biocompatibility with body tissues;
do not give adverse reactions;
indicated, including for diabetes mellitus - under the supervision of an endocrinologist.

Even the last stage of gonarthrosis is not a death sentence. Medicine does not stand still, so it’s too early to despair! Consult a specialist you trust and choose the most suitable treatment for you. And most importantly, maintain a positive attitude and faith in recovery!

Treatment of arthrosis of the knee joint

Treatment of arthrosis of the knee joint is complex, including drug therapy, physiotherapy, surgical interventions, therapeutic exercises, and diet therapy. The range of therapeutic measures depends on the degree of cartilage destruction and clinical manifestations.

Conservative treatment gives a positive result in the first, partly in the second stage of the disease, while most of the cartilage is not yet destroyed.

Drug treatment

Non-steroidal anti-inflammatory drugs (diclofenac, ketoprofen, indomethacin, meloxicam, etc.) are used to relieve pain and inflammation. It is not recommended to take them for a long time, as they negatively affect the synthesis of proteoglycans, which causes dehydration and accelerated cartilage destruction. In addition, they have unwanted side effects from the gastrointestinal tract.

Chondroprotectors (glucosamine and chondroitin sulfate) nourish cartilage tissue, promote regeneration, improve the production of intra-articular fluid, and normalize lubricating properties. Chondroprotectors are ineffective in the third stage of gonarthrosis, when the cartilage is practically destroyed. To obtain a real treatment result, 2-4 courses of treatment are needed (lasting up to one and a half years).

Glucocorticosteroids (diprospan, hydrocortisone, celeston) quickly and effectively relieve pain and inflammation during synovitis, but arthrosis itself is not treated. The first injection of GCS relieves symptoms more effectively than all subsequent ones. They have many side effects and, with frequent use, negatively affect cartilage tissue. Moreover, glucocorticoids are dangerous for diabetes mellitus, arterial hypertension, renal failure, and peptic ulcer disease.

Hyaluronic acid preparations are a modern and safe way to treat arthrosis. Act in the joint as a natural synovial fluid. Sodium hyaluronate covers damaged cartilage with a protective film, preventing further destruction and improves gliding. Penetrates deep into the cartilaginous lining, improving firmness and elasticity, restoring shock-absorbing properties. They start the process of producing their own hyaluronic acid. As a result, the biomechanics of the joint is normalized, pain is relieved, and mobility is restored.

Important!
HA drugs are destroyed in the inflamed joint. Therefore, you first need to stop the symptoms of synovitis with the help of GCS and NSAIDs.

HA preparations:

HYAL-SIN - 1% high molecular weight hyaluronic acid. The course of treatment includes three injections with an interval of 7-10 days.

HYAL-SIN PROLONG - 2% high molecular weight hyaluronic acid. The high concentration of hyaluronic acid makes it possible to reduce the course of treatment to two injections, while simultaneously enhancing the intra-articular effect of the drug and prolonging the effect.

GYAL-SYN PROLONG PLUS -2% long-acting high molecular weight HA (12-24 months) for single use. Intermolecular cross-linking of the HA chains of this drug is carried out for a longer effect and resistance to destruction. One injection per course of treatment. Applicable only to the knee joint.

The most effective is an integrated approach: when all methods of conservative therapy are used.

Surgery

For advanced forms of KLA, the method of choice is knee replacement. This is the replacement of the knee joint with a functional endoprosthesis. Implants made of high-tech alloys (titanium, cobol-chromium, etc.) are strong, rigid, elastic, and biocompatible with human tissue.

Endoscopic arthroscopy with minimally invasive manipulations is performed if the course of the disease is complicated by ruptures of the ligaments, meniscus, or the entry of a bone fragment into the joint capsule.

Physiotherapy

Complex treatment of stages 1-2 of OAC includes shock wave therapy, ultrasound, manual techniques, iontophoresis, mechanical traction of the joint, laser therapy, thermal treatment, cryotherapy (local cooling). A good effect is obtained by combining manual therapy with traction.

Diet therapy

Age-related osteoarthritis is associated with the loss of calcium salts, which provokes microcracks in bones and fragility of osteophytes. Patients with OAC are advised to follow a non-strict diet, which includes:

consumption of lean meat, fish, seafood;
introduction of high-protein ingredients (nuts, legumes, wheat germ) into the diet;
dishes that include plant and animal collagen (jelly, aspic, jellied meat);
dairy products;
ban on fatty, salty, spicy foods.

People who are overweight are prescribed a more strict diet to lose weight.

Physiotherapy

Therapeutic gymnastics strengthens muscles and activates blood circulation in the joint. Use exercises without maximum flexion and extension. Instead of the usual dynamic exercises, static ones are used. For example, lying on your back, raise your outstretched leg and keep it suspended for some time.

Important!
To strengthen muscles and ligaments, do static or slow dynamic exercises. If the exercise causes sharp pain, then it is contraindicated or performed incorrectly.