As a rule, excess weight creates an additional load on the joints, affects the musculoskeletal system, especially the spine, hip and knee joints. It is understandable: try to vilify a bucket of water in your hands for a couple of hours and you will feel how your joints will get tired. But for many overweight people, the extra weight is measured by more than one such bucket!

Experts have long calculated that every extra 500 g of weight increases the load on the spine and joints, contributing to the faster development of their degenerative-dystrophic changes, in which the cartilage tissue that covers the surface of the joint suffers first.

As the interarticular cartilage is destroyed and thinned, the tissues surrounding the joint (synovium, adjacent bone, muscles) also suffer. If this process is not stopped, the case may end with a chronic pain syndrome, and ultimately with the replacement of the affected joint.

Important Steps

If you are overweight (see table) or have back or joint pain, it is important to take immediate action to lose weight. To do this, it is enough to take a number of simple, but quite effective steps.

Step 1. Establish nutrition.

Its principles are simple: you need to minimize the consumption of salt (no more than 3-5 g per day), simple carbohydrates (sugar and sweets), alcohol, fats (fatty meat, fish, poultry with skin, lard, sausages, vegetable and butter , fatty dairy products, canned food, mayonnaise, confectionery).

You can also slightly reduce portions and eat fractionally - often and little by little, avoiding the feeling of hunger that makes us overeat. By the way, for the same reason, it is better to move the main meal to the morning and afternoon, and not to the evening, as is customary among many working citizens.

Step 2. Maintain adequate physical activity.

The best option is walking at a fast pace (preferably at least 10 thousand steps a day and in no way less than 150 minutes a week) and swimming (increased heat transfer occurs in the water, therefore both swimming for 40-50 minutes and exercises are useful in water, similar to rhythmic gymnastics).

By the way, if you are overweight, it is undesirable to engage in running and jumping sports: this will only increase the load on the joints. At the same time, in order to effectively get rid of fat reserves, it is necessary to increase physical activity due to the duration and volume of classes, and not due to an increase in their intensity.

Step 3. Start a course of chondroprotectors.

Until excess weight has caused serious damage to your joints, you need to start taking slow-acting combined chondroprotectors as soon as possible - drugs that are not only a building material for articular cartilage, but also stimulate its regeneration (recovery), which allows you to slow down the development and progression of osteoarthritis.

Check yourself!

Do you have extra pounds? This can be calculated using the formula BMI - body mass index.

BMI = your weight (in kg) divided by your height (m) squared.

For example: with a weight of 70 kg, a height of 1.7 m, the body mass index should be 70: 2.89, that is, 24.9.

Another sign of obesity is waist circumference. For women, this figure should not be more than 80 cm, for men - no more than 94 cm.

What does BMI mean?

• 18.5 -24.9 - normal body weight.
• 25.0 -29.9 - excessive (you have an increased risk of developing arthrosis).
• 30.0-34.9 - obesity of the first degree (high risk of developing arthrosis).
• 35.0-39.9 - obesity of the second degree (the risk of developing arthrosis is very high).
• 40 or more - obesity of the third degree (the risk of arthrosis is extremely high).

Modern technologies, which are designed to make our lives easier, lead to the fact that a person gradually practically stops moving. In this regard (as a result of a significant reduction in energy costs), obesity occurs.

The load on the joint increases with each extra kilogram.

Joint diseases and excess weight are directly dependent on each other. Obesity of varying degrees in a person who suffers from deforming osteoarthritis is common. In a full person, the load on the joints of the spine and lower extremities increases significantly.

Let us give an example of a calculation that will clarify the situation. The condyles of the femur in the knee joint are supported by menisci, whose area is 14.5 cm². If a person weighs no more than 70 kg, then the load per 1 cm² of his menisci will be approximately 4.5 kg. In proportion to the increase in body weight, the load on the supporting surface of the joints also increases. With a body weight of 100 kg, the pressure increases to 7 kg, and at 120 kg - up to about 8 kg, etc. The greater the load on the joint every day, the faster it wears out.

Consequences of obesity

In addition to the load on the joints, obesity has a negative effect on blood and lymph circulation, and therefore congestion is observed in the joints and tissues. Joint tissues do not receive nutrients in the right amount. Fat people are also more prone to flat feet than others.

Obesity is associated with metabolic disorders that cause non-inflammatory diseases of the spine and lower extremities, in this case, the cartilage tissue of the joints and intervertebral discs are affected by the pathology. Cracks form in the softened cartilage, and it begins to break down. The articular ends of the bones come together, between them during movement there is excessive friction.

The body tries to correct this situation, as a result of which bone tissue grows along the edges of the surface of the joints and the formation of spikes. These formations (so-called osteophytes) can injure the articular bag and ligaments. Most severely, this pathology affects the ankle, hip and knee joints.

Signs of joint damage

The initial stages of the disease are usually asymptomatic, however, a person has a crunch in the joints, fatigue. After some time, pain begins when moving, playing sports, long walking. If the patient feels pain that increases at the beginning of the movement, which then decreases, and in the evening can reach its highest point, then this indicates a progressive pathology.

Constantly increasing pain causes the muscles to contract reflexively, due to which the load on the articular surfaces of the cartilage and bones increases even more. In this case, patients often complain of difficult movements during extension and flexion, walking. All these symptoms cause inconvenience and force you to change your usual way of life - a person suffering from obesity begins to move even less, abandons sports. A vicious circle emerges.

If bones and joints crunch, this is not a harmless thing at all.

If you look, you can find out that this is often a harbinger of a serious illness.

Our joints should move silently and imperceptibly for us.

This is ensured by the production of synovial fluid during movement, which acts as a joint lubricant.

A crackling sound appears when the cartilage is damaged and less fluid is released. Because of this, friction occurs, which over time can develop into joint disease and even lead to disability.

Why do our joints crackle

Joints click most often for the following reasons:

Other reasons

Also, the cause of a crunch throughout the body or in a separate part of it can be:

1. Injuries - when the bones are cracked or fractured, the tissues and blood vessels adjacent to the joint are also damaged, resulting in inflammation that makes it difficult for the joints to move.
2. Infections.
3. Lack or excess of physical activity. A sedentary lifestyle often causes muscles to weaken and atrophy. As a result, the ligaments and the articular apparatus as a whole suffer. If a person is regularly exposed to excessive physical exertion, for example, during sports or at work that involves being constantly on their feet or carrying heavy loads, this can also provoke a crunch in the joints.
4. Irrational nutrition - people who abuse meat, chocolate, strong tea or coffee, spicy or salty foods and sweets can observe the appearance of a crunch.
5. Excess salt in the joints is often a problem for people living in areas where drinking water contains an increased amount of mineral salts.
6. Joint hypermobility is their too high mobility, most often observed in young women and is associated with the production of an altered connective tissue protein, collagen, in their body.
7. Inflammation in muscle tissue that occurs after overload.
8. Joint wear.
9. Overweight.
10. Disturbed metabolism.

This may be due to the fact that dissolved gas accumulates in the synovial fluid, which, increasing in volume, makes a click. The interval between such sounds should be at least 15 - 20 minutes.

Another reason for a normal crunch lies in the ligament or tendon touching a protruding bone fragment. At the same time, a dull click is heard.

If you suffer from a crunch all over your body

The sounds that the joints make are, in essence, a signal of their destruction and the presence of a risk of developing arthritis and similar diseases.

As a rule, joint damage occurs in a specific part of the body, but it also happens that the whole body begins to crackle periodically.

This is usually a consequence of articular hypermobility and is due to genetic inheritance.

The development of pathology in different parts of the body

A crunch in different parts of the body indicates the presence of problems in this area.

Distinguish:

1. Unpleasant sounds in the shoulder. Often the cause of this phenomenon is an excess of movement, as a result of which hypermobility of the joint develops. Ligaments weaken, painful clicks appear. This factor is transmitted at the gene level, so it is impossible to get rid of it. The only solution to this problem is the observance of preventive measures, which consist mainly in avoiding overload and overstretching of the ligaments. Also, a crunch can occur due to arthritis or other joint diseases.
2. Clicking in the hip joint. If the cause of the crunch was not an injury, then this may indicate arthrosis of the joint. As a result of this disease, the hardening and death of the articular tissues, as well as the restriction of their mobility, occurs. Also, the cause of clicks in the hip joint can be coxitis or coxarthrosis, that is, inflammation or degeneration of cartilage tissue.
3. Clicking joints in the knees. Normally, this part of the body should not make a crunch. The presence of this symptom indicates health problems. It is important to establish the cause of extraneous sounds in the joints in time and begin the correct treatment. The cause of a crunch in the knee, accompanied by pain, may be an injury, overweight, genetic predisposition, viral infections, problems with the endocrine system, physical overload, high-heeled shoes, a sedentary lifestyle. Accompanying each movement of the leg with pain and a crunch in the knee may indicate a disease of the joints.
4. Joints of hands hurt and crunch. Many practice the bad habit of cracking their fingers. At first glance, this is a rather harmless habit, but this is not entirely true. It is clear that after a working day or during psychological stress, you want to stretch your fingers. Quite often this comes as a relief. But the regular use of such a forced restoration of joint mobility over time leads to the fact that the cartilage is damaged and arthrosis begins to develop. Therefore, it will be much more useful to do a hand massage or simple physical exercises than to make your fingers crunch.
5. Pathological sound in the back usually occurs when a force is exerted on the joint that exceeds the resistance of the muscles and ligaments. This is normal. But if the clicks become regular, this may be a sign that the muscles are constantly in tension and are not doing their job. This happens, as a rule, due to physical overload, infection, malnutrition.

Constantly being in one position, the back muscles eventually lose the ability to relax on their own, their strength decreases, the vertebrae acquire excessive mobility, as a result of which the spine is struck by a short-term “shooting” pain.

If the knee joints click

Spine crunches - urgently see a doctor

To eliminate it, you need to perform special gymnastics.

Clicking joints in children

Why is pathology most often manifested in children? There are a number of reasons:

1. Connective tissue pathology. In this case, the child noted the presence of excessive mobility of the joints.
2. Temporary childhood hypermobility of the joints. Since the child's articular-ligamentous apparatus has not yet fully formed, from time to time a crunch may occur in his knees, which is not accompanied by pain. Over time, as the joints become stronger, the sound disappears. The cause for concern should be the appearance of a rattle in the joints, a feeling of discomfort. If this happens, then you need to seek medical help.

Details about the problem of crunching in children

How to get rid of pathology

What can and should be done if your joints crunch during the day.

In this case, it is worth taking certain measures to prevent the development of the disease:

1. So, while sitting, you need to change positions more often, at least once every one and a half hours you need to get up from your seat and perform a few simple exercises with your head and palms. There should be sports activities two to three times a week.
2. If the crunch occurred after an injury or disease of the joints, then you need to urgently contact an orthopedist-traumatologist. To make a diagnosis, he will prescribe an x-ray, ultrasound of the joints of the bones and computed tomography, and tell you how the treatment should take place.

joint inflammation

If inflamed joints crunch, then the decision on how to treat diseases in this case should only be a doctor.

In such cases:

1. Analgesics are prescribed to eliminate pain.
2. In the presence of inflammation and swelling, the doctor prescribes non-steroidal anti-inflammatory ointments - Ibuprofen, Diclofenac, Fastum gel.
3. If necessary, chondroprotectors are taken internally - drugs aimed at restoring the cartilage structure. These include glucosamine and chondroitin sulfates. The course of treatment in this case takes a lot of time. It is worth considering that chondroprotectors act more effectively at an early stage of the disease, when there is still no sensation of pain.
4. Sick joints need to be regularly unloaded, providing them with peace. For this, elastic bandages and special clamps are used.

If the cause of clicking sounds is a disease, then appropriate treatment is carried out:

1. With arthrosis, you need to free the joints from the load as much as possible, wear comfortable, and best of all, orthopedic shoes. If the patient has excess weight, it would be advisable to get rid of it, because in this case the joints and vessels of the legs will be less loaded. In the case of active progression of the disease, it is necessary to perform an operation, during which the joint will be replaced. This procedure is usually performed on the knee and hip osseous joints.
2. If the patient has gout, treatment includes diet and increased drinking regimen. In this case, the patient should consume at least two to three liters of fluid.
3. Patients suffering from arthritis, it will be useful to exclude starchy foods and sweets, as well as animal fats from their diet. It is useful to eat dairy products and plant foods.

Possible and common complications

If seeking help from a doctor is untimely, then a crunch in the joints can ultimately lead to the development of diseases such as osteoarthritis, arthritis, arthrosis, and bursitis.

The biomechanics of the spine also changes, a herniated disc and other complications occur.

Ultimately, the patient may become disabled, losing the ability to self-care or independent movement.

Preventive measures

In order to prevent unpleasant sounds in the joints, it is necessary to observe the following measures:

1. Eat more vegetables and fruits, and reduce the consumption of fatty meat dishes.
2. Foods that are a source of calcium and phosphorus will be useful for the body: sea fish, dairy products.
3. It is better to eat white meat instead of red meat.
4. It is better to replace fried and smoked dishes with stewed or baked ones, and instead of sweets, use fruit drinks, uzvar, fruit jelly.
5. It is useful to use sunflower seeds, pumpkin and sesame seeds, vegetable oil.
6. You need to drink at least 6 glasses of water a day in order to thin the blood in the body and prevent the formation of blood clots.
7. During the day, you need to move more, with sedentary work, change positions more often, get up from your seat and warm up.
8. Cycling, walking and swimming are good for joint health.
9. As far as possible, strong physical exertion, leading to injuries, destruction of cartilage tissue, and inflammation should be avoided.
10. In no case should you snap your fingers, because in this case the joints are injured and there is a risk of developing arthrosis.

Summing up, we can say that crunchy joints are a rather dangerous thing, since it is a harbinger of serious joint diseases. It is very important to make a diagnosis in a timely manner, find out the cause of this sound, and begin adequate treatment.

It is also important to observe preventive measures that prevent the appearance of unusual sounds in the body.

Many people are quite well aware of the situation when, from physical overstrain or for another reason, all the bones and joints hurt what to do in this situation, not everyone knows. Doctors note that the etiology of pain symptoms of this kind is diverse. Why do bones hurt? This may be an infection and metabolic disorders, tissue necrosis or a consequence of allergic reactions. These are the universal causes of pain. In total, there are about a hundred such reasons.

Today, this symptom is quite common, and even the World Health Organization became interested in this issue and conditionally designated the past decade as the peak years for the discovery of this pain symptom. What are the causes of the disease?

In modern medicine, joint and bone pain are combined into a group of rheumatic diseases. All of them combine diseases of an inflammatory and dystrophic nature.

The main causes that provoke diseases of the skeletal system, experts call:

1. Joint pain can occur due to overload in sports.
2. Tumor processes of bones. At first, the pain is present only at night or during physical hard work. The dynamics of pain depends on the rate of tumor development. Terms can be from several weeks to a year. As a result of tumor processes, the bone weakens. This leads to fractures. Joint and bone pain may be accompanied by chills, fever throughout the body, and weight loss.
3. Joint pain can be caused by systemic blood disorders. Painful symptoms of the joints of the whole body occur suddenly or with pressure on the bone. Most often, such signs are characteristic of diseases of the bone marrow, leukemia and myeloma. As for the latter disease, it is a malignant disease of the bone marrow, which is localized in the spine, pelvic bones and ribs. Most often, the disease affects men aged 60-70 years. At first, the development of the disease passes without any symptoms. This period can last up to 15 years. In the later stages of the disease, intense bone pain, fractures of the limbs and vertebrae are observed. At the stage of acute leukemia, in addition to subfebrile temperature, there is intense pain in the bones.
4. Pain in the joints and bones can be a symptom of Hodgkin's lymphoma. Against the background of a pain symptom, an increase in lymph nodes, weight loss and allergic reactions are observed.
5. Pain in the joints and bones can be in the case of malignant skin processes: melanoma, warts, papillomas.
6. Pain in the bones and joints of the knees can be in cases of chemotherapy for breast cancer. In this case, metastases can spread to the bone.
7. Intense pains in the joints of one of the knees at night are a manifestation of infectious diseases. In addition to the knees, they extend to the lower leg area.
8. Knee and shin pains are observed with intermittent fever and chills, which are transmitted by body lice.
9. Joint pain can occur due to benign tumor processes in the so-called lymphoreticulosis. The pain symptom often affects the tendons near the bone.
10. Another very serious disease provokes bone pain. This is tuberculosis of the bones. This occurs when a tubercle bacillus enters the spine from the lungs.
11. Osteomyelitis may be accompanied by bone pain and fever.

With metabolic disorders, pain may occur. This condition occurs due to a deficiency of mineral components in the diet and slow absorption into the intestinal tissue. The consequence of this condition may be a lack of vitamin D. In this case, bone softening occurs, and doctors diagnose osteoporosis. The misconception that bones need only calcium. In the case of an excess of calcium or its norm, with a lack of vitamin D, softening of the bone occurs. Basically, people with diseases of diabetes, kidneys and liver suffer from bone pain. Deficiency of the vitamin complex of group B, in addition to pain, provokes cramps in the muscle tissue of the limbs. Nerve endings do not receive enough vitamin and are destroyed. When you press on the muscle tissue, pain occurs near the bone.

A hormonal tumor of the thyroid gland also causes destruction of bone tissue. In this case, hormonal and mineral metabolism is disturbed. The early stage of the disease is characterized by bone pain, muscle weakness, and fatigue. Later, the bone softens so much that compression fractures occur.

Pain in the bones and joints occurs under the influence of the use of hormonal drugs by women during menopause, after childbirth or in the treatment of infertility.

Pain symptoms in the bones are characteristic of states of immobility. This process slows down the development of bone tissue.

Congenital features of collagen development contribute to the development of muscle and bone pain.

Pain of the entire skeletal system occurs due to the development of deforming osteitis. In this disease, the entire skeletal system is affected, and bone tissue remodeling is also impaired. The main symptom of the disease: severe pain at the sites of damage to the skeleton, deformity of the spine and lower extremities, neurological disorders.

The pain of bones throughout the body is often felt by a modern person. It's not strange. Since sitting at a computer and a sedentary lifestyle violates the water-salt balance of the body, a lack of water leads to depletion of the walls of the stomach. The protective function of the mucous membrane of the gastrointestinal tract loses its elasticity, the barrier function is destroyed. As a result, all salt components increase and exceed the quantitative threshold in the body. With a small amount of fluid intake and inactivity, excess salt fluid is retained in the body and absorbed into the muscle and bone tissue. This changes the structure of the tissue, irritating the nerve endings and causing pain.

Functional bone pain needs to be diagnosed, and only after that treatment can begin. It needs to be corrected by following a special diet, taking chondroprotectors and vitamin complexes. An important way to treat bone diseases is the normalization of nutrition. In no case should you limit the intake of carbohydrates and fats, you need to reduce their consumption. If you are overweight, you should follow a diet and limit yourself to a light dinner three hours before bedtime. To reduce weight, you should increase the intake of vegetables and fruits rich in vegetable fiber in the diet.

With functional diseases, bones and joints should not be subjected to unnecessary physical exertion and wear heavy things. To enhance metabolic processes, you should move more, play sports and perform simple exercises.

If, after the measures taken, there is no improvement in the general condition and a decrease in pain, then you should seek medical help.

This indicates more severe pathologies of the skeletal system.

Diet for arthritis and arthrosis of the joints, its features.

There are many diseases in the world today. Studies show that arthritis and arthrosis are among the most common.

The complex therapy used for these joint diseases includes not only drug treatment, physiotherapy and physical therapy, but it also takes into account the especially important issue of nutrition. In various cases, the doctor prescribes a special type of nutrition system, mode and menu. Diet for arthritis and arthrosis is considered a factor that particularly affects the human body, it is no less important than other methods of treatment. It is careful, daily dieting that can ease diseases, thus offering a chance to reduce the number of periods of flare-ups, and greatly increase the duration of periods of improvement.

General rules to follow

The goal of any diet is to improve the metabolic processes in the body, but in the case of arthrosis and arthritis, the restorative, anti-inflammatory and analgesic properties of a special diet will be directed to a certain part of the body and joints. It is vital to observe the daily routine, starting from the day the first signs of the disease appeared or there was a suspicion of its presence.

Since, in the presence of joint diseases, a person leads a measured, calm, sometimes even recumbent lifestyle, the diet should be appropriate. With arthrosis or arthritis, it is predominantly low-calorie or medium-calorie.

It is necessary to switch to a dietary diet gradually so that in the future there are no eating disorders and eating disorders. The food consumed should be varied according to the menu established by the diet.

Products of the "risk group"

There are a number of products that belong to the so-called "risk group", representing unhealthy, unhealthy foods. Nutritionists call such food “empty”, as it does not contain the vitamins, trace elements and minerals necessary for the body, and therefore does not bring any health benefits. The diet used as part of the treatment for arthritis and arthrosis of any joints in the body involves the rejection of such products. At first, it will be very difficult to rebuild the nutrition system and develop new habits, but over time, the body will get used to the new diet, and your health will be guaranteed to improve. Risk group products include:

The gradual rejection of the above products and replacing them with healthy, vitamin-rich ones will not only help to effectively fight ailments, but also significantly improve the general condition of the body.

Having listed the food groups that are recommended to be excluded from the new nutrition system, it is necessary to focus on the fact that a number of certain foods can be eaten, but the quantity and frequency of their use should be minimized, especially when following a special diet for arthritis and arthrosis.

• Strong tea and coffee. These drinks contribute to the leaching of calcium from the bone tissue and joints, which provokes the rapid progression of the disease. Therefore, in order to relieve acute symptoms, it is better to reduce their use to 1-2 cups per week and gradually stop.
• Meat dishes. Meat contains arachidonic acid, which, as a result of decay, increases inflammation in the body.
• Chocolate and other sweets. Their excessive use contributes to the rapid weight gain, which increases the load on the joints.
• Salt. Eating salty foods contributes to the accumulation of deposits in the bones, increases swelling and, as a result, increases the inflammatory process. When following a diet for arthritis and arthrosis, it is recommended to cook meals without salt, adding a little salt to the prepared food if necessary.
• Trans fats. Foods that contain "bad fats" are unhealthy and contribute to rapid weight gain. They are mainly present in fax food, chips, cakes, mayonnaise, chocolate.

The list of products that it is better to refuse or limit in use is not long enough. In addition, in modern gastronomy, you can easily find a replacement for them, following the rules of the diet, which is vital and necessary for diseases of the joints.

Another type of products that nutritionists highlight are useful and necessary for arthritis and arthrosis of the joints. They must be present in the diet, as they reduce the inflammatory process, have a beneficial effect on the articular surfaces, cartilage and bone tissue. Among them are:

• Fish of the salmon family. Rich in natural "healthy fats" and Omega-3 acids, thanks to the regular consumption of fish of this species, the body is saturated with vitamin D
• Almond. Walnut contains vitamin E, which strengthens the articular surfaces and capsules.
• Papaya. Storehouse of vitamin C and beta-carotene.
• Apples. They contribute to the production of collagen by the body - the most important substance for the joints, which restores cartilage tissue.
• Kale. It contains copper, calcium and manganese, it is recommended on a diet mainly in raw form, but cooked is also no less useful.
• Broccoli. Asparagus broccoli is rich in vitamins A and C, contains a significant amount of easily digestible calcium.
• Ginger. Ginger is considered one of the most useful products for the body, well reduces swelling and relieves pain.

Menu for arthritis and arthrosis

Composing the right menu, which would be complete and useful, is a difficult task. Therefore, in order for a diet for arthritis and arthrosis to bring exceptional benefits, it is usually prescribed by a specialist. We suggest that you consider an approximate menu for a week, which can be taken as a basis for a diet, supplemented and diversified depending on the stage of development of the disease.

Monday	Breakfast: oatmeal; fruit salad dressed with sour cream or unsweetened yogurt, you can add a little honey if necessary; a glass of tea.	Lunch: vegetable soup with meat broth; salad with celery, carrots and cucumber, seasoned with a teaspoon of olive or sunflower oil.	Dinner: baked apples with curd filling; boiled beets; a glass of kefir.
Tuesday	Breakfast: medium-fat cottage cheese, a couple of toasts with butter and a teaspoon of jam, a cup of herbal tea.	Lunch: boiled or baked chicken breast; vegetables or cereals; apple.	Dinner: baked fish; rice porridge with butter.
Wednesday	Breakfast: scrambled eggs with vegetables; a glass of green tea with ginger; yogurt jelly.	Lunch: fish meatballs; mashed potatoes or peas; cabbage salad with a teaspoon of oil.	Dinner: stewed rabbit or chicken; vegetable salad.
Thursday	Breakfast: cottage cheese casserole with dried fruits; a glass of juice or fruit drink.	Lunch: ear; Pasta with cheese; vegetable salad.	Dinner: fish aspic; carrot and cabbage salad; a glass of yogurt.
Friday	Breakfast: boiled eggs; toast with butter; apple; ginger tea.	Lunch: beetroot; minced meat zrazy; baked zucchini.	Dinner: beef or chicken soufflé; carrot cuts; a glass of juice.
Saturday	Breakfast: buckwheat porridge; sour cream jelly with berries; green tea.	Lunch: borscht; baked rabbit with zucchini.	Dinner: boiled fish; baked beans; a glass of ryazhenka.
Sunday	Breakfast: barley porridge with milk; ginger tea.	Lunch: cabbage soup with fresh cabbage; baked chicken; vegetable salad with radish and herbs.	Dinner: cottage cheese and carrot casserole; a glass of kefir.

Conclusion

If you have made the decision to fight such an ailment as arthritis or arthrosis of the joints, then you should not neglect nutrition. Changing the diet and the use of a special diet will create favorable conditions for the restoration of damaged joints, as well as strengthen the immune system and overall health.

Obesity is a subject of discussion not only for nutritionists, but also for other doctors, including those involved in the treatment of diseases of the musculoskeletal system. Excess weight and joints are closely related. With the load of excess kilograms on the articular structures, cartilage is damaged, connective tissue is destroyed, deforming osteoarthritis or other pathologies of the osteoarticular apparatus may occur.

How does extra weight affect joints?

With obesity, the load on the spine and lower limbs increases, which leads to accelerated wear of connective tissues, their deformation, and destruction. Such pathological processes provoke the development of joint diseases. In addition, being overweight has the following negative effects:

• changes lymph and blood circulation, which leads to stagnation;
• interferes with the receipt of useful substances by the articular tissue;
• provokes flat feet, osteochondrosis, arthrosis;
• due to impaired metabolism, it contributes to the destruction of cartilage, and as a result, bone growth on top of the joint and the appearance of osteophytes.

A large load with obesity can cause gonarthosis.

Problems with the musculoskeletal system can begin with a weight gain of 0.5 kg. Such a small increase can lead to displacement of the vertebrae, while knees may hurt when walking, squatting. This does not happen to all people. Much depends on the characteristics of the organism. The more weight, the stronger the pressure on the spine. A large load often affects the knees. Excess weight can cause a disease such as gonarthrosis. Its symptoms come on in stages:

1. Knee pain after sleeping and climbing stairs.
2. Soreness and crunching on movement.
3. The pain is constantly present. The joints are deformed and there is no complete flexion or extension.

How to understand that there is excess weight?

There are many methods for calculating excess weight. One of them is the calculation of body mass index. To do this, they weigh and measure their height. Then the weight indicator in kg is divided by the height (m) squared and the required index is obtained. A person has a normal weight if the indicator is in the range of 18-25. A value below 18 is underweight. With a number above 25 - there are extra pounds. If the result is 25, then the person needs to lose 4 kg (25=4 is the indicator).

What to do with the problem?

Before starting the fight against overweight, you must first consult with specialists to prescribe a set of measures in order to achieve an effect and not harm the body.

To get rid of the gained kilograms, it is initially recommended to identify the cause of their appearance.

When the legs, knees, joints hurt, the spine aches, then people seriously begin to think about their health. They want to quickly get rid of the extra pounds gained, which initially did not seem such a huge problem. But, in addition to desire, you must first find out the cause of weight gain, and then take action. Achieving this goal is difficult, but quite possible. This is easier than treating joint pathologies caused by excess kilograms.

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 the 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. People with 40% overweight have a 2 times higher risk of premature death compared to 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 strokes), respiratory diseases (sleep apnea syndrome, asthma) , cholelithiasis, non-alcoholic cirrhosis 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 various diseases of different etiologies that have the same biological, morphological and clinical outcomes, in which not only the articular cartilage, but the entire articular cartilage is involved in the pathological process. joint, including subchondral bone, ligaments, capsule, synovial membrane, and periarticular muscles. 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 articular insufficiency, 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 in the musculoskeletal motor apparatus 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/m2, the risk of developing knee OA was 4 times higher than in those with a BMI of 25 kg/m2. ) 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 radiological changes.A double controlled study by F. Cicuttini showed that an increase in body weight per kilogram increases the risk of radiological signs of OA of the knee and carpometacarpal joints.D. Hart and T. Spector in a study that included 1000 women, established the relative risk of developing unilateral and bilateral OA of the knee (according to radiological examination) in according to 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 likelihood of developing carpal tunnel syndrome in people with increased body weight is 2 times higher than in people with an average body weight, while in women, carpal tunnel syndrome developed 3 times more often than in 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 that included 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 - by 80-120 % and 300% higher in individuals with BMI >35 kg/m2. 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 UK women aged 50-69 recruited in 1996-2001 with a follow-up of 2.9 years (for primary hip and knee arthroplasty), found that the risk performing primary arthroplasty in middle-aged women is associated with an increase in 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, leading to 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 tissue sensitivity 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). 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 OA-associated changes 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 an increase in its 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 course of cardiovascular disease. 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. Summing up 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 no 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. Thus, cholesterol, depending on the dose used, 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) than in the case of using monotherapy with CS or GH.

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 study that included 60 patients aged 62.3 ± 4.7 years with OA of the knee joints II-III stage 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 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, there was a significant decrease in the degree of functional insufficiency, 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 blood pressure (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. Against the background of 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.

LITERATURE

1. Dedov I.I., Melnichenko G.A. Obesity: etiology, pathogenesis, clinical aspects. M: MIA 2004;9.
2. Nasonova V.A., Folomeeva O.M. Medical and social significance of the XIII class of diseases for the population of Russia. Scientific and practical rheumatology 2001;1:7-11.
3. Magliano M. Review Obesity and arthritis. Menopause International 2008;14:149-154.
4. Tukker A., ​​Visscher T.L.S., Picavet H.S.J. Overweight and health problems of the lower extremities: osteoarthritis, pain and disability. Public Health Nutr 2007;12:3:359-368.
5. The problem of obesity in the WHO European Region and strategies for its solution. Ed. Francesco Branca, Haik Nikogosian and Lobstein Tim. World Health Organization 2009;7.
6. Aus Tariq Ali, Nigel John Crowther. Health risks associated with obesity JEMDSA 2005;10:2.
7. Malnick S.D., Knobler H. The medical consequences of obesity. Q J Med 2006;99:565-579.
8. Calza S., Decarli A., Ferraroni M. Research article open access obesity and prevalence of chronic diseases in the 1999-2000 Italian National Health Survey. BMC Public Health 2008;8:140.
9. Alekseeva L.I., Chichasova N.V., Benevolenskaya L.I. Combination drug ARTRA in the treatment of osteoarthritis. Ter arch 2005;11:69-75.
10. Caremer P., Hochberg M.C. osteoarthritis. Lancet 1997;350:503-508.
11. Kuttner K., Goldberg V.M. osteoarthritic disorders. Rosemont. Am Acad Orthopedic Surg 1995;452-453.
12. Pelletier J.P., Martel-Pelletier J., Abramson S.B. Osteoarthritis, an inflammatory disease: Potential implication for the selection of new therapeutic targets. Arthr Rheum 2001;44:237-1247.
13. Pelletier J.P., Martel-Pelletier J. Commentary The Novartis-ILAR Rheumatology Prize 2001 Osteoarthritis: from molecule to man. Arthritis Res 2002;4:13-19.
14. Sharma L., Berenbaum F. (ed). Osteoarthritis: a companion to rheumatology. Philadelphia: Mosby Inc. 2007.
15. Felson D.T., Zhand Y. An update on the epidemiology of knee and hip osteoarthritis with a view to prevention. Arthr Reum 1998;41:1343-1355.
16. Kalichman L., Hernandez-Molina G. Hand osteoarthritis: an epidemiological perspective. Semin Arthritis Rheum 2010;39:6:465-476.
17. Zhang Y., Jordan J.M. Epidemiology of Osteoarthritis. Clin Geriatr Med 2010;26:3:355-369.
18. Felson D.T., Zhang Y., Hannan M.T. et al. Risk factors for incident radiographic knee osteoarthritis in the elderly: the Framingham Study. Arthritis Rheum 1997;40:728-733.
19. Spector T.D., Hart D.J., Doyle D.V. Incidence and progression of osteoarthritis in women with unilateral knee disease in the general population: the effect of obesity. Ann Rheum Dis 1994;53:565-568.
20. Hochberg M.C., Lethbridge-Cejku M., Scott W.W. Jr. et al. The association of body weight, body fatness and body fat distribution with osteoarthritis of the knee: data from the Baltimore Longitudinal Study of Aging. J Rheumatol 1995;22:488-493.
21. Gelber A.C., Hochberg M.C., Mead L.A. et al. Body mass index in young men and the risk of subsequent knee and hip osteoarthritis. Am J Med 1999;107:542-548.
22. Manek Nisha J., Hart D., Spector T.D., MacGregor Alexander J. The association of body mass index and osteoarthritis of the knee joint: an examination of genetic and environmental influences. Arthrit Rheum 2003;48:4:1024-1029.
23. Osteoarthritis And Obesity. A report by the Arthritis Research Campaign.
24. Cicuttini F.M., Baker J.R., Spector T.D. The association of obesity with osteoarthritis of the hand and knee in women: a twin study. J Rheumatol 1996;23:1221-1226.
25 Hart D.J., Spector T.D. The relationship of obesity, fat distribution and osteoarthritis in women in the general population: the Chingford Study. J Rheumatol 1993;20:331-335.
26. Davis M.A., Ettinger W.H., Neuhaus J.M. Obesity and osteoarthritis of the knee: evidence from the National Health and Nutrition Examination Survey (NHANES I). Semin Arthrit Rheum 1990;20:3:Suppl 1:34-41.
27. Sharma L., Lou C., Cahue S., Dunlop D.D. The mechanism of the effect of obesity in knee osteoarthritis: the mediating role of malalignment. Arthrit Rheum 2000;43:568-575.
28. Cooper C., Snow S., McAlindon T.E. et al. Risk factors for the incidence and progression of radiographic knee osteoarthritis. Arthrit Rheum 2000;43:995-1000.
29. Reijman M., Pols H.A., Bergink A.P. et al. Body mass index associated with onset and progression of osteoarthritis of the knee but not of the hip. The Rotterdam Study. Ann Rheum Dis 2007;66:158-162.
30. Felson D.T., Goggins J., Niu J. et al. The effect of body weight on progression of knee osteoarthritis is dependent on alignment. Arthrit Rheum 2004;50:3904-3909.
31. Adamson J., Ebrahim S., Dieppe P., Hunt K. Prevalence and risk factors for joint pain among men and women in the West of Scotland Twenty-07 study. Ann Rheum Dis 2006;65:520-524.
32. Busija L., Hollingsworth B., Buchbinder R., Osborne R.H. Role of age, sex, and obesity in the higher prevalence of arthritis among lower socioeconomic groups: a population-based survey. Arthrit Rheum 2007;57:553-561.
33. Becker J., Nora D.B., Gomes I. et al. An evaluation of gender, obesity, age and diabetes mellitus as risk factors for carpal tunnel syndrome. Clin Neurophysiol 2002;113:1429-1434.
34. Wendelboe A.M., Hegmann K.T., Gren L.H. et al. Associations between body-mass index and surgery for rotator cuff tendonitis. J Bone Joint Surg Am 2004;86A:743-747.
35. Leboeuf-Yde C, Kyvik K.O., Bruun N.H. Low back pain and lifestyle. Part II Obesity. Information from a population-based sample of 29,242 twin subjects. Spine 1999;15:779-783.
36. Aihie Sayer A., ​​Poole J., Cox V. et al. Weight From Birth to 53 Years: a longitudinal study of the influence on clinical hand osteoarthritis. Arthritis Rheum. 2003; 48:1030-1033.
37 Hart D.J., Spector T.D. The relationship of obesity, fatdistribution and osteoarthritis in women in the general population: The Chingford Study. J Rheumatol 1993;20:331-335.
38. Carman W.J., Sowers M.F., Hawthorne V.M., Weissfeld L.A. Obesity as a Risk Factor for Osteoarthritis of the Hand and Wrist: A Prospective Study. Am J Epidemiol 1994;139:119-129.
39. Hochberg M.C., Lethbridge-Cejku M., Plato C.C. et al. Factors associated with osteoarthritis of the hand in males: data from the Baltimore Longitudinal Study of Aging. Am J Epidemiol 1991;134:10:1121-1127.
40. Hochberg M.C., Lethbridge-Cejku M., Scott W.W. et al. Jr. Obesity and osteoarthritis of the hands in women. Osteoarthritis Cartilage 1993;1:2:129-135.
41. Grotle M., Hagen K.B., Natvig B. et al. Obesity and osteoarthritis in knee, hip and/or hand: An epidemiological study in the general population with 10 years follow-up. BMC Musculoskelet Disord 2008;9:132-137.
42. Erlangga Yusuf, Nelissen R.G., Andreea Ioan-Facsinay et al. Association between weight or body mass index and hand osteoarthritis: a systematic review. Ann Rheum Dis 2010;69:761-765.
43. Tepper S., Hochberg M.C. Factors associated with hip osteoarthritis: data from the First National Health and Nutrition Examination Survey (NHANES-I). Am J Epidemiol 1993;137:1081-1088.
44 Vingard E. Overweight predisposes to coxarthrosis. Body-mass index studied in 239 males with hip arthroplasty. Acta Orthop Scand 1991;62:106-109.
45. Cooper C., Inskip H., Croft P. et al. Individual risk factors for hip osteoarthritis: obesity, hip injury, and physical activity. Am J Epidemiol 1998;147:516-522.
46. ​​Liu B., Balkwil A., Cooper C. et al. on behalf of the Million Women Study Collaborators Reproductive history, hormonal factors and the incidence of hip and knee replacement for osteoarthritis in middle-aged women. Ann Rheumat Dis 2009;68:1165-1170.
47. Wang Y., Simpson J.A., Wluka A.E. et al. Relationship between body adiposity measures and risk of primary knee and hip replacement for osteoarthritis: a prospective cohort study. Arthrit Res Ther 2009;11:2:R31.
48. Millward-Sadler S.J., Salter D.M. Integrindependent signal cascades in chondrocyte mechanotransduction. Ann Biomed Eng 2004;32:435-446.
49 Guilak F., Fermor B., Keefe F.J. et al. The role of biomechanics and inflammation in cartilage injury and repair. Clin Orthop Relat Res 2004;423:17-26.
50. Pottie P., Presle N., Terlain B. et al. Obesity and osteoarthritis: more complex than predicted. Ann Rheum Dis 2006;65:1403-1405.
51. Matt C. Cave, Ryan T. Hurt, Thomas H. Frazier et al. McClain and Stephen Obesity, Inflammation, and the Potential Application of Pharmaconutrition Nutr. Clin Pract 2008; 23(1):16-34.
52. Das U.N. Is obesity an inflammatory condition? Nutrition 2001;17:953-966.
53. Miller G.D., Nicklas B.J., Loeser R.F. Inflammatory Biomarkers and Physical Function in Older, Obese Adults with Knee Pain and Self-Reported Osteoarthritis After Intensive Weight-Loss Therapy. J Am Geriatr Soc 2008;56:4:644-651.
54. Guerre-Millo M. Adipose tissue hormones. J Endocrinol Invest 2002;25:855-861.
55. Tilg H., Moschen A.R. Adipocytokines: mediators linking adipose tissue, inflammation and immunity. Nat Rev Immunol 2006;6:772-783.
56. Yamaguchi N., Argueta J. G., Masuhiro Y. et al. Adiponectin inhibits Toll-like receptor family-induced signaling. FEBS Lett 2005;579:6821-6826.
57. Wolf A.M., Wolf D., Rumpold H. et al. Adiponectin induces the antiinflammatory cytokines IL-10 and IL-1RA in human leukocytes. Biochem Biophys Res Commun 2004;323:630-635.
58. Mantzoros C. The role of leptin in human obesity and disease: a review of current evidence. Ann Int Med 1999;130:8:671-680.
59. Dumond H., Presle N, Terlain B. et al. Evidence for a key role of leptin in osteoarthritis. Arthrit Rheumat 2003;48:11:3118-3129.
60. Mainard D., Dumont H., Presle N. et al. Role of leptin in the pathogenesis of osteoarthritis: a clinical and experimental study. J Bone Joint Surg Br Proceedings 2008;90-B:254-255.
61. Lajeunesse D., Delalandre A., Fernandes J.C. Subchondral osteoblasts from patients show abnormal expression and production of leptin: Possible role in cartilage degradation. J Bone Min Res 2004;19:1:S149.
62. Chevalier X., Tyler J.A. Production of binding proteins and role of the insulin-like growth factor I binding protein 3 in human articular cartilage explants. Br J Rheumatol 1996;35:6:515-522.
63. Aspden R., Scheven B., Hutchison J. Osteoarthritis as a systemic disorder including stromal cell differentiation and lipid metabolism. Lancet 2001;357:1118-1120.
64. Gabriel Sh.E., Michaud K. Review Epidemiological studies in incidence, prevalence, mortality and comorbidity of the rheumatic diseases. J Arthr Res Ther 2009;11:229.
65. Denisov L.N., Nasonova B.A., Koreshkov G.G., Kashevarova N.G. The role of obesity in the development of osteoarthritis and associated diseases. Ter arch 2010;10:34-37.
66. Mendel O.I., Naumov A.V., Vertkin A.L. Osteoarthritis and cardiovascular diseases in the elderly: clinical and pathogenetic relationships. Uspekhi gerontol 2010;23:2:304-314.
67. Kadam U.T., Jordan K., Croft P.R. Clinical comorbidity in patients with osteoarthritis: a case-control study of general practice consultants in England and Wales. Ann Rheum Dis 2004;63:4:408-414.
68. Hochberg M.C. Mortality in osteoarthritis. Clin Exp Rheumat 2008;26:5: Suppl 51:120-124.
69. Loy G., Saltman D., Kidd M. Comorbidities of osteoarthritis. 2004 Research Conference, College of Health Sciences.
70. Jordan K.M., Arden N.K., Doherty M. et al. EULAR Recommendations 2003: an evidence based approach to the management of knee osteoarthritis: Report of a Task Force of the Standing Committee for International Clinical Studies Including Therapeutic Trials (ESCISIT). Ann Rheum Dis 2003;62:12:1145-1155.
71. Jordan K.M., Arden N.K., Doherty M. et al. EULAR evidence based recommendations for the management of hip osteoarthritis: report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis 2005;64:669-681.
72. Zhang W., Moskowitz R.W., Nuki G. et al. OARSI recommendations for the management of hip and knee osteoarthritis, Part II: OARSI evidence-based, expert consensus guidelines. Osteoarthritis Cartilage 2008;16:137-162.
73. Christensen R., Bartels E.M., Astrup A., Bliddal H. Effect of weight reduction in obese patients diagnosed with knee osteoarthritis: a systematic review and meta-analysis. Ann Rheum Dis 2007;66:4:433-439.
74. Felson D.T., Zhang Y., Anthony J.M. et al. Weight loss reduces the risk for symptomatic knee osteoarthritis in women. The Framingham Study. Ann Int Med 1992;116:535-539.
75. MacLean C.H., Mojica W.A., Morton S.C. et al. Effects of omega-3 fatty acids on inflammatory bowel disease, rheumatoid arthritis, renal disease, systemic lupus erythematosus and osteoporosis. Evidence Report/Technical Assessment no. 89. AHQR Publication no. 04-E012-2. Agency Healthcare Res Quality (Rockville) 2004.
76 Maroon J.C., Bost J.W. Omega-3 fatty acids (fish oil) as anti-inflammatory: an alternative to nonsteroidal anti-inflammatory drugs for discogenic pain. Surg Neurol 2006;65:4:326-331.
77. Nasonov E.L., Karateev A.E. Non-steroidal anti-inflammatory drugs: new aspects of application in rheumatology and cardiology. Rus med zhurn 2003;23:1280-1284.
78. Antman E.M., Bennett J.S., Daugherty A. et al. Use of Nonsteroidal Antiin-flammatory Drugs: An Update for Clinicians: A Scientific Statement From the American Heart Association. Circulation 2007;115:1634-1642.
79. Page J., Henry D. Consumption of NSAIDs and the development of congestive heart failure in eldery patient: an unrecognized public health problem. Arch Int Med 2000;160:777-784.
80. Alvarez-Soria M.A., Largo R., Calvo E. et al. Differential anticatabolic profile of glucosamine sulfate versus other anti-osteoarthritic drugs on human osteoarthritic chondrocytes and synovial fibroblast in culture. Osteoarthr Cartil 2005;13:Suppl A:309.
81. Clegg D., Reda D., Harris C.L. et al. Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis. N Engl J Med 2006;354:8:795-808.
82. Naumov A.V., Vertkin A.L., Mendel O.I. How to improve the safety and effectiveness of "anti-arthrosis" therapy in patients with somatic pathology. RMJ 2007;15:26:2012-2019.