Articular pathologies are extremely common among the population of various age groups. They are diagnosed in both the elderly and young people after 30-40 years. The type of damage to the articular structures can be different, and the degree of intensity of the pathological process is also not the same. But almost always, regardless of nosology (type of disease), in the clinical picture there is stiffness of the joints in the morning.

It can last no more than an hour, followed by a complete restoration of the joints. In other cases, joint stiffness can persist throughout the day. In addition, it rarely manifests itself in isolation, in most cases it is observed in combination with other pathological signs. Depending on what kind of disease a person has, stiffness can be observed either in one joint, or in several at once, for example, in the fingers.

The mechanism of development of stiffness

The main task of any joint is to ensure the full range of motion provided by physiology. To accomplish it, all the articular components work simultaneously and harmoniously. Bone structures slide relative to each other due to the smoothness and elasticity of hyaline cartilage, the synovial membrane produces a lubricating fluid and delivers oxygen and necessary nutrition to the cartilage tissue.

If any failure occurs in this mechanism of normal movements, then first of all their amplitude suffers, which becomes much smaller. Subjectively, this phenomenon is felt by a person precisely as stiffness and stiffness, or the inability to fully bend or straighten a limb, fingers, less often the spine.

Joint stiffness in the morning is not an independent diagnosis, it is always a symptom of some pathology. If the synovial membrane is affected, then it thickens and decreases in elasticity, and the amount of lubricating fluid decreases. This necessarily affects the ability to perform a full range of motion in the joint. When the layer of cartilaginous tissue is destroyed, the bone structures do not begin to slide, but constantly touch each other, which also reduces the amplitude. In each case, the restriction of movement is combined with other symptoms; most often it is the development of pain syndrome and signs of an inflammatory process.

Therefore, all mechanisms for the formation of morning stiffness can be divided into three groups:

• Degenerative-dystrophic processes in the cartilaginous tissue, which gradually lead to the destruction of hyaline cartilage, the formation of osteophytes (bone growths) and fibrous degeneration of the synovial membrane.
• Inflammatory processes in the joint, which can be of various origins (aseptic, infectious, allergic, autoimmune) and affect all joint structures.
• Tumor processes that are less common and disrupt the functionality of the joints mechanically (the neoplasm compresses the tissues and prevents them from performing their functions).

The more severe the disease, the more pronounced all its manifestations, including joint stiffness. But there are also pathologies in which morning stiffness in the joints does not always last long, regardless of the severity. This characteristic of the symptom, as well as its combination with other signs, is very helpful in the differential diagnosis of almost all joint pathologies.

Causes of morning stiffness

As already noted, stiffness of various localization is only a separate characteristic of a disease. Therefore, the causes of morning stiffness are a wide variety of pathologies. And not always the painful process affects the joint. There are diseases in which the osseous articulations, hyaline cartilage, synovial membrane and capsule remain intact, but the surrounding ligaments and muscles suffer, often as a result of nervous dysregulation. Such pathologies include, for example, Parkinson's disease or the consequences of acute cerebrovascular accident (ischemic or hemorrhagic stroke), when the innervation of the muscle groups surrounding the joint changes according to a certain type. As a result, the formation of articular stiffness is also noted.

In cases of a high degree of obesity, one should speak of false stiffness. The decrease in the amplitude of movements in these situations is associated, rather, with general motor insufficiency and muscle weakness than with pathological changes in the joints.

Short-term or longer-term stiffness can have various origins. It can form as a result of trauma, physical overload or surgical interventions.

But most often these are various diseases, and the most extensive group among them has an inflammatory nature. These are arthritis.

• rheumatoid;
• infectious (nonspecific and specific);
• gouty;
• Bechterew's disease, or ankylosing spondylitis;
• systemic;
• psoriatic;
• allergic.

In every disease in this group there is always a stiffness in the joints, large or small, which develops only in the morning or persists much longer. Since the pathological process is inflammatory in nature, there are other characteristic signs.

This may be swelling and hyperemia (redness) of the skin, pain of varying intensity, joint deformity, pronounced movement disorders, changes in skin sensitivity as a result of concomitant lesions of the central or peripheral nervous system. With each nosology, there is a certain combination of these signs, changes in the biological environment of the body (blood and urine), as well as morphological disorders (changes in the anatomy and structure of tissues), which are diagnosed using additional instrumental methods.

Another group of pathologies is more often associated with an inflammatory process or traumatic injury only at the beginning of its development. These are arthrosis, or osteoarthrosis, which can be of very different localization: in the joints of the arms, legs, spinal column. With each of them, inflammation “starts” a destructive degenerative process in the joint, which, starting with slight stiffness, gradually progresses and ends with almost complete joint immobility.

Of course, it does not make sense to treat morning stiffness separately from other pathological manifestations. After carrying out a full range of diagnostic measures for each patient, an individual therapy regimen is developed, which is designed to fight a specific disease. Therefore, it will be more convenient to consider each pathology separately, indicating the most characteristic symptoms and methods of treatment.

Rheumatoid arthritis

This is a very common joint disease that occurs in almost 2% of the population and is often one of the causes of disability in young and middle age. Many joints suffer at once, mostly small ones, according to the destructive-erosive type. In fact, rheumatoid arthritis is a polyarthritis in which the connective tissue that makes up the main part of the synovial membrane is affected.

By its nature, rheumatoid arthritis is considered an autoimmune pathology, that is, a peculiar and perverted reaction of the body to its own tissues, in particular, to connective. As a result, the resulting immune complexes cause an inflammatory process in the synovial membrane of the joints, its own tissue is destroyed, and fibrous structures are formed in its place.

These pathological processes are reflected in the condition and functionality of the synovial bag. It loses its elasticity, smoothness and elasticity, becoming rigid and uneven, which begins to interfere with the execution of movements in the joint with the required amplitude. Additionally, the production of lubricating fluid is also reduced, and its deficiency significantly affects the nutrition of cartilage tissue, leading to the onset of destruction of hyaline cartilage.

That is why one of the most characteristic manifestations of rheumatoid arthritis is morning stiffness in the joints. At first, it is noted in the small joints of the hands and fingers, but then, as the autoimmune process progresses and spreads, it moves to the medium and large joints of the whole body. Stiffness is felt by the patient as a feeling of tightness or constriction that does not allow movement.

After a few hours, as a rule, this symptom disappears and movements in the joints are partially or completely restored, but other manifestations of rheumatoid arthritis remain:

• swelling of the joint zone;
• redness of the skin;
• symmetry of the lesion;
• pain syndrome, most severe in the afternoon and at night;
• the pain intensifies when pressed and when trying to make a movement in the joint;
• the formation of dense nodules under the skin in natural folds, which is explained by a systemic lesion of the connective tissue;
• symptoms of chronic intoxication (weakness and malaise, headache, loss of appetite, weight loss);
• the gradual formation of joint deformity, which is manifested by a characteristic curvature, for example, of the fingers and is accompanied by a violation of blood circulation in them.

To get rid of stiffness in the joints, which, as can be seen from the indicated complex of clinical symptoms, is not the most painful and pronounced manifestation of rheumatoid arthritis, it is necessary to carry out treatment aimed at the nature of the pathology. It becomes lifelong, since arthritis of autoimmune origin cannot be completely cured, the disease will proceed with alternating exacerbations and remissions.

However, the intensity and frequency of exacerbations can be reduced and reduced by using the most potent drug combination available today. These are non-steroidal anti-inflammatory drugs (Diclofenac, Indomethacin, Ibuprofen and their derivatives), hormonal drugs (Prednisolone, Dexamethasone), as well as the so-called basic drugs (Azathioprine, Methotrexate, Cyclophosphamide) and biological agents (Actemra, Halofuginone, Humira, Orencia).

infectious arthritis

The clinical picture of infectious, or septic, arthritis is always pronounced, and the manifestation (the onset of pathology) occurs suddenly and acutely, that is, the symptoms develop quickly and with maximum intensity of manifestations. As a rule, the whole organism reacts to the inflammatory process in a separate joint, responding with the formation of an intoxication syndrome.

Therefore, in most cases, septic arthritis has the following symptoms:

• a feeling of stiffness is quickly replaced by a pronounced pain syndrome, which is aggravated by palpation (palpation) or an attempt to move;
• no symmetry of the lesion;
• the inflamed joint swells and swells, the skin over it turns red and becomes sharply painful and hot;
• the patient tries to keep the sore leg or arm in a forced position, which somewhat reduces the severity of pain;
• acute intoxication syndrome is expressed: fever up to 39-40 degrees, severe headache, severe weakness.

Bechterew's disease

Ankylosing spondylitis, or ankylosing spondylitis, is quite rare (about 400 thousand patients in Russia) and affects mainly small joints that connect the processes of the vertebrae, as well as the vertebral bodies themselves. However, there are other forms of the pathological process, which is localized in larger joints, such as the knee.

In Bechterew's disease, the synovial membrane primarily suffers, in which chronic inflammation develops. The formation of fibrous nodes in it and later joining bone growths significantly worsen the condition of the joints of the spine or limbs.

This disease can manifest itself in various forms, masquerading as other articular pathologies. Its symptoms may differ in men and women and depend on the age category. In general, in women, the disease develops somewhat more slowly and does not begin at such a young age as in men.

The main symptoms of Bechterew's disease are:

• pain and feeling of stiffness (not only in the morning) in the spine, upper or lower extremities;
• pain is characterized by significant irradiation;
• limitation of the range of motion in the affected joints;
• in the blood test, the ESR rises sharply, up to 60 mm / h.

It is impossible to completely cure this disease, like rheumatoid arthritis, but modern methods of treatment can significantly slow down the rate of its progression. For this, non-steroidal anti-inflammatory drugs, hormonal and basic agents, glucocorticoids, immunosuppressants, and cytostatics are used. Additionally, massage, physiotherapy, therapeutic exercises are needed.

Other types of arthritis

Arthritis of gouty nature develops if the metabolism of uric acid is disturbed in the human body. At the same time, its crystals can linger both in the renal tissue and inside the joints, forming salt deposits on the synovial membrane. In response to this, the inflammatory process begins to progress, negatively affecting all articular structures. A feeling of stiffness and pain, swelling and hyperemia, difficulty in movement and intoxication of the body are the main signs of this type of arthritis. Therapy consists in the use of a complex of medications, local procedures and a strict diet.

Systemic arthritis, like rheumatoid arthritis, has an autoimmune nature, with a pronounced element of heredity. If it begins in childhood, it is referred to as "Still's disease", or systemic juvenile arthritis. In addition to pain and stiffness in the joints, characteristic changes in the skin in the form of a rash are observed around them. Treatment is long and complex, including medications (NSAIDs, immunomodulators, hormones), physiotherapy and special physical education.

Arthritis of psoriatic origin is often called a variety of rheumatoid arthritis. The clinical pictures of these diseases are very similar, with a predominantly symmetrical lesion of small joints and their characteristic deformation. Psoriasis, gradually developing, "transfers" from the skin to the bone-articular frame and leads to the formation of arthropathy. Its treatment consists in the use of a complex of medicines, diet, folk methods of local therapy.

Arthritis of an allergic nature can develop in a person with an allergic predisposition. Most often this is possible if there is an allergy to certain foods, less often to pollen or household allergens. In the mechanism of development of this arthritis, the immune mechanism is pronounced, therefore, all signs of the disease (pain, stiffness, swelling, hyperemia) can be stopped using means of influencing the immune system. In the first place among them are antihistamines, hormones, immunosuppressors, cell membrane stabilizers.

Almost all diseases of the joints are accompanied by the presence of stiffness, often it becomes the very first manifestation of the pathology and signals trouble in the body. Therefore, with the development of this symptom, it is necessary to consult a doctor, diagnose and urgently begin treatment of the identified disease.

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Treatment of joints with gelatin is an effective adjuvant

Edible gelatin, which is used to make jellies and meat jellies, is a valuable source of collagen for the human body. It is produced on the basis of heat-treated connective tissue taken from animals. Treatment of joints with gelatin helps to strengthen them, get rid of the crunch and pain.

• The benefits of gelatin for joints
• Treatment with gelatin
• Gelatin tinctures
• Side effects and contraindications

The benefits of gelatin for joints

Edible gelatin (translated from Latin means frozen or frozen) is a crystalline powder that swells and turns into a viscous transparent mass upon contact with water. Gelatin is a denatured collagen found in cartilage, veins, skin and bones of animals.

Gelatin is good for hair growth because it contains protein. It also has a beneficial effect on human skin, which regularly needs a fresh portion of collagen. For this reason, various pharmacological preparations are produced in gelatin capsules (for example, vitamin E).

American physiologists have found that food gelatin is useful for the prevention and treatment of cartilage destruction in human joints. So, people suffering from the disease "osteoarthritis of the knee joints", after two weeks of regular consumption of gelatin, noticed muscle strengthening and restoration of joint mobility.

Gelatin powder helps with arthritis, pain in the spine and joints. The amino acids contained in gelatin maintain the elasticity of cartilage in the joints and slow down, and sometimes prevent, their deformation.

Official medicine also recognizes the effectiveness of treating joints with gelatin, but recommends it as an adjuvant, not excluding drug treatment prescribed by specialists.

Treatment with gelatin

Crunch and pain in the joints is often inherent not only in the elderly, but also in the younger generation. A simple compress with gelatin will help get rid of obsessive pain. Do it at night for seven days to achieve maximum effect.

To warm up a wide gauze bandage, it is dipped in hot water. After twisting to squeeze out excess moisture. Then the napkin is folded several times, and gelatin powder (about one teaspoon) is poured between the middle rows. A napkin is applied to the affected joint, covered with plastic wrap and wrapped in a terry towel or woolen scarf. To fix the bandage on top, it is fixed with a bandage.

Gelatin tinctures

On the water. The duration of the course is one month, during which it is necessary to prepare the tincture in the evening. To complete the full course, you need 150 grams of powder.

The cooking process is as simple as possible: you need 2 incomplete small spoons (or 5 grams) of gelatin powder, pour half a glass of water. During the night it will swell, and in the morning it must be diluted with warm water 1: 1. And the tincture is ready to use. It is taken on an empty stomach half an hour before a meal.

To improve the taste, the tincture can be sweetened. To do this, we dilute the gelatin mass swollen overnight not with water, but, for example, with your favorite fruit juice. You can also improve the taste of the tincture by adding a few drops of lemon juice to it.

On milk - almost ordinary milk jelly, which is not only a tasty and simple homemade delicacy, but also has incredible benefits for the body.

To prepare, take 5 grams of gelatin powder (or 2 small spoons) and stir in 2/3 cup of low-fat warm milk. To the resulting mixture add a couple of tablespoons of honey (you can sugar). The mass swells within an hour. Then it is heated over low heat, stirring constantly, until the particles are completely dissolved. It is not recommended to bring the mixture to a boil, because. after that it may not freeze. After the resulting mixture is cooled first at room temperature, and then in the refrigerator until completely solidified.

Take a gelatin "medicine" about 2-3 times a week. Gelatin tincture on milk helps not only with diseases in the joints, but can also help with nosebleeds, and also helps restore immunity and strengthen the body after suffering colds.

Traditional medicine advises the treatment of various joints with gelatin in courses of 10 days, followed by a break of 10 days. In addition to a beneficial effect on the joints, gelatin tinctures will strengthen the structure of hair and nails. And for those who want to lose weight, they will help in restoring muscle mass.

Side effects and contraindications

During the treatment of joints with gelatin, patients may experience side effects:

• constipation;
• inflammatory process in hemorrhoids;
• disorders in the gastrointestinal tract.

In order to exclude their appearance throughout the course of treatment, you need to additionally take dried fruits. They have a laxative effect and miraculously restore bowel function. Also, for this purpose, it is possible to prepare a home-made dietary supplement (BAA) from prunes, dried figs and dried apricots (200 grams each). Also, 50 grams of hay grass, which is commercially available in pharmacies, can be added to the mixture.

All ingredients are mixed, poured with boiling water (1 liter) and cooled. The resulting mixture is stored in a glass jar in the refrigerator or in a plastic container in the freezer. To normalize the work of the intestines, it is enough to take one teaspoon of this remedy, which is best consumed before bedtime.

However, it is worth remembering that treatment with gelatin should not be carried away by people suffering from increased blood clotting and having a predisposition to thrombophlebitis and thrombosis. Also, such treatment is contraindicated in people with oxalate kidney stones or suffering from urolithiasis or cholelithiasis.

Treatment of joints with gelatin is highly effective if the duration of the course of its use is at least two weeks.

Useful articles:

Obesity and joints

Joint diseases and obesity are directly related. In an obese person, the load on the joints, ligaments and spine increases. Pressure increases with body weight. Excess body weight contributes to the violation of blood and lymph flow, which leads to congestion and poor nutrition of the joints.

Obesity is a direct path to inflammatory diseases of the joints and spine, which are four times more common in obese people. Diseases arising from excess weight: arthrosis, osteochondrosis, spondylosis.

Intervertebral discs and cartilaginous tissue are severely affected. There is a softening and disintegration of the cartilage, cracks appear in it, it begins to completely collapse. Instead of cartilage, bone tissue grows, and the joints and spine begin to quickly lose mobility. The knee, hip, and ankle joints are severely affected. Then begins deforming arthrosis, which is accompanied by pain.

It is necessary to strive to prevent obesity, for which a balanced diet is used.

If you've ever loaded your car's luggage with heavy items or driven with four adult passengers, you may have noticed that the ride wasn't as smooth. Your car's shock absorbers probably didn't absorb the shocks from bumps and potholes, unlike a lighter load. Similarly, if you're carrying too much weight on your body, your knees can also end up in a rough ride. In this article, we will consider why the knees hurt when overweight.

Why do knees hurt when overweight

The bones that meet at your knees are covered in cartilage, providing a smooth sliding surface for the femur, tibia, and patella. They move within the joint as you walk, says Jonathan B. Shook, MD, an orthopedic surgeon who specializes in hip, shoulder and knee pain.

When you weigh more than you should, you put more force on that cartilage. “When you put more force on the cartilage, it will wear down faster,” says Dr. Shook. Various studies have found links between carrying excess body weight and knee pain. And, in many cases, a condition called osteoarthritis is the link between the two. .

Link between weight and knee pain

In a recent British study, researchers looked at the association between changes in body mass index (BMI) and knee pain in 594 women over 14 years. They found that women with a higher BMI were more likely to have knee pain by the end of the study. In another study, researchers in the Netherlands took x-rays of people's knees and then repeated them over six years later. Those with a BMI over 27 were three times more likely to develop osteoarthritis of the knee. For example, a woman with a height of 168 cm and a weight of 75.7 kg has a body mass index of 27.

Excess body fat can also lead to the release of the hormone leptin, which some experts believe may play a role in the development of osteoarthritis. In addition, body fat can release substances that promote inflammation in your body. Two of these, called tumor necrosis factor alpha and interleukin-1, appear to play an important role in the cartilage damage seen in osteoarthritis. ?

Weight management to reduce knee pain

Here's the good news: In a recent study of overweight and obese people with osteoarthritis of the knee, those who lost weight with diet and exercise reduced knee pain by about half. Weight loss is an important part of keeping your knees healthy, Shook says. The National Institutes of Health recommend the following steps for safely exercising knee pain.

Get advice. Talk to your doctor if you have chronic health problems or are concerned that exercise could lead to injury. If you already have knee pain, talk to your doctor about activities that may be safe for you.

Exercise. Good types of exercise for heavier people include walking—even for a few minutes when you start—cycling indoors or outdoors, and strength training to strengthen strong muscles. .

Be active. Just do more physical activity in your daily life. Take a walk while you're on the phone (that's why they're wireless, after all). Play actively with your children or grandchildren and make in-person visits at work instead of using email. Weight loss is something you can do on your own, Shook says. It is not expensive. And it could save you from knee surgery or other health issues down the road. Why knees hurt when overweight, see above.

Weight problems cause many obstacles and difficulties for any woman.

And, unfortunately, this is not only dissatisfaction with the physical forms of one's body, but also a wide range of other more serious deviations.

Very strongly overweight is reflected in the condition and injuries of the spine.

But, much to the surprise, many women do not think that they worsen the quality of their lives by not paying attention to their bodies. We are not talking about physical beauty, but about richness and the ability to perform elementary things.

No one will argue that you can get great pleasure from the surrounding nature and the world, just a little closer to it.

But it is unlikely that you will be able to admire the lovely view from the top of the hill, or just run a race with a child, with strong ones.

Doctors note that extra pounds affect the spine and blood vessels in the same way as injuries or excessive physical exertion.

Therefore, it is safe to say that excess kilograms indirectly take away many wonderful moments of their lives from the weaker and stronger sex.

Direct link between extra pounds and back health

The concept of being overweight in many women has different characteristics and extreme limits.

Just think about half a kg, they can cause displacement of the vertebrae. This is not a serious weight at all, but a very serious problem for the spine.

Of course, weight gain up to 1 kg does not cause such a serious pathology in all women. It depends on many individual factors and inclinations of the organism.

But nevertheless, the greater the weight, the more it puts pressure on the spine. And the greater the likelihood of developing pathologies in, from constant pressure.

Many experts give an example with a heavy backpack. After you wear a briefcase weighing at least 5 kg for 3 hours, you will certainly feel relief when you remove it.

But at the spine and joints, there is no such opportunity to remove the load in order to rest. And they have to not only walk, but also run, jump with extra pounds (and this is even more excessive pressure).

How to determine if you are overweight

There are a lot of methods for calculating excess weight described on the Internet. The simplest and most popular among them is the body mass index ( BMI ).

What problems with the spine can occur

Excessive pressure on the spine caused by extra pounds can not only cause the development of new diseases, but also aggravate the flow of existing ones.

Here are the possible complications:

1. Injuries in the intervertebral discs. It can be or. With strong pressure, it is possible to infringe on the spinal nerves. Their slightest infringement causes sharp and intolerable pain.
2. Violations in the mobility of the spinal column. Naturally, overweight people are less mobile and less abrupt in their movements. Excess weight in the initial stages makes it harder to pass any physical activity. Therefore, most people simply refuse to work on themselves in order to avoid pain.
3. Rachiocampsis. With a lot of weight it is very difficult. This requires a lot of physical effort. Not everyone can handle it. Therefore, the spine gets used to bend in certain places, thereby causing scoliosis.

How joints suffer from overweight

The joints, like the spine, wear out very much and suffer under the influence of excess weight.

An important part of the joints in the form of cartilaginous tissue, if the BMI is exceeded by at least one point, wears out faster by 11%. But the restoration of cartilage takes decades.

It is at this moment that the negative impact of extra pounds on.

We list the possible manifestations of pathological changes in the joints with excess weight.

• . The minimum amount of physical activity and any movement leads to the fact that the cartilage loses its elasticity and can change shape and consistency.
• Arthritis and. The destruction of the joints is caused by unbearable weight pressure. Those. joints are simply injured under strong pressure on them. Excess weight is tantamount to received blows and bruises.

Fighting extra pounds is difficult, but possible. And most importantly, it is easier to deal with kilograms than to treat diseases of the spine and.

Think about the fact that almost all pathologies of the joints and spine easily pass into the chronic stage. This means that they will remind themselves of themselves again and again throughout their lives.

It is much easier and more interesting to develop and improve your body in order to avoid the pathologies listed above.

If you are overweight, to relieve pressure on your back, orthopedists advise you to pay attention to:

• Compliance with a balanced diet
• Instructor-led gradual introduction
• Purchasing a medium-hard mattress for sleeping (this allows the spine to rest a little and not sag under the weight of the weight)

Do not forget that any back pain should be consulted with professionals for accurate and effective treatment.

Published in the magazine:
"PREVENTIVE MEDICINE"; No. 1; 2011; pp. 29-37.

Acad. RAMS V.A. NASONOV 2 , Ph.D. O.I. MENDEL, MD head of laboratory L.N. DENISOV 2 , MD, prof. A.L. VERTKIN 1 , MD, head of laboratory L.I. ALEKSEEVA 2 , MD, Assoc. A.V. NAUMOV 1

1 Moscow State University of Medicine and Dentistry, 2 Research Institute of Rheumatology, Russian Academy of Medical Sciences, Moscow

Keywords: obesity, osteoarthritis, risk factors, leptin, metabolic disorders, weight loss.

Osteoarthrosis and obesity: clinical and pathogenetic associations

V.A. NASSONOVA, O.I. MENDEL, L.N. DENISOV, A.L. VERTKIN, L.I. ALEKSEYEVA, A.V. NAUMOV

key words: obesity, osteoarthrosis, risk factors, leptin, metabolic disturbances, weight reduction.

Obesity and osteoarthritis (OA) are one of the most urgent medical and social problems of modern society. This is due to both their extremely high prevalence and high comorbidity with other conditions and diseases that have a significant impact on the quality of life and life prognosis of patients. According to modern data, obesity is a risk factor for OA and many other diseases associated with metabolic disorders, and dysfunction and disability, usually accompanying OA, in turn lead to an increase in body mass index (BMI) and induce the development of cardiovascular diseases and diabetes.

According to the WHO definition, overweight and obesity is defined as abnormal or excessive accumulation of fat that can lead to health problems. According to the WHO definition, "overweight" corresponds to BMI ≥25, and "obesity" - BMI ≥30. BMI is a weight-for-height ratio widely used to classify overweight and obese conditions in the adult population (BMI=body weight (kg)//height 2 (m 2)). In 2005, according to WHO, approximately 1.6 billion adults (over 15 years of age) worldwide were overweight and at least 400 million adults were obese. The results of selective studies conducted in Russia indicate that at least 30% of the working-age population are overweight and 25% are obese. By 2015, approximately 2.3 billion adults are projected to be overweight and over 700 million obese. From an etiological and pathogenetic point of view, obesity is a chronic heterogeneous, progressive disease associated with a number of genetic, behavioral, environmental, hormonal and neurological factors leading to eating disorders, disorders of all types of metabolism and energy imbalance. Numerous studies have shown that obesity leads to the development of various diseases, high disability and a decrease in the overall life expectancy of patients. The risk of their development increases progressively as BMI increases. Individuals with 40% excess body weight have a 2 times higher risk of premature death compared with people with an average body weight. The range of diseases associated with obesity is quite wide. The most commonly associated with obesity are: type 2 diabetes mellitus (DM), arterial hypertension (AH), dyslipidemia, coronary artery disease, heart failure (HF), cerebrovascular disease (increased risk of stroke), respiratory disease (sleep apnea, asthma), cholelithiasis, non-alcoholic cirrhosis of the liver and OA.

Osteoarthritis is the most common and common age-related joint disease, leading to the development of functional insufficiency and subsequent disability in adults. According to current projections, increasing life expectancy and global population aging by 2020 could make OA the fourth leading cause of disability (WHO). Until 1986, there was no clear definition of the disease. Most authors considered OA to be a disease of unknown etiology, in which articular cartilage and subchondral bone are initially affected, in contrast to rheumatoid arthritis, where changes in the synovial membrane primarily occur. Around the same year, the American College of Rheumatology's subcommittee on OA proposed defining OA as a heterogeneous group of conditions resulting in symptoms and signs associated with loss of articular cartilage integrity and subchondral bone changes. The current definition of the disease was adopted in 1994 at the workshop "New Perspectives on the Study of OA" and characterizes OA as a group of overlapping different diseases of different etiologies that have the same biological, morphological and clinical outcomes, in which not only the articular cartilage, but the entire joint, including the subchondral bone, ligaments, capsule, synovial membrane and periarticular muscles, is involved in the pathological process. It should be noted that traditionally OA was considered a degenerative disease of the joints, but recently there is more and more evidence that inflammation plays a significant role in its pathogenesis. That is why in foreign literature the disease is usually called "osteoarthritis". In general, OA is characterized by focal loss of articular cartilage and central and marginal new bone formation. In Russia, about 15 million people suffer from OA, which is 10-12% of the country's population, and the incidence rate is at the level of about 20% per year. In the US, OA is diagnosed in more than half of people over the age of 65 and in virtually every person over 75 years of age. According to WHO forecasts, by 2020 OA will affect 71% of the population over the age of 65 years.

OA is divided into primary (or idiopathic) and secondary (associated with other conditions). Primary OA can be localized (localized in one joint) and generalized (three or more joints). There is no clear relationship between clinical symptoms and radiographic findings. For example, it was found that people aged 65 to 93 years in 33% of cases have radiological signs of OA, but only 9.5% of them have its clinical manifestations. At the same time, in a number of patients with a pain syndrome characteristic of OA, minimal radiological changes are not detected or are detected. The classification (criteria) of Kellgren and Lawrence is most widely used to establish the diagnosis and assess the progression of OA. Most epidemiological studies rely on the radiological manifestations of OA and the duration of pain in the joint. According to various researchers, the incidence of OA at autopsy is significantly higher compared to its clinical manifestations. It ranges from 48 to 65%.

In general, the etiology of OA is multifactorial and includes both generalized constitutional factors (old age, gender, obesity, heredity, reproductive function) and mechanical factors. The opinion that OA is a group of diseases that differ, in particular, in the affected joints, but have signs of a common pathological process that leads to joint failure, arose to a greater extent as a result of the analysis of risk factors for various localizations of the disease. Osteoarthritis of the knee is more common in women and often affects black Americans. This disease is usually preceded by traumatic injury to the joints. Local mechanical factors play an important role in the progression of knee OA. Valgus or varus deformity significantly increases the risk of progression of tibiofemoral OA. Bruises (damage) to the joints significantly increase the risk of OA. A retrospective analysis shows that knee injuries in childhood or adolescence significantly increase the risk of knee OA at 65 years of age. There are no gender differences in OA of the hip joints, it is rarely diagnosed in Asians, congenital developmental defects are common: congenital hip dysplasia, Legg-Calve-Pertes disease, etc. The risk of developing OA in people with congenital defects of the musculoskeletal system is increased by 7.7 times. OA of the joints of the hands is a heterogeneous, gender-dependent disease, more common in women over the age of 50 years. In the elderly population, radiological signs of hand OA occur in 80% of cases. Genetic factors increase the risk of developing primary hand OA. So, Stecher (1941) suggested that the formation of Heberden's nodules is a congenital autosomal sex-mediated feature of OA, since, according to his data, Heberden's nodules were found in women 10 times more often than in men. At the same time, Heberden's nodules were detected in mothers and sisters of patients, respectively, 2 and 3 times more often than in women of the same age in the population. The incidence of OA in families of patients with OA is 2 times higher than in the population.

Obesity as a risk factor for the development and progression of OA
Obesity is one of the most serious risk factors for the development and progression of OA. First of all, this applies to primary OA of the knee joints, in which a clear relationship was found between the level of BMI and the risk of OA.

Numerous studies (Fremingham, Chindford, Baltimore), as well as studies conducted in other countries, have demonstrated a strong relationship between obesity (BMI> 30) and the presence of radiographic signs of knee OA. According to the Medical Research Council's Epidemiology Resource Center Southampton University (England), the risk of knee OA progressively increases with increasing BMI. This conclusion was made based on an analysis of the effect of BMI on the severity of knee OA in 525 men and women aged 45 years and older: in people with a BMI> 30 kg / m 2, the risk of developing knee OA was 4 times higher than in people with a BMI of 25 kg / m 2. In people with a high degree of obesity (BMI 36 kg / m 2 and more), the risk of knee OA was 14 times higher than in people with a normal BMI. In addition, obesity was associated with both symptomatic OA and OA without clinical manifestations, but with radiographic changes. A double controlled study by F. Cicuttini showed that an increase in body weight per kilogram increases the risk of radiographic signs of OA of the knee and carpomet D. Hart and T. Spector, in a study of 1000 women, established the relative risk of developing unilateral and bilateral OA of the knee (according to X-ray examination) depending on BMI: 6.2 for BMI<23,4 кг/м 2 и 18 для ИМТ>26.4 kg / m 2. When comparing BMI<23.4 кг/м 2 с ИМТ 23,4-26,4 кг/м 2 относительный риск ОА был увеличен для колена в 2,9 раза, для карпометакарпальных суставов - в 1,7 раза и для проксимальных межфаланговых суставов - в 1,2 раза. M. Davis и соавт. , обследовав около 4000 человек в возрасте от 45 до 74 лет (включая рентгенографию суставов), установили, что ожирение ассоциируется как с двусторонним, так и односторонним ОА коленных суставов, но более строго - с билатеральным. L. Sharma и соавт. показали, что ИМТ положительно коррелирует с большей тяжестью повреждения медиальной тибиофеморальной области у пациентов с варусным нарушением оси нижней конечности, но не в случае вальгусного или нормального расположения оси конечности. При варусном положении коленного сустава ожирение способствует перенесению оси тяжести тела и выраженному поражению медиальных тибиофеморальных сочленений. Проспективные исследования показали, что повышенная масса тела способствует прогрессии рентгенологических проявлений ОА коленных суставов, при этом влияние высокого ИМТ на заболеваемость ОА выше, чем на прогрессирование ОА . D. Felson и соавт. отметили четкую связь между увеличением ИМТ и прогрессированием ОА коленных суставов у пациентов с умеренными нарушениями механической оси конечности.

However, there is an association of obesity not only with the risk of knee OA. Numerous studies have shown that obesity increases the risk of developing OA of the joints of the hands, hip joints, as well as other pathologies of the musculoskeletal system. The review by M. Magliano summarizes publications on the topic "obesity and arthritis - OA and RA" in the English-language electronic Internet databases Medline (1966-February 2008), Pubmed, Embase (1980-February 2008) and Cochrane Library. In a review by J. Adamson et al. among 858 Scots aged 58 years, there was a high prevalence of pain in the knee, hip, hand, back and neck joints, with the frequency of pain in the knee and hip joints being 2 times higher in obese individuals. In a review by L. Busija et al. , which included 7800 Australians, people with overweight were 2 times more likely to be diagnosed with OA than people who had a normal BMI (the groups were comparable in age and socioeconomic status). According to the Italian National Health Survey 1999-2000. , OA and back pain were significantly more common in women with II-III degree obesity than in women with normal body weight (OR 2.48 vs. 0.64, OR 2.06 vs. 0.57, respectively). The probability of developing carpal tunnel syndrome in people with increased body weight is 2 times higher than in people with an average body weight, while women developed carpal tunnel syndrome 3 times more often than men. It has also been found that in obese individuals, the risk of developing rotator cuff compression syndrome is significantly higher than in the general population. In a case-control study involving 311 patients undergoing surgical treatment for rotator cuff compression syndrome, it was found that the risk of developing this syndrome in people with increased body weight is 25% higher, with moderate obesity - 80-120% and 300% higher in people with a BMI> 35 kg / m 2. A Danish study of 29,424 twins found an association between chronic and recurrent back pain and obesity.

There is ample evidence that hand OA is associated with obesity. M. Hochberg et al. in the framework of the Baltimore study found a relationship between metabolic and some physiological factors (including age) and OA of the joints of the hands in men. The same researchers (1993) presented data on the association of OA of the joints of the hands in women with age, the value of the waist / hip index above the average and the percentage of fat. Researchers found no relationship between OA of the hands and BMI. F. Cicuttini et al. in a study of middle-aged twin women, obesity was found to be an important risk factor for both knee and carpometacarpal hand OA, with a significant increase in risk of 9-13% per kilogram of body weight. A. Sayer et al. in a cohort study of 1467 men and 1519 women born in 1946 found that OA of the hand joints in men was associated with increased body weight at ages 26, 43 and 53 and at birth. However, the authors did not find a similar relationship in women. M. Grotle et al. in a 10-year prospective cohort study of 1894 subjects found that hand and knee OA in both men and women was significantly associated with high BMI (>30) but not with hip OA. In a recent systematic review by Erlangga Yusuf et al. analyzed 25 studies on hand OA and obesity. These included 2 cohort, 3 case-controlled, and 20 cross-sectional studies, 15 of which were classified as high quality studies. Analysis of the results led to the conclusion that there is a positive relationship between body weight, or BMI, and hand OA. The level of evidence was moderate, with an approximate hazard ratio of 1.9, and additional high-quality cohort or randomly controlled studies are needed. Although the mechanism by which obesity may increase the risk of developing OA remains completely unclear, these data support the important role of obesity in the development of OA of the joints of the hands.

Literature data reflecting the relationship between obesity and hip OA are ambiguous. A number of researchers have found a clear relationship between BMI and the risk of hip OA, others have not found it. So, S. Tepper et al. in a cross-sectional in-depth study in the United States of 2358 people over the age of 55 found no relationship between increased body weight and the type of fat distribution on the body and hips. In contrast, a case-controlled study in Sweden (E. Vingard et al.) of 259 men undergoing arthroplasty for primary hip OA showed a positive association between severe hip OA and high BMI. Large cohort studies have confirmed this correlation. G. Flugsrud et al. in 2006, after studying the data of 1.2 million people aged 18 to 67 years, examined for tuberculosis, including those with a study of the hip joints, 28,425 people were identified who subsequently underwent total hip arthroplasty for primary OA. The researchers found a clear association between height, BMI, and hip arthroplasty. An increase in BMI by 5 kg/m 2 increased the risk of surgery by 66% (95% CI 62-74%) in men and by 35% (95% CI 33-37%) in women. Obese men had more than 8 times the risk compared to underweight men, while obese women had 5 times the risk compared to underweight women. The authors established an important fact - obesity at a young age is a more significant risk factor for the development of hip OA than obesity that developed at an older age (according to the authors, this is due to the greater vulnerability of cartilage to the effects of obesity factors at a young age). A 10 cm height increase increased the risk of subsequent arthroplasty by 17% (95% CI 13-21%) in men and by 46% (95% CI 43-50%) in women. B. Liu et al. In a prospective cohort study of 490,532 United Kingdom women aged 50-69 years selected in 1996-2001, followed up for 2.9 years (for primary hip and knee arthroplasty), found that the risk of primary arthroplasty in middle-aged women was associated with increased BMI and height. According to these researchers, 27% of hip arthroplasty and 69% of knee arthroplasty in middle-aged women in the UK are attributes of obesity. This clinical and epidemiological study found that reproductive history and hormonal factors affect the risk of hip and knee arthroplasty in OA in middle-aged women, and to a greater extent - the knee than the hip. Early onset of menstruation slightly increases the risk of hip and knee arthroplasty. Menopausal status and age at menopause were not associated with the risk of hip and knee arthroplasty. The use of hormone replacement therapy was associated with a significant increase in hip and knee arthroplasty, while previous use of oral contraceptives had no effect.

Y. Wang et al. in a prospective cohort study conducted in Australia, including 39,023 healthy volunteers, found that the risk of primary knee and hip arthroplasty in OA was associated with the amount of fat mass and central type of obesity. According to the authors, this relationship suggests general and biochemical and metabolic mechanisms associated with increased weight and contributing to the risk of joint replacement, more significant for the knee than the hip.

Thus, most authors draw attention to the existing causal relationship between OA and obesity. The effect of increased stress on articular cartilage in overweight people may explain the increased risk of knee OA. Undoubtedly, the increased mass of adipose tissue itself increases the load on the skeleton and leads to damage to the musculoskeletal tissue. Recently, mechanoreceptors, sensitive to pressure and associated with the extracellular matrix by a signaling cascade, have been found on the surface of chondrocytes. Three types of signaling receptors have been found on chondrocytes: stretch-activated channels, α5β1-integrin, and CD44. Contraction and stretch stimulate integrin and stretch-activated channels, resulting in both activation of the signaling pathway (mitogen-activated protein kinase, NFχB) and production of second messengers (calcium, triphosphatinositol, and cyclic adenosine monophosphate). Upon activation of mechanoreceptors, cytokines, metalloproteinases, prostaglandins, or NO can be expressed. As experimental studies have shown, under certain conditions, overload can serve as a trigger for inhibition of matrix synthesis and cartilage degradation. In turn, it can be assumed that obesity can induce cartilage damage through the activation of mechanoreceptors.

However, the current scientific evidence allows us to assess the role of obesity as a risk factor for OA and other chronic conditions much more than just the impact of elevated BMI. The effect of increased stress on articular cartilage in overweight people may explain the increased risk of knee OA. However, the fact that OA often develops in joints that are not directly affected by increased weight suggests that there are other mechanisms associated with obesity that can alter cartilage and bone metabolism and lead to the development of the disease.

Metabolic disorders in OA and obesity
Adipose tissue is not a passive energy storage, it is an active metabolic and endocrine organ that produces hormonal and biologically active substances, and plays a key role in the development of obesity, metabolic syndrome, type 2 diabetes and other pathologies. It has been established that a large number of adipokines or adipocytokines - peptide hormones - are produced in adipose tissue. Adipokines have a variety of biological effects and affect the severity of processes in many organs directly or through neuroendocrine mechanisms, interacting with pituitary hormones, insulin, catecholamines. They also play a role in the relationship between obesity and concomitant diseases. Adipokines produced by fat cells (adipocytes) and the stroma of the vascular fraction of white adipose tissue cells can be divided into 3 types: the first type - cytokines: TNF-α, interleukins (IL-1, IL-6, IL-8, IL-10), transforming growth factor (TGF), interferon (IFN), leptin, adiponectin, resistin, angiotensinogen; the second type - factors of the complement system: plasminogen activation inhibitor-1 (PAI-1), fibrinogen, angiopoietin-related proteins, complement factor-3; 3rd type - chemoattractants (chemotactic molecules): chemotactic monocytic protein-1 (MCP-1), macrophage inflammatory protein (MIP-a1). The fact that adipose tissue produces and accumulates a number of pro-inflammatory cytokines suggests that obesity is a mild inflammatory condition. This also combines obesity with OA, which is also regarded as a low-inflammatory condition: both of these diseases have high levels of inflammatory biomarkers - IL-β, TNF-α, TNF-α receptors sTNFR1 and sTNFR2, C-reactive protein (CRP) .

Special consideration deserves such adipokines as leptin and adiponectin, which affect cartilage, bone tissue and the vascular wall. Adiponectin is a critical mediator of obesity-associated insulin resistance and tissue inflammation. The action of adiponectin is aimed at reducing inflammation and increasing the sensitivity of tissues to insulin. The content of adiponectin in people with visceral obesity is markedly reduced compared to people with normal body weight. Adiponectin exerts its anti-inflammatory effect through opposition to TNF-α. Adiponectin reduces the macrophage response to TLR4 by activating ADIPOR1. Thus, adiponectin suppresses TLR4-induced NFaB activation and suppresses LPS-produced interferon-α secretion. By inhibiting the expression of adhesion molecules induced by TNF-α, adiponectin reduces macrophage adhesion, phagocytic capacity, and transmigration.

Leptin is a cytokine peptide. Structurally, it is similar to such pro-inflammatory cytokines as IL-6 and IL-12. Produced by white adipose tissue. Leptin circulates in the blood in two forms: free and bound to specific proteins. Serum leptin levels are proportional to total fat mass. Leptin regulates neuroendocrine functions, energy homeostasis, hematopoiesis, and angiogenesis. Leptin modulates food intake and body energy balance through appetite control. The action of leptin is based on the activation of the leptin receptor (LR). The binding of leptin to LR activates the JAK factor, which affects the expression of many hypothalamic neuropeptides: neuropeptide U, which regulates the function of the hypothalamic-pituitary-gonadal system, thyroid-stimulating hormone, and corticoliberin. The inhibitory effect of leptin on the production of neuropeptide U leads to a decrease in appetite, an increase in the tone of the sympathetic nervous system and energy expenditure, as well as a change in metabolism in peripheral organs and tissues. In addition, leptin plays a role in the inflammatory response. Leptin can increase the production of pro-inflammatory cytokines (TNF-α, IL-6 and IL-12) by macrophages.

Recent studies have established that adipokines may accompany changes associated with OA and, moreover, may be involved in the local regulation of articular cartilage metabolism. Leptin, resistin, and adiponectin have been found in the synovial fluid of patients with OA. Leptin is found in both osteophytes and cartilage of OA patients with increased expression in areas of matrix depletion, fibrillation, and chondrocyte accumulation. The level of leptin in articular tissues correlates with BMI. The expression and production of leptin are increased in subchondral osteoblasts in OA compared with the norm. Leptin induces the expression of growth factors, stimulates the synthesis of proteoglycans and collagen, increases the stimulating effect of pro-inflammatory cytokines on the production of nitrogen nitrite in chondrocytes. D. Mainard et al. in the experiment demonstrated the important role of leptin in the pathogenesis of osteoarthritis due to its influence on the synthesis of insulin-like growth factor (IGF1) and transforming factor p1 (TGFP1). The presence of leptin, IGF1 and TGFP1 in cartilage tissue (osteophytes) in OA has been established immunohistologically. In patients with OA, a high level of leptin was determined in the synovial fluid and in the subchondral bone. Normally, leptin is not detected in cartilage tissue. It has been established that chondrocytes in OA produce IGF1 and TGFP1. Expression of TGFP1 is strongly associated with osteophytes. TGFP induces fibrous changes in the synovial membrane, bone sclerosis, differentiation of stem cells from the periosteal layer with the formation of osteophytes. The experiment proved that injections of leptin into the joint of healthy rats can mimic the signs of OA. G. Miller et al. studied the relationship between serum leptin levels, obesity and progression of knee OA (the study included patients over the age of 60 years, with a BMI of 28.0 kg/m 2 or more). These results led the authors to conclude that a decrease in serum leptin may be one of the mechanisms by which weight loss slows the progression of OA.

Thus, at present, OA can be considered as a systemic disease, in which dysregulation of lipid homeostasis can be one of the main pathophysiological mechanisms leading to the development of OA. Obesity and OA are connected in a vicious circle: obesity is a risk factor for OA and many other diseases associated with metabolic disorders, and dysfunction and disability, as a rule, accompanying OA, in turn also lead to an increase in BMI and induce the development of diabetes and cardiovascular diseases. According to available data, OA is most often combined with arterial hypertension (AH) and other cardiovascular diseases (atherosclerosis, coronary artery disease). Cardiovascular disease occurs in more than 50% of patients with OA. Analysis of publications in Medline from 1966 to 2004 showed that the combination of OA with hypertension occurs in 48-65% of patients with OA in the population and in more than 65% of patients with OA over 80 years of age who need knee arthroplasty. In a study conducted by L.N. Denisov and V.A. Nasonova in 2010 included 298 patients with overt OA of the knee and hip joints. The relationship between obesity and the incidence of other diseases, disorders of fat metabolism and the progression of OA of various localizations was studied. There was a clear increase in the prevalence of cardiovascular disease and DM with increasing BMI. In the group with obesity (BMI>30-35 kg/m 2 ), stage II-III OA prevailed (in 97%), in the group of patients with BMI>40 kg/m 2 80% had stage III-IV OA.

Thus, modern scientific data allow us to consider OA as a disease pathogenetically interconnected with obesity, cardiovascular diseases and other metabolic conditions, which dictates the need for an integrated approach to the choice of treatment methods.

Principles of treatment of patients with OA with increased body weight and comorbidity
More than 50 methods of non-pharmacological, pharmacological and surgical treatment for OA of peripheral joints, mainly knee and hip, are described in the medical literature. The generally accepted treatment regimens for OA are based on recommendations developed by leading scientific organizations that study all aspects of the problem of OA, including its therapy from the point of view of evidence-based medicine. Treatment of a patient with OA is carried out in accordance with international recommendations developed by OARSI (Osteoarthritis Research Society International) and EULAR (European League Against Rheumatism). These recommendations are based on an analysis of past studies and expert opinion and are presented in a clear evidence-based format. According to the recommendations, OA treatment should be carried out taking into account risk factors: general risk factors - age, comorbidity (obesity, cardiovascular diseases, etc.), pain intensity level and functional insufficiency, presence or absence of signs of inflammation, localization and severity of structural changes. Optimal management of OA should include a combination of non-pharmacological and pharmacological therapies.

Non-pharmacological treatments for OA include regular patronage and patient education; development of skills of motor mode, work and rest; regular exercise therapy and aerobics; the use of special orthopedic devices; dietary advice. The positive effect of exercise therapy on the reduction of pain in the joints in OA has been established in a number of studies. The exercise therapy complex should be selected individually, taking into account the patient's diseases and their severity. From the standpoint of mechanical unloading of the joints, as well as the prevention of cardiovascular pathology, it is necessary to orient patients towards maintaining a normal body weight.

For a patient with OA and obesity, taking measures to reduce body weight is a priority both in terms of mechanical load and in terms of preventing cardiovascular diseases. Weight loss is recommended if BMI>25 kg/m 2 . Competent correction of body weight will reduce the intensity of pain in the affected joints, will help slow down the progression of OA, and will also significantly reduce the risk of cardiovascular complications. A systematic review of the literature on obese individuals diagnosed with knee OA concluded that OA-related disability can be significantly reduced with a 5.1% reduction in body weight. In a study by D. Felson et al. , which included 800 women, it was demonstrated that a decrease in BMI by 2 kg / m 2 over 10 years reduced the risk of developing OA by more than 50%. The most effective combination of diet and exercise. G. Miller et al. studied the relationship between serum leptin levels, obesity, and disease progression in patients with knee OA. The study included patients with symptoms of knee OA over the age of 60 years, BMI of 28.0 kg/m2 or more. The duration of the study was 18 months. All patients with OA were randomly divided into 4 groups depending on the method of weight loss: a control group leading a healthy lifestyle; diet group; group of physical activity; group of a combination of physical activity and diet. The greatest weight loss was achieved in the "diet" and "diet + exercise" groups - by 5.3 and 6.1%, respectively; to a lesser extent, the group "physical exercises" reduced body weight - 2.9%. The decrease in serum leptin levels at 6 and 18 months was significant in the diet and diet+exercise groups compared with the other two groups (b=0.245; p<0,01). Результаты исследования свидетельствуют о том, что снижение уровня сывороточного лептина может быть одним из механизмов, с помощью которого снижение массы тела может замедлить прогрессирование ОА. В диету больных с ОА рекомендуется включать рыбные продукты (как минимум 2 раза в неделю), содержащие омега-3 полиненасыщенные жирные кислоты (омега-3 ПНЖК). Омега-3 ПНЖК не вырабатываются в организме человека, но жизненно ему необходимы: они способны подавлять воспалительные реакции в организме, нормализуют жировой обмен, положительно влияют на сосудистую стенку и реологические свойства крови . С целью полной компенсации дефицита омега-3 ПНЖК и физиологической коррекции жирового обмена целесообразно назначать лекарственные препараты омега-3 ПНЖК. Безрецептурный лекарственный препарат Витрум кардио Омега-3 содержит в 1 капсуле 500 мг (300 мг эйкозопентаеновой и 200 мг докозогексаеновой кислоты), т.е. суточную потребность здорового человека в омега-3 ПНЖК. Более высокие дозы препарата 1-3 капсулы (1500 мг/сут экозопентаевой и докозогексаеновой кислот) в день способны оказывать лечебный эффект. В ряде исследований показано, что при ревматоидном артрите высокие дозы омега-3 ПНЖК (более 2000 мг/сут) оказывают достоверное обезболивающее и противовоспалительное действие.

The main objectives of the pharmacological treatment of OA are the effective reduction of pain, suppression of the inflammatory process in the joint, improvement of the functional abilities of the joint and inhibition of disease progression. Relief of pain in OA is possible with the help of several groups of drugs that differ in the mechanism of action, the speed of onset and the strength of the analgesic effect, as well as the safety and tolerability profile. Taking into account the fact that a patient with OA, as a rule, has several somatic diseases at the same time, primarily cardiovascular diseases, dictates the need for a rigorous assessment of the expected benefits and possible risks from the prescribed antiarthrosis therapy. Against the background of comorbidity, excessive and irrational prescribing of drugs without taking into account the peculiarities of their interaction leads to a sharp increase in the likelihood of developing undesirable effects of therapy and aggravation of the course of diseases.

In international guidelines for the treatment of OA (EULAR, 2003; OARSI, 2008), non-steroidal anti-inflammatory drugs (NSAIDs) are indicated as the drugs of choice for pain relief in OA (in case of paracetamol ineffectiveness). NSAIDs, both non-selective and selective, have a pronounced anti-inflammatory and analgesic effect, however, in patients with OA and metabolic diseases or a high risk of their development (obesity, hypertension, coronary artery disease, etc.), they can have a number of side effects that aggravate the course of cardiovascular pathology. An increased risk of cardiovascular events (myocardial infarction, stroke and sudden coronary death) can be considered as a class-specific side effect for all NSAIDs. Taking NSAIDs can lead to destabilization of hypertension and progression of heart failure. It has been established that the use of NSAIDs by patients with a history of heart disease increases by 10 times the likelihood (0R=10.5) of hospitalization for heart failure compared with patients not taking NSAIDs (OR=1.6). It should also be borne in mind that NSAIDs can reduce the effectiveness of drugs used in standard CVD therapy (β-blockers, diuretics, ACE inhibitors and, to a lesser extent, calcium channel antagonists).

Currently, symptomatic drugs with a possible structure-modifying effect (SYSODOA) occupy an increasingly important place in the treatment of OA. They, like NSAIDs, are included in the EULAR and OARSI guidelines for the treatment of OA. These include glucosamine (GA) and chondroitin sulfate (CS), diaceriin, hyaluronic acid preparations for intra-articular injections, and avocado and soy extracts. The greatest evidence for efficacy in the treatment of OA has been obtained for cholesterol and GA. Summarizing the results of clinical studies conducted with CS and GA preparations, we can conclude that they are characterized by a slowly developing anti-inflammatory effect comparable to NSAIDs and allowing to reduce the dose of the latter, the possibility of combining with paracetamol and NSAIDs, long-term preservation of the therapeutic effect, high safety and the absence of serious side effects. At the same time, they help slow down the progression of OA (according to x-ray studies). The mechanism of the therapeutic action of cholesterol and GA in OA is associated with their ability to suppress catabolic (degenerative) and activate anabolic (recovery) processes in cartilage tissue, to have their own anti-inflammatory and analgesic effect. So, depending on the dose used, cholesterol suppresses the synthesis of prostaglandins stimulated by IL-1 by synovial fibroblasts, cancels the inhibition of hyaluronic acid synthesis associated with IL-1, reduces the synthesis of collagenase and aggrecanase activity dependent on IL-1, which indicates the ability of cholesterol to reduce collagenolytic activity and increase the production of matrix components; is able to suppress the synthesis of aggressive matrix metalloproteinases and activate the synthesis of their inhibitors, which helps to restore the balance between anabolic and catabolic processes in the cartilage matrix. In addition, cholesterol suppresses NO-induced apoptosis of chondrocytes, improves microcirculation of subchondral bone due to inhibition of lipid synthesis, binding of E-selectin, mobilization of fibrin, lipids and cholesterol in the blood vessels of subchondral bone. GA suppresses the pro-inflammatory and vasoconstriction effects of IL-1 and inhibits the activation of the nuclear factor NFχB pathway. Through this mechanism, GA can suppress gene expression and protein synthesis of cyclooxygenase-2 (COX-2), selectively through COX-1, thus preventing the release of prostaglandin PGE2 in the nutrient medium. The action of NFχB is suppressed by GA at the level of both chondrocytes and synoviocytes, while providing a parallel decrease in the synthesis of COX-2 proteins, the release of prostaglandin E 2 , and the release of NO in chondrocytes. In addition, GA consistently reduces IL-1 mediated synthesis of matrix metalloproteinases in both cell types. At the same time, it was found that cholesterol and GA have not quite identical pharmacological effects, they complement and enhance the effects of each other, which determines the prospects for their combined use in the treatment of OA. In a recent double-blind, placebo-controlled study "Glucosamine/Chondroitin Arthritis Intervention Trial (GAIT)", when evaluating the effect of various treatment regimens on pain (WOMAC) after 6 months of therapy, it was found that in patients with OA with severe pain in the knee joints (WOMAC 301-400 mm), the effectiveness of therapy with a combination of cholesterol and GH was significantly higher (79.2%, p = 0.002 vs. placebo). cebo) than in the case of using monotherapy with cholesterol or GG.

The efficacy and high safety of the combined drug Artra (1 tablet contains 500 mg of cholesterol and 500 mg of glucosamine hydrochloride) in the treatment of knee OA in patients with somatic pathology was studied in a clinical trial that included 60 patients aged 62.3 ± 4.7 years with stage II-III knee OA and concomitant somatic pathology. BMI>25 kg/m 2 was in 100% of patients, 60% suffered from hypertension and 19% of coronary artery disease. Patients were randomized into two groups matched by sex, age, severity of OA (intensity of pain syndrome and degree of functional limitations) and concomitant therapeutic pathology. Patients of the main group received Artra together with NSAIDs, patients of the control group - only NSAIDs. In the course of treatment, NSAIDs were canceled in the absence of pain and exacerbation of the latter without NSAID therapy. The duration of therapy was 6 months, the effectiveness was evaluated: clinical - after 3 and 6 months, MRI - after 9 months. In the dynamics, the effect of therapy on pain (VAS, WOMAC indices), cancellation or reduction of the dose of NSAIDs taken, functional state (WOMAC, walking speed for 15 m), disease progression (MRI of the knee joints), the state of the cardiovascular system and the gastrointestinal tract were evaluated.

Assessment of pain syndrome dynamics (WOMAC pain) showed that in patients taking Arthra, after 3 months from the start of therapy, a more pronounced regression of pain syndrome was observed compared to the control group. After 6 months of therapy in patients of the main group, the level of intensity of pain syndrome was significantly lower than in patients of the control group (178.3±37.2 versus 287.4±42.8, respectively, p=0.02). Assessment of functional impairment according to the WOMAC scale at the start of the study did not reveal significant differences between the observation groups. After 6 months of therapy in both groups, a significant decrease in the degree of functional insufficiency was observed, however, in the main group, the average score was 427.3, in the control group - 658.9 (p=0.002). Thus, in patients receiving Artra, after the end of the planned observation period, there was a pronounced positive dynamics of the pain syndrome and improvement in functional ability. Visual assessment of the condition of the knee joints by MRI before treatment and after 9 months of therapy established an improvement in the visualization of the articular cartilage in 60% of patients in the main group, while in 63.3% of patients in the control group there was a negative trend. Thus, the positive effect of therapy in the group of patients treated with Artra, from the point of view of the clinical picture, was confirmed by the data of an objective research method - MRI. To study the effect of therapy on the state of the cardiovascular system in patients with OA and somatic pathology, the dynamics of systolic BP (SBP), the frequency of painful ischemia (PI) and painless ischemia (PAI) of the myocardium were evaluated according to the Holter study (at the beginning and after 6 months of the study). It was found that during the treatment with Artra there was a significant decrease in the level of SBP. The difference in the average daily SBP before the start of therapy and after 6 months of observation was 7.3 mm Hg in the main group. (R<0,05), в то время как в контрольной группе - 3,6 мм рт.ст. (р>0.05). According to Holter monitoring data, patients of the main group had a smaller number of episodes of SI and ASI than patients in the control group. The positive effect of Artra in patients with OA and somatic pathology on the state of the cardiovascular system is apparently due to a more effective relief of pain in the joints, improvement in the functional state, a decrease in the dose of NSAIDs taken by patients and an associated decrease in the risk of side effects caused by them. During the treatment with Artra in patients with OA, the number of rehospitalizations due to exacerbations of somatic diseases decreased: in the main group, 43% of patients (13 people) were rehospitalized over the next 9 months of observation, while in the control group rehospitalizations were in 76% of patients (23). The total number of hospitalizations per 1 patient was 1.2 in the main group and 1.7 in the control group. Thus, taking into account the positive effect of the drug on the dynamics of concomitant cardiovascular diseases in patients with OA and its high safety, Arthra is reasonably the drug of choice for the basic therapy of OA in patients with comorbid pathology.

Given the above data, it should be concluded that the treatment of clinical manifestations of OA in patients with obesity and other metabolic diseases (hypertension, coronary artery disease, etc. or their high risk) should be carefully considered by the doctor. When forming a treatment regimen, much attention should be paid to non-drug methods of treatment - exercise therapy, a diet aimed at reducing BMI, organizing a work and rest regimen. Throughout the course of treatment, strict control of the level of blood pressure, ECG is necessary. With regard to drug therapy, in patients with OA and a high risk of cardiovascular complications, NSAIDs should be prescribed with great caution, following accepted recommendations. Given the proven clinical efficacy, high safety (comparable to placebo) and good tolerability of cholesterol and GA drugs, they can be considered as the most preferred drugs for the treatment of clinical manifestations of OA in patients with comorbid pathology.

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