TREATMENT AND PREVENTION OF OSTEOARTHROSIS: DRUGS OF CHOICE (Part 1)

The cartilaginous joints of the bones are covered with a synovial membrane, which provides protection and reliable “grip”. It also secretes synovial fluid, which performs 2 important tasks:

• provides nutrition that maintains cartilage in working condition;
• serves as a lubricant between cartilages to reduce friction.

Osteoarthritis affects the cells that produce the main element of synovial fluid - glucosamine. Due to lack of nutrition, cartilage loses its elasticity and cracks. The distance between them at the ends of the bones (articular space) decreases, and the lack of lubrication increases friction and accelerates the process of thinning of the cartilage tissue. As a result, the joint loses functionality. All these changes lead to pain, and then to the inability to move normally.

Symptoms of osteoarthritis (osteoarthritis)

The difficulty of timely diagnosis of the disease lies in the fact that in the early stages patients practically do not notice any deviations from the norm. There is no pain (or it is mild), movements are not constrained. You can find out about the development of osteoarthritis from the results of an x-ray or ultrasound. The cartilage begins to lose its smoothness, and bone growths appear.

The first symptoms of osteoarthritis for which you should consult a specialist are:

• Pain when moving or even just trying to perform any action;
• Limitation of mobility in the first time after sleep;
• Painful sensations when touching the joint.

Another option is possible: in some patients, pain appears immediately in the early stages of the disease. This is due to the inflammatory process in the joint. Broken pieces of destroyed cartilage irritate the joint lining, causing inflammation. This process does not go unnoticed and interferes with movement. Particularly severe pain occurs at night, closer to the morning.

As the disease progresses, osteoarthritis increasingly affects cartilage tissue. To compensate for the damage, the body tries to expand the surface of the joint, which is why bone spurs appear. At this stage, discomfort increases significantly. Every movement becomes difficult and painful. The joints cannot cope with the load, and bone growths only aggravate the situation, reducing mobility.

Ultimately, the disease leads to complete loss of joint functionality. The cartilage tissue is destroyed, the friction between the bones becomes maximum. In fact, a person loses the ability to move. In addition, the muscles next to the joint become damaged and lose their ability to contract (muscle atrophy).

Common symptoms of osteoarthritis are:

• Pain in the joint (when moving, at night, when trying to move - “starting pain”);
• Reduced mobility (heaviness when performing actions, restrictions due to acute pain);
• Characteristic crunching sound during movements;
• Stiffness or stiffness (in the morning);
• Loss of mobility (last stage of the disease).

Drug treatment of osteoarthritis

ABOUT

Steoarthrosis (OA) is a heterogeneous disease that occurs most often in people over 60 years of age and is characterized by severe pain and often the presence of inflammatory signs that bring the patient to the doctor.
Pain is the most common symptom in OA
, so treatment of the disease is aimed primarily at reducing pain and, as a result, improving joint function.
10–30% of patients with OA develop varying degrees of disability, so the ability to influence the natural history of the disease would be of great social and economic importance. Traditional treatment for OA
consists primarily of pain management, which begins with various
non-pharmacological methods
, including patient education, physical therapy, transcutaneous stimulation, and others.
However, if non-pharmacological treatment methods are insufficiently effective, drug therapy is required. The action of most drugs is aimed primarily at treating the symptoms of the disease, although some of them are considered as drugs that affect the catabolic and anabolic processes that occur when cartilage is damaged. These drugs are classified as disease-modifying drugs. The choice of drugs and the selection of combinations of various treatment methods remain strictly individual (Table 1). Knowledge of the mechanisms of action, effectiveness, contraindications when prescribing drugs, and the safety profile of drugs is extremely important. Despite the relatively long period of drug use, many questions remain regarding symptomatic treatment. Hierarchically, the first place is occupied by analgesic drugs
. The use of acetaminophen in OA was first recommended by Bradley et al. [1], who showed that 4.0 g of acetaminophen per day was comparable in effectiveness to two doses of ibuprofen (1200 mg and 2400 mg) in patients with OA of the knee and hip joints, and the drug was better tolerated. A study of the mechanism of action of the drug revealed the presence of high analgesic, antipyretic and slight anti-inflammatory activity [3,4]. In vitro, high doses of acetaminophen inhibited prostaglandin synthesis [5]. Acetaminophen appears to act on the central nervous system through inhibition of prostaglandin E2 synthesis and has no effect on prostaglandin synthesis in peripheral tissues [b].

Further study of acetaminophen in terms of its effectiveness, the risk of adverse reactions, as well as the cost of treatment, showed the advantage of its use in patients with OA with mild to moderate pain, but it was noted that clinical effectiveness is higher with non-steroidal anti-inflammatory drugs

(NSAIDs) [2]. In addition, there is evidence of hepatotoxicity and the potential damaging effects of acetaminophen on the kidneys [7], in connection with which attention is drawn to the fact that when taking about 60 g of alcohol per day, the dose of acetaminophen should not exceed 2.0 g per day. The advantage of the drug over other analgesics is its low toxicity for the gastrointestinal tract (GIT), however, in patients with severe pain and inflammation, analgesics are not effective enough and the prescription of NSAIDs is required.

NSAIDs, having anti-inflammatory, analgesic and antipyretic properties, are widely used to reduce pain, gel syndrome, and improve joint function in patients with OA. The choice of NSAID is usually based on the opinion of the doctor. At therapeutic doses, the clinical effectiveness of NSAIDs is approximately the same, but individual response to drugs varies widely [8]. Differences in clinical effectiveness are also influenced by the pharmacokinetic, pharmacodynamic and metabolic properties of the drugs. Although the variability in response can be explained (in part) by drug adsorption, distribution and metabolism, the most important reason for the differences in effectiveness appears to lie in potential differences in the mechanism of action of the drugs [9].

Most NSAIDs are weak organic acids and are completely absorbed when taken orally, about 95% of the drug taken is bound to serum albumin, so hypoalbuminemia, especially in older people with chronic somatic diseases, can lead to increased serum concentrations of NSAIDs and, as a consequence, to increased toxicity. Taking NSAIDs with food can reduce its absorption, as for example, this is shown for naproxen, the adsorption of which is reduced by 16% under these conditions. NSAIDs are metabolized mainly in the liver and excreted in the urine, which must be taken into account when prescribing these drugs to patients with impaired liver or kidney function. Plasma concentrations of drugs vary widely and depend on renal clearance and metabolic rate.

The residence time of drugs in plasma is of some importance in explaining the various clinical effects, according to which NSAIDs are divided into “short- and long-lived”.

The anti-inflammatory and analgesic activity of NSAIDs is associated with a decrease in the production of prostaglandins E. NSAIDs have also been shown to inhibit the formation of prostacyclin and thromboxane, exerting a complex effect on vascular permeability and platelet aggregation. The anti-inflammatory effect of NSAIDs is apparently due to inhibition of cyclooxygenase activity

(COX) is the main enzyme in the metabolism of arachidonic acid on the path of its conversion into prostaglandins.
There are at least two isoforms of COX. And although their amino acid sequence is 60% identical, they are the product of two different genes. COX-1
regulates normal cellular processes and is stimulated by hormones or growth factors. COX-1 is expressed on most tissues of the body and is inhibited to varying degrees by all NSAIDs, so many adverse reactions from the gastrointestinal tract are explained by this inhibition [13].

Another isoform, COX-2

, which is usually not detected in tissues, is expressed during inflammation and is also inhibited by all existing NSAIDs to a greater or lesser extent, as well as by glucocorticosteroids [34], which distinguishes it from COX-1.

Based on these data, a new group of drugs was created - specific COX-2 inhibitors, which include celecoxib and rofecoxib, which are approximately 300 times more effective in suppressing COX-2 compared to COX-1 [15]. Clinical studies in OA showed that both drugs had an effect on pain comparable to the effect of naproxen, ibuprofen and diclofenac, and had almost no damaging effect on the gastrointestinal mucosa and platelet aggregation [16,17,18].

However, evidence is accumulating that the anti-inflammatory and analgesic effects of NSAIDs are not explained solely by COX inhibition. It is assumed that NSAIDs inhibit the activation and chemotaxis of neutrophils and reduce the production of toxic oxygen radicals in stimulated neutrophils [5], inhibit the activity of the transcription factor NF-kB, thus inhibiting the stimulation of nitric oxide synthetase [20].

In addition, NSAIDs, being inhibitors of prostaglandins, which are believed to inhibit apoptosis (programmed cell death), can help normalize the life cycle of cells at the site of inflammation [14].

Arachidonic acid is exposed not only to COX, but also to 5- and 12-lipoxygenases. To date, evidence is accumulating that the mechanism of development of NSAID-induced gastropathy may include alternative processes of conversion of arachidonic acid into leukotrienes under the influence of 5-lipoxygenase (5-LOX). This was the reason for the creation of a new group of drugs capable of inhibiting COX-1 and COX-2. The first study of such a drug - licofelone

(200 mg x 2 times a day) was carried out in 148 patients with OA in a comparative trial with naproxen (500 mg x 2 times a day) and placebo [19]. Licofelon turned out to be equal in effectiveness to NSAIDs, was extremely well tolerated and did not cause damage to the gastrointestinal tract,

Thus, the study of the mechanisms of action of NSAIDs led to the creation of a new classification of drugs (Table 2), based on the selectivity of action against COX, allowing the doctor to individually select the most effective and safe drug.

Numerous controlled studies indicate a significantly higher effectiveness of NSAIDs compared to placebo, therefore, when choosing a drug, it is necessary to take into account its safety, effect on cartilage, and, given the age of patients with OA, and the presence of a large number of concomitant pathologies, compatibility with other drugs.

The general principles of using NSAIDs for OA are to use the minimum effective dose, take no more than one NSAID at a time, discontinue the drug if there is no pain, and evaluate the effectiveness of treatment after 2-4 weeks from the start of use.

For OA, the most optimal are “short-lived” drugs: ibuprofen, diclofenac, ketoprofen. The doses of drugs used for OA are usually lower than for inflammatory diseases of the joints (Table 3). To quickly relieve pain, drugs with high analgesic activity are prescribed: potassium salt of diclofenac (Rapten Rapid)

. The drug has a persistent analgesic effect much faster and longer than the sodium form of diclofenac and other NSAIDs. In addition, the drug has minimal side effects compared to ibuprofen and indomethacin. Rapten Rapid can also be recommended for introductory therapy to relieve pain with subsequent transition to another analgesic. A decrease in pain during treatment with NSAIDs is observed in approximately 60–70% of patients with OA. At the same time, individual differences in the effectiveness of NSAIDs vary widely, so the first place comes not only to the selection of the most effective drug (Rapten Rapid, etc.), but also to the assessment of real differences in the toxicity of drugs. Adverse reactions observed with NSAID treatment are presented in Table 4.

The most clinically significant are adverse reactions from the gastrointestinal tract; their occurrence is likely due to local and systemic inhibition of prostaglandin synthesis.
The spectrum of damage to the gastrointestinal tract is quite wide - from the development of esophagitis to bleeding and perforation of peptic ulcers, sometimes leading to death [13]. Data are provided on damage to the mucosa of the small and large intestines [23]. Endoscopic studies have shown that the prepyloric and antral parts of the stomach are most often affected. They are usually asymptomatic, making it difficult to estimate their true prevalence. Risk factors for the development of NSAID gastropathy include the age of patients over 60 years of age, a history of ulcers, taking antiulcer drugs for any reason, the combined use of glucocorticosteroids, and the presence of severe concomitant diseases, for example, cardiovascular [21,22]. Based on numerous clinical studies, the relative risk for gastric ulcers is 4.0–5.0; for duodenal ulcers – 1.1–1.6 and from 4.5 to 5.0 – for gastric ulcers with bleeding, perforation or death. “Long-living” NSAIDs, such as piroxicam, have greater gastrointestinal toxicity. Significantly better results were obtained using predominantly selective COX-2 inhibitors: meloxicam and nimesulide. Individual clinical studies indicate similar efficacy to standard NSAIDs, but higher safety in relation to gastrointestinal lesions.

The use of specific COX-2 inhibitors is associated with a significant reduction in the incidence of gastrointestinal ulcers compared with diclofenac and ibuprofen. In addition, severe gastroenterological adverse reactions (bleeding, perforation) occur 2–3 times less often when taking rofecoxib and celecoxib. In recent years, questions about the risk/benefit of NSAIDs in OA and the costs of gastroenterological adverse reactions have been constantly discussed. Apparently, selective COX-2 inhibitors can significantly improve the safety of treatment, especially in elderly patients with high risk factors.

If NSAIDs are insufficiently effective and poorly tolerated, other analgesic drugs are prescribed. Tramadol

– a synthetic analgesic of central action, which does not cause physical and mental dependence, is effective for pain of various origins. Schnitzer et al. [24] showed that the drug is effective against pain; in addition, the combined use of tramadol with naproxen made it possible to reduce the dose of the latter. Tramadol is used for OA in doses of 50 to 200 mg per day. Relatively common adverse reactions when using the drug (nausea, dizziness, constipation and drowsiness) can be significantly reduced by titrating the dose (over 3 days, increasing the dose by 25 mg).

In case of isolated articular damage, local remedies are used for the treatment of OA in the form of ointments, NSAID-based creams, which avoids systemic adverse reactions, especially in the elderly, and chondroitin sulfate in combination with dimethyl sulfoxide ( Chondroxide

). A form of NSAID in the form of a patch containing diclofenac has been created, which turned out to be more effective than placebo in a 2-week study in 155 patients with gonarthrosis [25], which may reduce the need for systemic drugs.

Moore et al. analyzed 86 studies to assess the effectiveness and toxicity of topical agents for the treatment of acute and chronic pain, including OA. The authors concluded that these drugs are quite effective and safe [26].

In patients with gonarthrosis in the presence of joint effusion, intra-articular injections of corticosteroids

. Unfortunately, certain aspects of this therapy remain controversial (its relative effectiveness, potentially damaging effects and potentially structure-modifying effects), so the place of long-term use of intra-articular corticosteroid therapy for the treatment of OA remains unclear - long-term double-blind studies are required. Currently, it is believed that the number of intra-articular injections into one joint should not exceed 3-4 over the course of one year.

Although NSAIDs reduce pain and inflammation, it has not yet been shown whether they slow the progression of OA or protect cartilage from mechanical or inflammatory damage.

Attempts to influence the disease began with the study of risk factors, such as obesity, excess joint stress, and were limited to recommendations for weight loss and the use of various physical exercises. Currently, agents are being developed that can slow the progression of OA. The range of drugs being studied is quite wide: from antibiotics with anti-collagenolytic activity, hyaluronate and polysaccharides to more complex drugs, including growth factors and cytokines. These drugs are called structure-modifying drugs, their role is the ability to prevent, slow down, stabilize or reverse the development of the osteoarthritis process not only in cartilage, but also in the entire joint, considered as an organ as a whole. Currently, there is no clear evidence of structure-modifying properties for humans for any drug, but certain data have been obtained for some of them.

Chondroitin sulfate

(CS) and
glucosamine sulfate
(GS) are sulfated glycosaminoglycans that are found in the extracellular matrix of articular cartilage. When taken orally, they are well adsorbed and found in high concentrations in the joint cavity. The mechanism of their action is not fully understood. Evidence has been obtained that cholesterol and HS stimulate the synthesis of hyaluronic acid and proteoglycans and inhibit the action of proteolytic enzymes, thereby enhancing anabolic processes in cartilage and suppressing catabolic ones, which may underlie their structure-modifying effect. There is evidence of their ability to suppress the formation of superoxide radicals and the synthesis of nitric oxide, which apparently determines their analgesic effect. In vivo experimental studies found that oral or intramuscular administration of cholesterol to rabbits (with cartilage degeneration caused by chymopapain) significantly increased the content of cartilage proteoglycans compared to control animals, indicating that cholesterol protects cartilage when damaged and has the ability to support resynthesis of matrix proteoglycans [27].

Treatment of cholesterol leads to a significant reduction in pain, improvement in the functional ability of joints and allows a reduction in the dose of NSAIDs taken. The drug is well tolerated, causing virtually no side effects [28,29,30]. A meta-analysis of double-blind, placebo-controlled studies of cholesterol in 372 and 404 patients with gonorrhea and coxarthrosis confirmed the effectiveness of the drug compared to placebo and NSAIDs [31,32]. A study conducted in Switzerland [33] over the course of a year raised the question of whether cholesterol has structure-modifying properties, since the drug had a stabilizing effect on the width of the joint space and metabolic processes in the subchondral bone and cartilage, and thus, apparently, on the course of the disease. At the annual European Congress of Rheumatology, held in Stockholm (2002), the results of long-term, for 2 years, use of cholesterol (800 mg/day) in 300 patients with gonarthrosis were reported, which showed the ability of the drug to slow down the progression of OA [34 ].

Earlier short-term studies showed the effectiveness of GS compared with placebo and NSAIDs [35,36]. Recently, long-term (for 3 years) use of GS (1500 mg/day) in 212 patients with gonarthrosis confirmed not only the symptomatic effect of the drug (decrease in the functional WOMAC index), but also its ability to slow down radiological progression, which was assessed by changes in the width of the joint gaps [37].

Relatively recently, work on the combined use of

these drugs.
Thus, a double-blind placebo-controlled study for 16 weeks of a combination of glucosamine hydrochloride
(1500 mg/day) and
cholesterol
(1200 mg/day) in 34 men with gonarthrosis and pain in the lower back showed a significant reduction in joint pain, but not in back [38]. Another study reported combination therapy for temporomandibular joint OA [39]. However, promising data on the structure-modifying effects of cholesterol and GS require further confirmation in long-term controlled studies.

Hyaluronate

(GL) is a polysaccharide consisting of a long chain of disaccharides, produced in joints by chondrocytes and synovial cells. Currently, 2 GL drugs are used, administered intra-articularly: low molecular weight (m.v. 500,000–730,000 daltons) and high-molecular weight (m.w. 6,000,000 daltons). The clinical use of GL was due to studies of synovial fluid in OA, which showed a significant change in its rheological properties compared to synovial fluid of a healthy joint. Therefore, it was assumed that the introduction of GL would restore the protective and so-called shock-absorbing properties of synovial fluid [40]. However, the long-term clinical effect could not be explained by these reasons alone, since the half-life of the drug was 2–8 days. Based on further studies, it was suggested that the mechanism of action of the drug is associated with the inhibition of inflammatory mediators (cytokines and prostaglandins), stimulation of anabolic and slowdown of catabolic processes in the cartilage matrix [41,42].

High molecular weight GL [43], when comparing 3 weekly injections with NSAIDs or a combination of NSAIDs and GL, was more effective than NSAIDs, and can probably be used instead of or together with NSAIDs. In a retrospective study of 336 patients with gonarthrosis, a good response was observed in 76% [44], with the treatment effect maintaining an average of 8 months. Local adverse reactions were observed in 8% of patients, ranging from minor to the development of acute synovitis with effusion, requiring intra-articular corticosteroids or a short course of NSAIDs.

A comparative study of high- and low-molecular-weight GL in 70 patients with knee OA (3 weekly injections) revealed a higher effectiveness of the first drug, with an equally small number of adverse local reactions [45]. However, the use of high and low molecular weight GL requires further research to better determine the place of this therapy and especially to assess the effect of long-term use on slowing down or reversing the development of cartilage degradation. GL is currently defined as a disease-modifying agent and is recommended for patients who do not respond to other therapies or who cannot tolerate NSAIDs.

Confirming the structure-modifying properties of drugs in humans is extremely difficult, since OA is usually a very slowly progressive disease. It must be taken into account that it is possible that any remedy effective against the symptoms of a disease may potentially have structure-modifying properties. Likewise, it is known that any drug with structure-modifying properties has a small and, as a rule, delayed effect on the symptoms of the disease. In addition, methods for studying disease progression are limited, making clinical testing of structure-modifying drugs challenging. To demonstrate structure-modifying properties, clinical trials often use knee radiographs to assess OA outcomes; Methods are being developed that can assess the surface and volume of cartilage.

Drugs that modify symptoms of the disease have some advantage in assessing the effectiveness of OA treatment

. However, treating patients with OA is challenging. First, in a heterogeneous disease with an unpredictable course, such as OA, it is important to remember that treatment should not harm the patient. Secondly, it is difficult to create a unified treatment algorithm, since individual differences in the course of the disease are also great. Therefore, treatment of patients with OA should be considered taking into account an assessment of the benefits/risks of the therapy.

An important point at the beginning of treatment is the characterization of the pain syndrome in terms of the presence or absence of inflammatory changes. The assumption that a significant proportion of patients had only pain without signs of inflammation formed the basis for the creation of an algorithm for the treatment of patients with OA of the knee and hip joints, proposed by the American College of Rheumatology in 1995 [10,11]. If non-pharmacological treatments were insufficiently effective, analgesics (acetominophen 4.0 per day) were recommended as first-line drugs, followed by local therapy (except for hip OA), low doses of NSAIDs or other analgesics such as tramadol, and then therapeutic doses NSAIDs, intra-articular injections of glucocorticosteroids, hyaluronic acid, sulfated glycosaminoglycans. For patients at high risk of developing gastrointestinal complications, preventive treatment

misoprostol, proton pump inhibitors, high doses of H2-histamine receptor antagonists.

And although these recommendations have not lost their relevance, evidence is accumulating on the need for earlier prescription of anti-inflammatory therapy [12]. In addition, acetaminophen was not completely safe as reported in early studies, and Pincus et al. [2] noted the greater effectiveness of NSAIDs compared to simple analgesics.

Specific COX-2 inhibitors have a significantly higher benefit/risk ratio compared to traditional NSAIDs. These drugs appear to be considered as first-line drugs, particularly in patients with moderate to severe pain, with or without signs of inflammation, joint swelling and joint effusion. Patients with insufficient effectiveness and poor tolerability of these drugs should be treated with traditional NSAIDs with mandatory combination with preventive therapy, especially in those patients who have risk factors for the development of adverse events. It must be taken into account that most patients over 60 years of age have at least one risk factor for complications.

If there is a large effusion in the joint, the condition is significantly alleviated by intra-articular injection of steroids (injection into the hip joint is undesirable), but not more than 1-2 times a year.

The introduction of hyaluronic acid is especially indicated when treatment with analgesics and NSAIDs is ineffective, and there are also contraindications for their use.

Sulfated glycosaminoglycans may turn out to be very promising, not only because of their effectiveness and, possibly, structure-modifying effects, but also due to their good tolerability, which does not require medical monitoring, unlike taking NSAIDs.

Probably, the time of treating OA with monotherapy is becoming a thing of the past, and the expansion and deepening of knowledge about the pathogenesis of the disease, the mechanisms of action of drugs on different pathogenetic links of the disease allows us to hope that treatment regimens and new drugs will soon be developed that will be able to change the natural course of OA.
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45. Wobig M, Bach G, Beks P, et al. The role of elastoviscosity in the efficacy of viscosupplementation for osteoarthritis of the knee: a comparison of hylan G–F 20 and a lower–molecular–weight hyaluronan. Clin Ther, 1999 Sep; 21(9): 1549–1562.

Causes of osteoarthritis (osteoarthritis)

There is no specific cause of osteoarthritis. Most often, a combination of various factors leads to the disease. However, there are certain risk groups that are most susceptible to this disease. The likelihood of developing osteoarthritis increases in the presence of the following circumstances:

1. Aging. With age, all mechanisms of the body begin to lose their power. Most patients with osteoarthritis are people over 40 years of age. Age is not a necessary factor for the onset of arthrosis, but the presence of additional provocateurs increases the risk.

2. Injuries. One of the common causes of the disease. Bruises, fractures, and dislocations do not lead to the immediate appearance of osteoarthritis, but weaken the joint, which causes the development of the disease in the future.

3. Regular increased load. Heavy physical labor leads to microtrauma of the joint. For example, football players develop arthrosis of the knee joint, and boxers develop arthrosis of the wrist.

4. Concomitant diseases. Any disease weakens the body. Osteoarthritis often affects people who are overweight, diabetes, and varicose veins.

5. Climax. During menopause, the production of important hormones that can protect the body decreases. This is a combination of two factors: age and weakened immunity. As a result, women get sick more often than men.

6. Flat feet. Flattening of the arches of the feet interferes with shock absorption when walking. The load from the foot is transferred to the knee joint, as a result of which arthrosis of the knee joint can develop.

7. Congenital abnormalities. Some congenital anomalies (connective tissue dysplasia, dislocations, scoliosis) significantly increase the likelihood of osteoarthritis. But with timely and correct treatment, the disease will not appear.

A general definition of the cause of osteoarthritis is a discrepancy between the load and the body’s capabilities.

Diet

Proper nutrition is not the main factor in the prevention of osteoarthritis, but it will also make its contribution to maintaining healthy joints. Recommended:

• a diet balanced in calories, macro- and micronutrients;
• sufficient amounts of vitamins and minerals;
• exclusion of spicy, canned, excessively fatty foods, alcohol, as well as products with artificial flavors and dyes;
• minimizing fast carbohydrates.

Collagen and omega-3 acids have a good effect on the condition of cartilage, which is why aspic and sea fish and olive oil should always be present in the diet.

Gonarthrosis (arthrosis of the knee joint)

Despite the commonality of symptoms, the consequences of the disease vary depending on the location of the lesion. Therefore, let us dwell in more detail on the types of arthrosis.

One of the most common forms of arthrosis. The knee joint is under attack. Most often the disease manifests itself after 45 years. Additional provocateurs are excess weight, injuries or bruises.

The risk group also includes athletes: football players, track and field athletes, weightlifters, etc. At the same time, according to statistics, more women fall ill. The disease can affect both legs or one. In this case, painful sensations may appear only on one leg.

OA treatment algorithm developed by ESCEO

ESCEO recommendations, which determine the priority of treatment measures in patients with knee OA, were presented in 2014 [8], and they were supplemented in 2021 [9]. In 2021, taking into account new evidence of the effectiveness and safety of drugs used to treat OA, the algorithm was updated [10]. The developers reaffirmed that treatment should include a combination of nonpharmacological and pharmacological methods (Fig. 1).

Non-drug treatment is recommended throughout the entire period of patient management. In addition to educational programs, physical therapy (exercises should be personalized and adapted to the needs and preferences of each patient) and weight loss, treatment should include correction of the disturbed joint axis (varus/valgus) using orthopedic devices (orthoses, arch supports), unloading of joints during late stages of OA (use of a cane, crutches, walkers, etc.).

In this version of the ESCEO algorithm, in addition to thermal treatment methods (using cold or heat) and manual therapy, for the first time the following are recommended: mechanotherapy, hydrotherapy, exercises in water, taping and Tai Chi.

As for drug treatment, the step-by-step prescription of drugs was retained (see Fig. 1).

Coxarthrosis (arthrosis of the hip joint)

Arthrosis of the hip joint is one of the most severe forms of arthrosis.

This type of osteoarthritis is the most difficult to treat. The disease manifests itself at retirement age, but in the presence of congenital anomalies, young people also become ill. Women tolerate this form of arthrosis worse, since the specific structure of the pelvic bones plays an important role in bearing and giving birth to a child.

The main symptom of coxarthrosis is severe pain in the pelvic area. It can cause lameness and changes in gait. Inflammations are outwardly invisible, but touching the sore spot is accompanied by painful sensations.

A serious side effect is spinal curvature. To reduce pain, a person begins to lean forward, which increases the load on the intervertebral joints. In addition, a change in gait.

Consequences and complications

Without timely treatment, osteoarthritis can cause disability, especially with bilateral damage.

It causes:

• severe joint deformation;
• bone curvature;
• loss of mobility;
• shortening of the limb (with coxarthrosis and gonarthrosis).

When the large joints of the legs are affected, a person’s gait and posture change so much that this inevitably leads to problems with the spine, pain in the neck and lower back.

Arthrosis of the interphalangeal joints of the hands

This form most often occurs in women after menopause. A clear sign of osteoarthritis are small lumps - nodules that can be felt on the fingers. Patients feel burning and tingling in their fingers. The functionality of the phalanges of the fingers is reduced. When diagnosing, it is important not to confuse it with rheumatoid arthritis. It also often affects the fingers, but with osteoarthritis these are the “end” joints, located closer to the tips of the fingers, and with rheumatoid arthritis, these are the “inner” joints, located at the base of the finger.

Advantages of the clinic

“Health Energy” is a multidisciplinary clinic with modern equipment and experienced staff. We are always aware of new developments in the field of treatment and prevention of diseases and offer our patients not only time-tested methods, but also modern, advanced methods.

Come to us if you need:

• fast and effective diagnostics;
• assistance from experienced doctors;
• an integrated approach to the treatment of diseases;
• comfortable conditions in the clinic;
• affordable prices for all medical services.

Osteoarthritis is a disease that begins gradually, develops slowly, but ultimately often leads to disability. Don’t let it change your life, sign up for a consultation with the orthopedists at Energy of Health.

Main symptoms of the disease

Considering the clinical picture of the disease, we can distinguish three main symptoms of joint osteoarthritis:

• painful sensations of a mechanical nature, which have varying degrees of severity and are localized in the area of ​​the affected joint;
• increased volume of joints, swelling;
• crepitus (crunching sound when moving a joint).

In addition, osteoarthritis is often accompanied by diseases such as varicose veins (dilated veins) of the lower extremities, thrombophleitis (inflammation of the vein wall and the formation of blood clots).

Instrumental diagnosis of the disease

A rheumatologist or orthopedist diagnoses joint osteoarthritis.

There are two ways to diagnose the disease:

• laboratory;
• instrumental.

Instrumental diagnosis of arthrosis is the most informative. So, after conducting an initial examination of the patient, collecting an anamnesis and ordering a number of laboratory tests, the attending physician can use such instrumental diagnostic methods as:

• X-ray of the joint is the most effective way to determine the narrowing of the lumen of the joint space and the presence of osteophytes. Allows you not only to confirm and assess the degree of development of the disease, but also to exclude its likelihood;
• Ultrasound examination of the joint (ultrasound) is characterized by mobility, accessibility and speed of execution. Makes it possible to assess the condition of cartilage tissue and determine the volume of synovial fluid in the joint cavity;
• arthroscopy - a study aimed at determining degenerative changes in the menisci and ligamentous apparatus, as well as assessing the changes that have occurred in the tissues of the cartilage and the condition of the synovial membrane;
• magnetic resonance imaging - allows you to determine even minor changes in the structure of articular tissues.