Obesity is a cause of leg and back pain. Why do fat people have joint pain? Scientists have found out how losing weight affects the condition of the knee joints. Does obesity of the 2nd degree affect the joints?

R. S. EVTEEVA, Candidate of Medical Sciences

The direct dependence of joint diseases on obesity is evidenced by the following fact: among patients with deforming arthrosis, approximately half are overweight. This pattern is explained by: that in an obese person the load on the joints and ligaments of the legs and spine increases.

Here's a simple arithmetic calculation. At the knee joint, the femoral condyles rest on the menisci. The area of ​​each meniscus is 14.5 square centimeters. When walking, a person whose body weight does not exceed 65-70 kilograms, the load on each square centimeter of the meniscus is 4.5 kilograms.

The pressure on the supporting surface of the joint increases according to the increase in body weight. So, with a body weight of 1OO kilograms, it increases to 6.9 kilograms, and with a body weight of 120 kilograms, it increases to 8.3 kilograms per square centimeter.

Thus, excess body weight plays a critical role in the development of joint disease, and the more stress a joint experiences, the faster it wears out.

Excess body weight also contributes to impaired blood and lymph circulation, which, in turn, leads to stagnation and deterioration in the nutrition of joint tissues. In obese people, metabolic processes usually suffer and flat feet develop.

Obesity is becoming one of the causes of non-inflammatory diseases of the joints of the legs and spine, which are observed 4 times more often than inflammatory diseases. Most of them belong to the group of so-called degenerative-dystrophic ones. This is deforming arthrosis of various joints of the limbs, osteochondrosis, spondylosis.

In these diseases, the pathological process develops primarily in the intervertebral discs and cartilage tissue covering the articular ends of the bones.

With the diseases in question, the cartilage softens, disintegrates, cracks appear in it, and in some places it even completely collapses, as a result of which the articular ends of the bones come closer together and friction occurs during movement. Along with this, bone tissue grows along the edges of the articular surfaces of the bones, where the mechanical load is less. Spikes of various shapes are formed, which damage nearby soft tissues - the joint capsule and ligaments. The knee, hip, and ankle joints are more often and more severely affected.

The onset of the disease is usually invisible to a person and can be manifested by rapid physical fatigue, a crunch in the joint. Further

deforming arthrosis makes itself felt by pain. At first it occurs only when moving after a state of rest, then after prolonged or increased load. If the process progresses, the pain intensifies in the morning when moving, then subsides, in the evening it increases again as the load increases, and at night at rest it gradually subsides.

Pain causes muscle contraction, which increases pressure on the articular surfaces of the bones, and consequently on the cartilage, which changes even more. Patients feel “tightening”, “stiffness” in the joints, the function of which is impaired: flexion, extension, walking up stairs, and using transport are difficult. All this causes great suffering, forces you to change your usual way of life, and often impairs your ability to work.

A kind of vicious circle develops. Due to pain in the joints, a person tries to limit movements, and physical inactivity contributes to an even greater increase in body weight and the progression of joint disease. This is more often observed in women. After all, among them there are 2-3 times more obese than among men.

We, doctors, prescribe various medications and physiotherapeutic methods of treatment to such patients. But the main, decisive factor in the development of joint diseases of non-inflammatory origin is the reduction of the patient’s body weight. This can be achieved by reducing the calorie content of food, limiting foods rich in carbohydrates: sugar, jam, confectionery and flour products and, conversely, increasing the proportion of vegetables and fruits in the diet that give a feeling of fullness.

But it’s even better to prevent weight gain and constantly keep it at a normal level.

Academician RAMS V.A. NASONOVA 2, Ph.D. O.I. MENDEL, MD head of the laboratory L.N. DENISOV 2, doctor of medical sciences, prof. A.L. VERTKIN 1, Doctor of Medical Sciences, Head of Lab. L.I. ALEXEEVA 2, Doctor of Medical Sciences, Associate Professor. A.V. NAUMOV 1

1 Moscow State Medical and Dental University, 2 Research Institute of Rheumatology of the 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 among the most pressing 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, as a rule, 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 are defined as abnormal or excessive accumulation of fat that can lead to health problems. According to the WHO definition, “overweight” corresponds to a BMI≥25, and “obesity” corresponds to a BMI≥30. BMI is a weight-for-height ratio widely used to classify the conditions of overweight and obesity in the adult population (BMI = body weight (kg) / /height 2 (m 2)). According to WHO, in 2005, approximately 1.6 billion adults (over 15 years of age) worldwide were overweight and at least 400 million adults were obese. The results of sample 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 more than 700 million to be obese. From an etiological and pathogenetic point of view, obesity is understood as 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 demonstrated 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 progressively increases as BMI increases. People with 40% excess body weight have a 2 times higher risk of premature death compared to people with average body weight. The range of diseases associated with obesity is quite wide. Most often associated with obesity: diabetes mellitus (DM) type 2, arterial hypertension (AH), dyslipidemia, coronary artery disease, heart failure (HF), cerebrovascular diseases (increased risk of strokes), respiratory diseases (sleep apnea syndrome, asthma) , cholelithiasis, non-alcoholic cirrhosis of the liver and OA.

Osteoarthritis is the most common and widespread joint disease associated with age, leading to the development of functional failure and subsequent disability in adults. According to current forecasts, increasing life expectancy and global population aging may make OA the fourth leading cause of disability by 2020 (WHO). Before 1986, there was no clear definition of the disease. Most authors considered OA to be a disease of unknown etiology, which primarily affects articular cartilage and subchondral bone, in contrast to rheumatoid arthritis, where changes primarily occur in the synovial membrane. Around the same year, the OA Subcommittee of the American College of Rheumatology proposed to define OA as a heterogeneous group of conditions that produce symptoms and signs that are associated with disruption of articular cartilage integrity and changes in subchondral bone. The present definition of the disease was adopted in 1994 at the workshop “New Perspectives in 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 joint, including subchondral bone, ligaments, capsule, synovial membrane and periarticular muscles. It should be noted that traditionally OA was considered a degenerative joint disease, but recently more and more evidence has emerged 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 formation of new bone tissue. In Russia, about 15 million people suffer from OA, which is 10-12% of the country's population, and the incidence growth rate is approximately 20% per year. In the United States, OA affects more than half of people over the age of 65 and virtually every person over 75. 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 local (localized in one joint) or generalized (three joints or more). There is no clear relationship between clinical symptoms and radiographic findings. For example, it has been found that people aged 65 to 93 years have radiological signs of OA in 33% of cases, but only 9.5% of them have clinical manifestations. At the same time, in a number of patients with pain syndrome characteristic of OA, no or minimal radiological changes are detected. To establish a diagnosis and assess the progression of OA, the classification (criteria) of Kellgren and Lawrence is most widely used. Most epidemiological studies rely on radiological manifestations of OA and the duration of pain in the joint. According to various researchers, the frequency of detection of OA in autopsies 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 general constitutional factors (old age, gender, obesity, heredity, reproductive function) and mechanical factors. The opinion that OA is a group of diseases that differ, in particular, in the affected joints, but have signs of a common pathological process that leads to joint failure, arose largely as a result of the analysis of risk factors for different localizations of the disease. Knee osteoarthritis is more common in women and often affects black Americans. This disease is usually preceded by traumatic damage to the joints. Local mechanical factors play a major role in the progression of knee OA. Valgus or varus deformity significantly increases the risk of progression of tibiofemoral OA. Contusions (injuries) to the joints significantly increase the risk of OA. Retrospective analyzes show that knee injuries in childhood or adolescence significantly increase the risk of knee OA at age 65 years. 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-Perthes disease, etc. The risk of developing OA in people with congenital musculoskeletal defects musculoskeletal system increased 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. Thus, Stecher (1941) suggested that the formation of Heberden's nodes is a congenital autosomal sex-mediated feature of OA, since, according to his data, Heberden's nodes were found 10 times more often in women than in men. Moreover, in mothers and sisters of patients, Heberden's nodules were detected 2 and 3 times more often, respectively, than in women of the same age in the population. The incidence of OA in families of patients suffering from 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. This primarily applies to primary OA of the knee joints, in which a clear relationship has been identified between the level of BMI and the risk of OA.

Numerous studies (Framingham, 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 information center of 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 people with a BMI of 25 kg/m2. In people with a high degree of obesity (BMI 36 kg/m2 or more ) the risk of knee OA was 14 times higher than in people with a normal BMI. In addition, obesity was associated with both symptomatic OA and OA without clinical manifestations but with radiographic changes. A double-controlled study by F. Cicuttini showed that each kilogram increase in body weight increases the risk of developing radiographic 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 joints (according to radiographic examination) in depending on BMI: 6.2 for BMI<23,4 кг/м 2 и 18 для ИМТ>26.4 kg/m2. 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. As numerous studies have shown, 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, a high prevalence of pain in the knees, hips, hands, back and neck was found, and the incidence of pain in the knees and hips was 2 times higher in obese people. In a review by L. Busija et al. In a study of 7,800 Australians, overweight people were twice as likely to be diagnosed with OA than those with a normal BMI (groups matched by age and socioeconomic status). According to the Italian National Health Survey for 1999-2000. , OA and back pain were significantly more common in women with grade II-III 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 average body weight, while in women, carpal tunnel syndrome developed 3 times more often than in men. It has also been found that obese individuals have a significantly higher risk of developing rotator cuff impingement syndrome than the general population. In a case-control study involving 311 patients undergoing surgical treatment for rotator cuff compression syndrome, it was found that the risk of developing this syndrome in people with increased body weight is 25% higher, and in people with moderate obesity - 80-120% higher. % and 300% higher in individuals with a BMI >35 kg/m2. A Danish study of 29,424 twins found a relationship between chronic and recurrent back pain and obesity.

There is enough data indicating a connection between OA of the hand joints and obesity. M. Hochberg et al. in the framework of the Baltimore study, they found a relationship between metabolic and some physiological factors (including age) and OA of the hand joints in men. The same researchers (1993) presented data on the association of OA of the joints of the hands in women with age, waist/hip index above average and percentage of fat. Researchers did not find any connection between hand OA and BMI. F. Cicuttini et al. in a study of middle-aged female twins found that obesity is an important risk factor for the development of OA of both the knee and carpometacarpal joints of the hands, with a significant increase in risk of 9-13% for each kilogram of body weight. A. Sayer et al. A cohort study of 1467 men and 1519 women born in 1946 found that hand OA in men was associated with increased body weight at ages 26, 43, and 53 years and at birth. However, the authors did not find a similar relationship in women. M. Grotle et al. A 10-year prospective cohort study of 1894 people 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 recently published systematic review by Erlangga Yusuf et al. 25 studies on hand OA and obesity were analyzed. 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 estimated risk ratio of 1.9, and further high-quality cohort or randomized controlled studies are needed. Although the mechanism by which obesity may increase the risk of developing OA remains unclear, these findings support the important role of obesity in the development of hand joint OA.

Literature data reflecting the relationship between obesity and hip OA are mixed. A number of researchers have identified a clear relationship between BMI and the risk of hip OA, while others have not found it. Thus, S. Tepper et al. A cross-sectional cross-sectional study in the United States of 2,358 people over the age of 55 found no association between increased body weight and the distribution of body and thigh fat. In contrast, a case-controlled study conducted in Sweden (E. Vingard et al.) involving 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, having studied the data of 1.2 million people aged 18 to 67 years examined for tuberculosis, including examination of the hip joints, they identified 28,425 people who subsequently underwent total hip arthroplasty for primary OA. Researchers found a clear association between height, BMI and hip arthroplasty. An increase in BMI by 5 kg/m2 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 a more than 8-fold higher risk compared with underweight men, while obese women had a 5-fold higher risk compared with 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 develops 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 increase in height increased the risk of subsequent arthroplasty by 17% (95% CI 13–21%) among men and by 46% (95% CI 43–50%) among women. B. Liu et al. A prospective cohort study of 490,532 UK women aged 50–69 years recruited from 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 arthroplasties and 69% of knee arthroplasties in middle-aged women in the UK are attributed to obesity. This clinical epidemiological study found that reproductive history and hormonal factors influence the risk of hip and knee arthroplasty for OA in middle-aged women, more so for the knee than for 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. Use of hormone replacement therapy was associated with a significant increase in hip and knee arthroplasty rates, whereas previous use of oral contraceptives had no effect.

Y. Wang et al. in an Australian prospective cohort study of 39,023 healthy volunteers, found that the risk of primary knee and hip arthroplasty for OA was associated with the amount of fat mass and central 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 are more significant in the knee than in the hip.

Thus, most authors pay attention to the existing cause-and-effect relationship between OA and obesity. The effect of increased stress on articular cartilage in people with increased body weight may explain the increased risk of knee OA. Undoubtedly, increased adipose tissue mass itself increases the load on the skeleton and leads to damage to musculoskeletal tissue. Recently, pressure-sensitive mechano-receptors connected to the extracellular matrix by a signaling cascade have been discovered on the surface of chondrocytes. Three types of signaling receptors have been found on chondrocytes: stretch-activated channels, α5β1-integrin, and CD44. Compression and stretch stimulate integrin and stretch-activated channels, leading to both the activation of a signaling cascade of reactions (mitogen-activated protein kinase, NFχB) and the production of second messengers (calcium, tri-phosphatinositol and cyclic adenosine monophosphate). Once mechanoreceptors are activated, cytokines, metalloproteinases, prostaglandins, or NO may 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 activation of mechanoreceptors.

However, current scientific evidence allows us to evaluate the role of obesity as a risk factor for OA and other chronic conditions much more broadly than simply the effect of increased BMI. The effect of increased stress on articular cartilage in people with increased body weight may explain the increased risk of knee OA. However, the fact that OA often develops in joints unrelated to the direct effects of increased weight suggests that there are some other mechanisms associated with obesity that can alter the metabolism of cartilage and bone tissue and lead to the development of the disease.

Metabolic disorders in OA and obesity
Adipose tissue is not a passive energy store; 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 adipose tissue produces a large amount of adipokines or adipocytokines - peptide hormones. Adipokines have a variety of biological effects and influence the severity of processes in many organs directly or through neuroendocrine mechanisms, interacting with pituitary hormones, insulin, and catecholamines. They also play a certain 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 - complement system factors: plasminogen activation inhibitor-1 (PAI-1), fibrinogen, angiopoietin-related proteins, complement factor-3; Type 3 - chemoattractants (chemotactic molecules): chemotactic monocyte protein-1 (MCP-1), macrophage inflammatory protein (MIP-a1). The fact that adipose tissue produces and accumulates a number of pro-inflammatory cytokines gives grounds to regard obesity as a mild inflammatory condition. This also combines obesity with OA, which is also regarded as a low-inflammatory condition: in both of these diseases, high levels of inflammatory biomarkers are determined - IL-β, TNF-α, TNF-α receptors sTNFR1 and sTNFR2, C-reactive protein (CRP).

Adipokines such as leptin and adiponectin, which act on cartilage, bone tissue and the vascular wall, deserve special consideration. Adiponectin is a key 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 macrophage response to TLR4 by activating ADIPOR1. Thus, adiponectin suppresses TLR4-induced NFaB activation and suppresses the secretion of interferon-α produced by LPS. By inhibiting TNF-α-induced adhesion molecule expression, adiponectin reduces macrophage adhesion, phagocytic capacity, and transmigration.

Leptin is a cytokine peptide. Structurally similar to pro-inflammatory cytokines such 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 the body's energy balance through appetite control. The action of leptin is based on the activation of the leptin receptor (LR). The binding of leptin to the 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 changes in metabolism in peripheral organs and tissues. In addition, leptin plays a role in the inflammatory response. Leptin can increase the production of proinflammatory cytokines (TNF-α, IL-6 and IL-12) by macrophages.

Recent studies have found that adipokines may accompany changes associated with OA and, moreover, may be involved in the local regulation of articular cartilage metabolism. Leptin, resistin and adiponectin are found in the synovial fluid of patients with OA. Leptin is found in both osteophytes and cartilage tissue of patients with OA, with increased expression in areas of matrix depletion, fibrillation, and chondrocyte accumulation. The level of leptin in joint tissues correlates with BMI. Leptin expression and production are increased in subchondral osteoblasts in OA compared to normal. Leptin induces the expression of growth factors, stimulates the synthesis of proteoglycans and collagen, and increases the stimulating effect of proinflammatory cytokines on the production of nitrogen nitrite in chondrocytes. D. Mainard et al. 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). Immunohistologically, the presence of leptin, IGF1 and TGFP1 in cartilage tissue (osteophytes) in OA was established. In patients with OA, high levels of leptin were determined in the synovial fluid and in the subchondral bone. Normally, leptin is not detected in cartilage tissue. It has been established that IGF1 and TGFP1 are produced by chondrocytes in OA. TGFP1 expression is strictly associated with osteophytes. TGFP induces fibrotic 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 imitate 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/m2 or more). The findings led the authors to conclude that a decrease in serum leptin levels 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 may be one of the main pathophysiological mechanisms leading to the development of OA. Obesity and OA are linked in a vicious circle: obesity is a risk factor for OA and many other diseases associated with metabolic disorders, and the dysfunction and disability that typically accompanies OA also leads to an increase in BMI and induces the development of diabetes and cardiovascular disease . According to available data, OA is most often combined with arterial hypertension (AH) and other cardiovascular diseases (atherosclerosis, ischemic heart disease). Cardiovascular disease is observed in more than 50% of patients with OA. An 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 requiring knee arthroplasty. In a study conducted by L.N. Denisov and V.A. Nasonova in 2010, 298 patients with manifest OA of the knee and hip joints were included. The relationship between obesity and the incidence of other diseases, lipid metabolism disorders and the progression of OA of various localizations was studied. There was a clear increase in the prevalence of cardiovascular diseases and diabetes as BMI increased. In the obese group (BMI>30-35 kg/m2), stage II-III OA predominated (97%), in the group of patients with BMI>40 kg/m2, 80% had stage III-IV OA.

Thus, modern scientific data allow us to consider OA as a disease pathogenetically interrelated 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 OA patients with increased body weight and comorbidity
The medical literature describes more than 50 methods of non-pharmacological, pharmacological and surgical treatment for OA of peripheral joints, mainly of the knee and hip. Generally accepted treatment regimens for OA are based on recommendations developed by leading scientific organizations involved in studying 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 research and expert opinion and are presented in a clear evidence-based format. According to the recommendations, treatment of OA should be carried out taking into account risk factors: general risk factors - age, comorbidity (obesity, cardiovascular diseases, etc.), level of pain intensity and functional impairment, presence or absence of signs of inflammation, localization and severity of structural changes. Optimal treatment for OA should include a combination of non-pharmacological and pharmacological treatments.

Non-pharmacological treatments for OA include regular patient care and education; practicing motor skills, work and rest; regular exercise therapy and aerobics; use of special orthopedic devices; dietary recommendations. The positive effect of exercise therapy on reducing joint pain 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 joints, as well as the prevention of cardiovascular pathology, it is necessary to orient patients to maintain normal body weight.

For a patient with OA and obesity, weight loss measures are a top priority, both from a mechanical stress point of view and from a cardiovascular disease prevention point of view. Weight loss is recommended if BMI>25 kg/m2. Proper correction of body weight will reduce the intensity of pain in the affected joints, help slow the progression of OA, and also significantly reduce the risk of cardiovascular complications. A systematic review of the literature examining obese individuals with diagnosed knee OA concluded that OA-related disability could be significantly reduced with a 5.1% reduction in body weight. In a study by D. Felson et al. In a study of 800 women, it was demonstrated that reducing BMI by 2 kg/m2 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 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; physical activity group; group of combinations of physical activity and diet. The greatest reduction in body weight was achieved in the “diet” and “diet + exercise” groups - by 5.3 and 6.1%, respectively; The “physical exercise” group reduced body weight to a lesser extent - 2.9%. The decrease in serum leptin levels after 6 and 18 months was significant in the “diet” and “diet + exercise” groups compared with the other two groups (β = 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 pharmacological treatment of OA are to effectively reduce pain, suppress the inflammatory process in the joint, improve the functional abilities of the joint and inhibit the progression of the disease. Relief of pain in OA is possible with the help of drugs from several groups that differ in the mechanism of action, the speed of onset and strength of the analgesic effect, as well as the safety and tolerability profile. Considering the fact that a patient with OA, as a rule, simultaneously has several somatic diseases, primarily cardiovascular diseases, dictates the need for a rigorous assessment of the expected benefits and possible risks of prescribed anti-arthrosis therapy. Against the background of comorbidity, excessive and irrational prescription 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.

International recommendations for the treatment of OA (EULAR, 2003; OARSI, 2008) indicate non-steroidal anti-inflammatory drugs (NSAIDs) as the drugs of choice for the relief of pain in OA (if paracetamol is ineffective). 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 pathology. An increased risk of cardiovascular events (myocardial infarction, stroke and sudden coronary death) may be considered a class-specific side effect for all NSAIDs. Taking NSAIDs can lead to destabilization of hypertension and progression of heart failure. It was found that taking NSAIDs in patients with a history of heart disease increases the likelihood (OR=10.5) of hospitalization for HF by 10 times 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 therapy for CVD (beta-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 recommendations for the treatment of OA. These include glucosamine (GA) and chondroitin sulfate (CS), diaceriin, hyaluronic acid preparations for intra-articular injections and avocado and soybean extracts. The greatest evidence regarding effectiveness in the treatment of OA has been obtained for cholesterol and GA. Summarizing the results of clinical studies conducted with CS and GA drugs, we can conclude that they are characterized by a slowly developing anti-inflammatory effect, comparable to NSAIDs and allowing the dose of the latter to be reduced, the possibility of combination 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 the progression of OA (according to X-ray studies). The mechanism of the therapeutic effect of cholesterol and GA in OA is associated with their ability to suppress catabolic (degenerative) and activate anabolic (restorative) processes in cartilage tissue, and provide their own anti-inflammatory and analgesic effect. Thus, cholesterol, depending on the dose used, suppresses IL-1-stimulated synthesis of prostaglandins by synovial fibroblasts, abolishes IL-1-related inhibition of hyaluronic acid synthesis, reduces IL-1-dependent collagenase synthesis and aggrecanase activity, 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 restore the balance between anabolic and catabolic processes in the cartilage matrix. In addition, cholesterol suppresses NO-induced apoptosis of chondrocytes, improves microcirculation of the subchondral bone due to inhibition of lipid synthesis, binding of E-selectin, mobilization of fibrin, lipids and cholesterol in the blood vessels of the subchondral bone. GA stops the pro-inflammatory and vascular-damaging effects of IL-1, suppresses 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, thereby preventing the release of prostaglandin PGE2 in the culture 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. It has been established that cholesterol and GA do not have entirely identical pharmacological effects; they complement and enhance each other’s effects, which determines the prospects for their joint use in the treatment of OA. A recent double-blind, placebo-controlled study, the Glucosamine/Chondroitin Arthritis Intervention Trial (GAIT), assessed the effects of different treatment regimens on pain (WOMAC) after 6 months of therapy and found that OA patients with severe knee pain (WOMAC 301) -400 mm) the effectiveness of therapy with a combination of cholesterol and GG was significantly higher (79.2%, p = 0.002 versus placebo) than in the case of monotherapy with cholesterol or GG.

The effectiveness 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 OA of the knee joints 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 stage II-III and concomitant somatic pathology. BMI>25 kg/m2 was in 100% of patients, 60% suffered from hypertension and 19% from coronary artery disease. Patients were randomized into two groups comparable in gender, age, severity of OA (pain intensity and degree of functional limitations) and concomitant therapeutic pathology. Patients in the main group received Artra together with NSAIDs, patients in the control group received only NSAIDs. During treatment, NSAIDs were discontinued in the absence of pain and exacerbation of the latter without NSAID therapy. The duration of therapy was 6 months, the effectiveness was assessed: clinical - after 3 and 6 months, MRI - after 9 months. The effect of therapy on pain (VAS, WOMAC indices), discontinuation or reduction of the dose of NSAIDs taken, functional status (WOMAC, walking speed at 15 m), disease progression (MRI of the knee joints), state of the cardiovascular system and gastrointestinal tract were assessed over time.

Assessment of the dynamics of pain syndrome (WOMAC pain) demonstrated that patients taking Artra, already 3 months from the start of therapy, had a more pronounced regression of pain syndrome compared to the control group. After 6 months of therapy, the level of pain intensity in patients of the main group was significantly lower than in patients in the control group (178.3±37.2 versus 287.4±42.8, respectively, p=0.02). The assessment of functional impairment on the WOMAC scale at the start of the study did not reveal significant differences between the observation groups. After 6 months of therapy, a significant decrease in the degree of functional impairment was observed in both groups, but 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 in pain syndrome and improvement in functional ability. Visual assessment of the condition of the knee joints using MRI before treatment and after 9 months of therapy revealed an improvement in the visualization of articular cartilage in 60% of patients in the main group, while 63.3% of patients in the control group showed negative dynamics. Thus, the positive effect of therapy in the group of patients receiving Artra, from the point of view of the clinical picture, was confirmed by data from 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 silent ischemia (PAI) of the myocardium were assessed according to the Holter study (at the beginning and after 6 months of the study ). It was found that during treatment with Artra, a significant decrease in SBP levels was observed. The difference in 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, patients in the main group had fewer episodes of BI and BBI 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 more effective relief of pain in the joints, improved functional status, a reduction in the dose of NSAIDs taken by patients and an associated reduction in the risk of side effects caused by them. During treatment with Artra in patients with OA, the number of re-hospitalizations for exacerbations of somatic diseases decreased: in the main group, 43% of patients (13 people) were re-hospitalized over the next 9 months of observation, while in the control group, 76% of patients were re-hospitalized (23 ). The total number of hospitalizations per 1 patient was 1.2 in the main group and 1.7 in the control group. Thus, given the positive effect of the drug on the dynamics of concomitant cardiovascular diseases in patients with OA and its high safety, Artra is justifiably the drug of choice for the basic treatment of OA in patients with comorbid pathology.

Considering 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 treatment methods - exercise therapy, a diet aimed at reducing BMI, organizing a work and rest schedule. Throughout the entire course of treatment, strict monitoring of blood pressure levels and ECG is necessary. As for drug therapy, NSAIDs should be prescribed to patients with OA and a high risk of cardiovascular complications with great caution, following accepted recommendations. Considering the proven clinical effectiveness, high safety (comparable to placebo) and good tolerability of cholesterol and GA drugs, they can be considered as the most preferable drugs for the treatment of clinical manifestations of OA in patients with comorbid pathology.

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Good afternoon It's finally time to talk about obesity.

This is truly an interdisciplinary problem. But I will not cite dry statistics now and say that obesity is a colossal burden on the joints. You already know all this very well. Let's approach this issue from the other side, namely, let's discuss what danger adipose tissue poses to joints.

Adipose tissue is a type of connective tissue that consists of an extensive network of vessels, collagen fibers, fibroblasts and cells of the immune system, surrounded by lipid cells - adipocytes. One of the least studied functions of adipose tissue is endocrine.

Adipose tissue produces many biologically active substances, among which adipokines and adipocytokines occupy an important place. Several dozen adipokines are already known, including leptin, adiponectin, resistin, visfatin, etc., which can secrete pro-inflammatory cytokines, such as tumor necrosis factor α (TNFα), interleukin 6 (IL6), plasminogen activator inhibitor 1, etc.

Adipokines are biologically active substances that are produced by white adipose tissue and are involved in a wide range of metabolic processes, including influencing immune and inflammatory responses. Adipokines contribute to the chronic inflammatory process, acting in conjunction with other cytokines, which together enhance the processes of proliferation in the joint.

Studies have shown that adipokine levels in patients with arthrosis are noticeably higher than in people without joint complaints. Particularly high levels of adiponectin and leptin are associated with female gender and high body mass index.

Leptin– one of the main adipokines involved in metabolic processes in arthrosis. The inflammatory process enhances the formation of leptin. Leptin is capable of inducing the synthesis of enzymes involved in cartilage damage during arthrosis. Leptin also affects the function of bone cells called osteoblasts. An increase in leptin levels by 5 ng/ml in the blood serum is associated with the progression of radiological signs of arthrosis by 38%!!!

Data on the role of other adipokines - adiponectin, resistin, visfatin - in the development and progression of osteoarthritis are contradictory.

Infrapatellar adipose tissue (surrounding the knee joint) contains not only adipocytes, but also a large number of macrophages, lymphocytes and granulocytes. It is capable of producing and releasing large amounts of leptin and adiponectin, as well as synthesizing inflammatory mediators (TNFα, IL6) in higher concentrations than even subcutaneous fat. Thus, the fatty tissue surrounding the joint will only maintain inflammation in the joint.

Friends, when we tell you that you need to lose weight, we, of course, do not want to offend you, but we only want you personally (!) to be interested in treating your disease and make an effort to do so. In the treatment of osteoarthritis, fat is definitely not your friend.

Approaches to weight loss

♀️Among non-pharmacological methods of treating osteoarthritis (osteoarthritis), much attention is paid to reducing body weight.

Maintaining normal body weight reduces the risk of arthrosis, and reducing body mass index in patients with an established diagnosis allows for a reduction in the clinical manifestations of arthrosis.

Losing weight has been shown to have a beneficial effect on joint pain. Reducing body weight by at least 5% helps reduce joint pain.

There is a dependence of the severity of clinical manifestations on the degree of weight loss. A 3-year OAI (Osteoarthritis Initiative) and a 30-month MOST (Multicenter Osteoarthritis) study involving 1,410 patients found that a 10% weight loss reduced pain more than a 5% or less weight loss. That is, the more weight loss, the better :)

The National Institutes of Health (NIH) has published clinical guidelines for identifying, assessing, and treating excess weight in adults. The basic principle of these recommendations is: “The initial goal of obesity treatment should be a reduction of body weight by 10% compared with baseline.” Although these recommendations are not intended specifically for patients with arthrosis, they should also apply to patients with joint complaints and obesity.

To reduce the body weight of patients with osteoarthritis, sometimes it is not enough just to follow a diet and exercise, which requires the inclusion of additional methods of treating obesity: drug therapy and bariatric surgery.

Although short-term weight loss can be achieved through diet and exercise, not everyone is able to maintain the results for a long time. About 75% of patients on the diet gain back most of what they lost within 1 year. The addition of drug therapy not only makes weight loss easier, but may also prevent weight gain from returning. Prescription of drugs is indicated for those patients with obesity (BMI >30 kg/m2) who cannot achieve or maintain a clinically significant degree of weight loss using diet and exercise.

In conclusion, I would like to emphasize once again that obesity is defined as a chronic low-inflammatory condition, which dictates the need for long-term treatment aimed at achieving a stable reduction in body weight, preventing or reducing the severity of serious concomitant diseases. Losing body weight in patients with arthrosis helps reduce pain and improve the functional status of patients, and also has a positive effect on the course of concomitant diseases.

Pathological increase in body weight negatively affects the condition of bones, joints, ligaments and the performance of their functions. This influence is due to several factors.

Factors that influence excess weight on the spine

In the foreground is the increased mechanical load of increased body weight on the musculoskeletal system. The main impact is taken by the spine, or more precisely, by its lumbosacral region, which bears the lion's share of the load with body weight. Due to the increased load, the intervertebral (or intervertebral) discs suffer. They consist of cartilage tissue and act as shock absorbers and spacers - they reduce the force of external influences on the spine during movement and protect the bone tissue of the vertebrae from wear.

But at the same time, they themselves often wear out prematurely. And one of the reasons for this pathological process, called osteochondrosis, is obesity. Increased mechanical pressure on the spinal column caused by obesity leads to decreased elasticity of the intervertebral discs. At the same time, the thickness of the discs, and, accordingly, the height of the intervertebral spaces, decreases. In addition, a disc that has lost elasticity and decreased in height easily displaces - a disc herniation occurs. These factors cause infringement of the sensory and motor roots of the spinal nerves between the vertebrae. Lumbosacral radiculitis forms, the leading manifestations of which are pain and limitation of movements in the lumbar region.

Further more. Over time, sensory and motor disturbances spread to the lower extremities. The muscles of the legs and thighs undergo atrophy. The final result of these pathological changes is cauda equina syndrome. The cauda equina is a figurative name for a bundle of nerve fibers passing through the spinal canal. Displacement of the vertebrae and disc herniation due to osteochondrosis lead to pinching of the cauda equina in the spinal canal. Intense pain occurs in the lower back, groin area and lower extremities. Against this background, control over the pelvic organs is often lost, and erectile dysfunction develops in men.

Structural changes occur not only in the spine, but also in the joints. With obesity, large joints are predominantly affected - the knee and hip, which are most susceptible to mechanical wear. Arthrosis forms in them - dystrophy and deformation of articular cartilage and the underlying bone tissue. In this case, the configuration of the joint is disrupted, which leads to difficulty in movements, or even to their complete absence. When knee or hip arthrosis is advanced, there is a need for endoprosthetics - replacing worn-out joints with synthetic prostheses. However, the normal functioning of endoprostheses in obesity is also problematic.

Consequences of obesity for bone tissue

Another negative consequence of obesity is osteoporosis. This term refers to a decrease in bone density. Previously, it was believed that increasing body weight automatically leads to increased strength and compaction of bones. This compensatory mechanism is supposedly designed to increase the resistance of the musculoskeletal system to increased load.

But recently it has been found that in fact everything is not so, and bone density does not increase, but, on the contrary, decreases. This is partly due to a deficiency of vitamins A, E, D and minerals - calcium, magnesium, zinc, the balance of which is disturbed by obesity. But there is another reason - hormonal. Obesity is accompanied by a change in the ratio of hormones of the pancreas, adrenal glands, pituitary gland, and thyroid gland. Hormonal imbalance leads to impaired absorption of minerals by bone tissue. The fat cells themselves (adipocytes) are also hormone-producing. The biologically active substances they secrete, including cytokines, adiponectin, and others, activate osteoclasts. Osteoclasts are specific cells in bone tissue. The action of these cells is aimed at leaching minerals from the bones and destroying collagen, the protein that ensures bone strength.

Clinically, osteoporosis is manifested by fragility and pathological fragility of bones. For patients suffering from osteoporosis, a small impact (a push, a fall on the spot) is enough to cause a fracture. Sometimes fractures occur spontaneously - the so-called. spontaneous fractures. In addition, osteoporosis serves as an additional factor in the development of osteochondrosis, arthrosis, and spinal curvature. All these changes in the musculoskeletal system are essentially irreversible. However, losing body weight slows down their progression and makes their course easier.

The most complete answers to questions on the topic: “obesity and joint diseases presentation.”

More articles: How much does knee replacement surgery cost?

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