RHEUMATOLOGY. OSTEOARTHROSIS: A MODERN VIEW AT THE PROBLEM

Concept and classification of osteoarthritis

Osteoarthritis predominantly affects weight-bearing joints: knees, hips, shoulders and lumbosacral joints.
A 2011 comparative study found that the topical analgesic capsaicin was 50% more effective as a pain reliever for OA than placebo. An inhibitor of neuronal reuptake of serotonin and norepinephrine, a third-generation antidepressant, duloxetine is more effective than placebo in relieving pain in OA. OA is a heterogeneous group of conditions with different etiologies and similar biological, morphological and clinical manifestations. OA primarily affects weight-bearing joints: knees, hips, shoulders, and lumbosacral joints. The distal and proximal interphalangeal joints and metacarpal joints may be affected, but such localization is much less common. Daily loads, which are mostly placed on weight-bearing joints, play an important role in the development of the disease.

Primary, or idiopathic, is osteoarthritis, the cause of which remains unknown. It can be local (one or two joints are affected) or generalized (three or more joints are affected). Local OA is most often associated with damage to the knee joints (gonarthrosis) and hip joints (coxarthrosis). In secondary OA, there is an obvious cause of the disease: trauma, metabolic disorders, a history of other rheumatological diseases, and so on.

Risk factors for osteoarthritis

The causes of osteoarthritis of the joints may be the following:

• age
• obesity
• injury
• heredity (family history of OA)
• low estrogen levels in women
• muscle weakness
• characteristics of work (for example, regular heavy physical activity)
• infection
• acromegaly
• history of inflammatory arthrosis (for example, rheumatoid arthritis)
• hereditary metabolic disorders (eg, alkaptonuria, hemochromatosis, Wilson's disease)
• hemoglobinopathies (eg, sickle cell anemia, thalassemia)
• neuropathic disorders leading to the development of Charcot's joint (syringomyelia, tabes dorsalis, diabetes mellitus)
• morphological risk factors (eg, congenital hip dislocation)
• damage to bone tissue (Paget's disease, aseptic necrosis and others)
• history of joint surgery (for example, meniscectomy)

Pathophysiology of OA

Vascularization of cartilage is a feature of the development of osteoarthritis. Blood vessels grow into the cartilaginous continuation of the articular surface, and ossification of the articular capsule begins from the subchondral zone

Primary and secondary OA have a common pathological basis. OA was previously thought to be a degenerative disorder resulting from the biochemical breakdown of hyaline cartilage in synovial joints. However, today a slightly different point of view is accepted, which suggests that not only the articular cartilage suffers, but also the entire joint, including the subchondral bone, synovial membrane and nearby tissues.

Despite the degenerative nature of OA, there is increasing evidence that after the synthesis of cytokines by chondrocytes and the release of cytokines into the joint cavity, an inflammatory process develops. Proinflammatory mediators (cytokines interleukin-1 and tumor necrosis factor) are not involved in matrix degradation [2], but activate chondrocytes in the superficial layer of cartilage, which increases the synthesis of matrix metalloproteinases and, consequently, degeneration of articular cartilage.

In the initial stage of OA, due to increased synthesis of proteoglycans, the main component of the matrix, swelling of the cartilage occurs. This stage can last several years or even decades, and its main manifestation is hypertrophy of the articular cartilage.

Further, as OA progresses, the level of proteoglycans decreases to extremely low values, and their qualitative composition changes. Damaged cartilage is subject to overload, as a result of which the synthesis of metalloproteinases (collagenase, stromelysin and others) increases. They contribute to the further destruction of proteoglycans and the entire collagen network, which determines the progressive degeneration of cartilage. As a result, the cartilage softens and loses its elasticity and becomes increasingly damaged. Microscopically, peeling and vertical clefts are noticeable on the smooth surface of the articular cartilage at this stage of the disease.

OA is characterized by vascularization of cartilage and changes in the subchondral bone. An actively mineralizing osteoid is formed in it, and then subchondral cysts and microfractures form. This leads to the development of subchondral sclerosis.

... Restoring a damaged joint

Currently, quite a lot of products have appeared on the Russian pharmaceutical market, which are based on two molecules - glucosamine and chondroitin, which are found in normal cartilage. Drugs of this series allow you to restore intra-articular cartilage and alleviate the course of the disease. In particular, such drugs as Dona, Structum, Chondro, Sustavit have a restorative effect. They must be taken for certain long periods, several months, because they do not begin to act from the first day. By the end of the first - the middle of the second month, anti-inflammatory and analgesic effects appear, the structure of the cartilage is modified, that is, these drugs act in all directions, while they are completely harmless and do not have any negative effect on the function of other organs. In addition, a drug has appeared that is administered intra-articularly. This is a preparation of hyaluronic acid, which is part of the normal intra-articular fluid, the state of which changes with arthrosis. The introduction of hyaluronic acid also has several effects: firstly, it enhances the activity of chondrocytes themselves - cartilage cells, secondly, it restores joint mobility, roughly speaking, lubricates it, thirdly, it has an anti-inflammatory effect. This drug is administered once a week; on average, a person requires about five procedures in one knee joint. If the injection has a positive effect, a stable (6-8 months to a year) remission occurs. These drugs include Ostenil, Fermatron. If drug therapy is not effective or the cartilage is so destroyed that the joint does not perform its functions, then in this situation either arthroscopic surgery or prosthetic surgery of the joint itself is performed.

Symptoms of osteoarthritis

Typical symptoms requiring treatment:

• joint pain (the first sign of the disease, may appear in the early stages);
• decreased range of motion, crepitus - crunching in the joints (often present);
• feeling of stiffness during or after rest. Joint stiffness is common after sleep, usually for less than 30 minutes.

Symptoms of osteoarthritis of the hands:

• the distal interphalangeal joints are most often affected;
• the proximal interphalangeal joints and the joints at the base of the thumb may be affected;
• Heberden's nodes (palpable osteophytes in the distal interphalangeal joints) are more common in women than in men;
• inflammatory changes, as a rule, are absent or remain unnoticed (mild).

Rheumatoid arthritis (RA) primarily affects the wrists and the metacarpophalangeal and proximal interphalangeal joints. Damage to the distal interphalangeal or lumbosacral joints is not typical for it. In addition, RA is associated with prolonged (more than 1 hour) morning stiffness, swelling, and increased joint temperature.

OA should also be differentiated from:

• avascular necrosis of bone tissue
• fibromyalgia
• gout and pseudogout
• ankylosing spondylitis
• neuropathic arthropathy (Charcot's joint)
• Lyme disease
• patellofemoral syndrome
• psoriatic arthritis

Diagnostics

Diagnosis of osteoarthritis is based on clinical and radiological examination data. Clinical studies have examined the ability to measure autoantibodies and synovial fluid markers as indicators of OA [4]. None of these indicators have proven reliable for diagnosing and monitoring OA.

As a rule, indicators of the acute phase of inflammation in OA are within normal limits. In the case of erosive arthritis, an increase in ESR is possible. In the synovial fluid, leukocytes are detected in quantities below 2000 per μl, with a predominance of mononuclear cells.

The method of choice in diagnosing OA is radiographic examination [5]. Some features of articular cartilage and soft tissue that are not visible on radiographs can be visualized using MRI. However, in most patients with OA, MRI is not necessary.

Ultrasound has no role in the routine clinical assessment of a patient with OA. It can be used as a tool for monitoring cartilage degeneration, as well as for intra-articular injections.

Arthrocentesis can help rule out inflammatory arthritis, infection, or crystalline arthropathy associated with deposition of microcrystals of varying composition.

The diagnostic results determine which methods will be used to treat osteoarthritis.

If therapy doesn't help...

In our Center, a rheumatologist diagnoses and treats osteoarthritis, and in advanced stages, when surgical care is required, a traumatologist. We do not yet perform prosthetics, but arthroscopic operations are performed in such severe conditions where drug therapy is ineffective.

Traumatologist - orthopedist Vitaly Semenovich Marina
“The arthroscopic method has long been successfully mastered by the specialists of the surgical department of our Center. We have experience in performing more than 600 operations; among our patients there are many athletes - national champions and Olympic participants. One of the most important advantages of arthroscopic surgery is minimal trauma and, as a result, a short rehabilitation period and absence of pain in the postoperative period. The operation is performed through three-millimeter punctures and consists of two stages: the first consists of examining all parts of the joint to make the most accurate diagnosis, the second is surgical. During the operation, fragments of cartilage that float inside the joint are removed, and the joint is washed. The operation is performed on an outpatient basis - the patient stays in the department for 6-8 hours and goes home in the evening. The patient's performance is restored, as a rule, 10-12 days after the operation. After the operation, the patient is observed by a rheumatologist, who, based on the results of the examination, prescribes adequate drug therapy. In our clinic, using arthroscopic technology, in addition to the treatment of deforming arthrosis, it is possible to remove a damaged meniscus, loose intra-articular bodies, restore damaged joint ligaments and much more.”

Therapy

Treatment of osteoarthritis is aimed at relieving pain and improving the functional state of the joint. Optimally, patients should receive a combination of non-pharmacological techniques and pharmacotherapy [6].

The inflammatory reaction in the joint is catalyzed by cyclooxygenase (COX) and lipoxygenase (LOX), producing mediators of inflammation and pain (prostaglandins, including prostaglandin E2 and leukotrienes). The latter, in addition to direct participation in the pathogenesis of inflammation, reduce the threshold for pain perception in the affected joint, thereby increasing pain sensations

Non-drug ways to control OA:

• weight normalization [7]
• physiotherapy
• physiotherapy
• occupational therapy
• unloading of some joints (for example, knee, hip)

Relieving pain...

If we talk about relieving pain in patients suffering from osteoarthritis, the simplest and most commonly used remedy, especially in the West, is regular Paracetamol. It is believed that in terms of effectiveness (when taken in substantial dosages, say up to 4 grams per day) it is comparable to Diclofenac, and at the same time it is quite safe for the gastrointestinal tract. But in our country, the most common drugs are nonspecific anti-inflammatory drugs, such as Diclofenac, Indomethacin. Currently, experts are focusing on the latest generation of drugs that do not negatively affect the gastrointestinal tract or blood pressure, these are the so-called “selective COX-2 inhibitors”, such as Movalis, Celebrex.

In addition, there are situations, especially at certain stages of arthrosis, when the joint becomes inflamed and fluid appears in it, then doctors often resort to intra-articular administration of corticosteroid drugs, which are aimed at relieving the exacerbation. It is recommended to administer them for certain indications, especially for elderly people, so as not to increase structural changes.

Pharmacotherapy of OA, recommendations of the International Society for the Study of OA (OARSI), 2014

The following drugs are used to treat osteoarthritis:

Paracetamol

Inflammatory mediators can stimulate angiogenesis. Thus, hypoxia, which often occurs during the inflammatory process, stimulates the synthesis of vascular endothelial growth factor (VEGF). Vascular growth can also be stimulated by fibrinogen and inflammatory cells: macrophages, lymphocytes, mast cells and fibroblasts.

A 2010 meta-analysis confirmed the effectiveness of paracetamol as a moderate pain reliever for OA [8]. However, studies have shown an increased risk of side effects associated with paracetamol use, including gastrointestinal (GI) manifestations and multiorgan disorders [8]. In connection with these data, OARSI recommends using the drug strictly in accordance with the dosage and duration of the course.

Capsaicin

A 2011 comparative, double-blind, randomized study of 100 patients with knee OA found that the topical analgesic capsaicin was 50% more effective as an analgesic for osteoarthritis than placebo [9].

Corticosteroids (intra-articular injections)

Recent studies demonstrate a clinically significant short-term analgesic effect [10]. There are several other recommended medications for the treatment of osteoarthritis.

Chondroitin

Four studies examining the use of chondroitin in OA showed mixed results. Some trials showed some analgesic effects, while others showed chondroitin's effect was no different from placebo [11]. In addition, specialists from the International Society for the Study of OA - OARSI note a high degree of heterogeneity of studies and their low quality, and therefore a final assessment of the effectiveness of chondroitin is extremely difficult. Thus, the effect of chondroitin as a symptomatic remedy is considered questionable, and it is not recommended as a drug for the treatment of OA.

Diacerein

A 2010 meta-analysis examining data from six studies involving 1533 patients found a relatively modest but statistically significant analgesic effect of the non-narcotic analgesic diacerein compared with placebo [12]. The meta-analysis also noted a significant increase in the risk of diarrhea among volunteers taking diacerein. However, diacerein is considered safer than NSAIDs.

Duloxetine

Studies have proven that the inhibitor of neuronal reuptake of serotonin and norepinephrine, the third generation antidepressant duloxetine, is more effective than placebo in relieving pain in OA [13]. However, 16.3% of patients receiving duloxetine experienced side effects (compared to 5.6% in the placebo group). These include nausea, dry mouth, drowsiness, fatigue, decreased appetite, and hyperhidrosis. In this regard, the need for the use of duloxetine for the treatment of OA in persons with concomitant diseases (diabetes mellitus, arterial hypertension and other cardiovascular diseases, renal failure, gastrointestinal bleeding, depression, limitation of physical activity, including due to obesity) is recognized doubtful*.

Glucosamine

A meta-analysis of three randomized controlled trials found a beneficial effect of rosehip powder (5 g/day) as an analgesic for OA compared with placebo, but these data require further study.

Two large studies evaluating the effectiveness of glucosamine in the treatment of OA yielded conflicting results [6]. One study showed a statistically significant analgesic effect, while another showed no effect. The latest meta-analysis, which included a large-scale study, did not prove the effectiveness of glucosamine at all. Based on these data, OARSI experts came to the conclusion that the effectiveness of glucosamine as a symptomatic agent for OA is questionable. It is not recommended as a treatment for OA [6].

Hyaluronic acid (intra-articular injections)

The results of clinical trials (CTs) examining the effectiveness of intra-articular injection of hyaluronic acid (HA) have been controversial [6]. Conflicting data from meta-analyses and individual studies cast doubt on the advisability of using hyaluronic acid preparations for OA of the knee and hip joints. For OA of several joints, GC is not recommended.

Oral NSAIDs

Taking these drugs is included in recommendations for the treatment of osteoarthritis for patients without concomitant diseases. For concomitant gastrointestinal diseases, it is necessary to prescribe proton pump inhibitors along with NSAIDs. For patients at high risk (GI bleeding, myocardial infarction, history of chronic renal failure), oral NSAIDs are strictly not recommended.

Risedronic acid

A review of the literature conducted by Japanese scientists in 2010 suggests that high doses of risedronic acid do not reduce the severity of OA symptoms, but may help reduce the progression of OA by maintaining the structural integrity of the subchondral bone [14]. Laboratoryly, this effect is manifested by a decrease in the level of the cartilage degradation marker CTX-II. Thus, the effectiveness of residronic acid requires further study.

Opioids

Studies have shown moderate effectiveness of codeine and morphine for OA of the knee and hip. A 2006 Cochrane meta-analysis of placebo-controlled trials involving 1019 patients found statistically significant benefits for tramadol compared with placebo [15].

List of sources

1. Folomeeva O. M., Erdes Sh. F. Prevalence and social significance of rheumatic diseases in the Russian Federation // Doctor (rheumatology). 2007. No. 10. P. 3–12.
2. Poole AR. An introduction to the pathophysiology of osteoarthritis. Front Biosci. 1999 Oct 15. 4: D662–70.
3. van Baarsen LG et al. Heterogeneous expression pattern of interleukin 17A (IL-17A), IL-17F and their receptors in synovium of rheumatoid arthritis, psoriatic arthritis and osteoarthritis… Arthritis Res Ther. 2014. 16 (4):426.
4. Brandt KD. A pessimistic view of serologic markers for diagnosis and management of osteoarthritis. Biochemical, immunologic and clinicopathologic barriers. J Rheumatol Suppl. 1989 Aug. 18:39–42.
5. Recht MP et al. Abnormalities of articular cartilage in the knee: analysis of available MR techniques. Radiology. 1993 May. 187(2):473–8.
6. Zhang W et al. OARSI recommendations for the management of hip and knee osteoarthritis, part I: critical appraisal of existing treatment guidelines and systematic review of current research evidence. Osteoarthritis Cartilage. 2007 Sep. 15(9):981–1000.
7. Felson DT et al. Weight loss reduces the risk for symptomatic knee osteoarthritis in women. The Framingham Study. Ann Intern Med. 1992 Apr 1. 116 (7):535–9.
8. Bannuru RRDU, McAlindon TE. Reassessing the role of acetaminophen in osteoarthritis: systematic review and meta-analysis. Osteoarthritis Research Society International World Congress; 2010 Sep 23–26; Brussels, Belgium. Osteoarthritis Cartilage 2010; 18 (Suppl 2):P 250.
9. Kosuwon W et al. Efficacy of symptomatic control of knee osteoarthritis with 0.0125% of capsaicin versus placebo. J Med Assoc Thai¼Chotmaihet Thangphaet 2010; 93(10):118e95. Epub 2010/10/27.
10. Bannuru RR et al. Therapeutic trajectory of hyaluronic acid versus corticosteroids in the treatment of knee osteoarthritis: a systematic review and meta-analysis. Arthritis Rheum 2009; 61 (12):1704–11.
11. McAlindon TE et al. OARSI guidelines for the non-surgical management of knee osteoarthritis //Osteoarthritis and Cartilage. - 2014. - T. 22. - No. 3. - pp. 363–388.
12. Bartels EM et al. Symptomatic efficacy and safety of diacerein in the treatment of osteoarthritis: a meta-analysis of randomized placebo-controlled trials. Osteoarthritis and Cartilage/OARS. Osteoarthritis Research Society 2010; 18(3):289–96.
13. Citrome L, Weiss-Citrome A. A systematic review of duloxetine for osteoarthritic pain: what is the number needed to treat, number needed to harm, and likelihood to be helped or harmed? Postgrad Med 2012; 124(1):83.
14. Iwamoto J. et al. Effects of risedronate on osteoarthritis of the knee //Yonsei medical journal. 2010. No. 2. 164–170 pp.
15. Cepeda MS, Camargo F, Zea C, Valencia L. Tramadol for osteoarthritis. Cochrane Database Syst Rev 2006; (3):CD005 522. Epub 2006/07/21.

RHEUMATOLOGY. OSTEOARTHROSIS: A MODERN VIEW AT THE PROBLEM

Epidemiology

The definition of OA itself remains unclear. In 1995, the following definition was adopted: “OA is the result of both mechanical and biological influences that disrupt the balance of degradation and synthesis of chondrocytes and the extracellular matrix of articular cartilage, as well as subchondral bone.” The onset of OA is provoked by very diverse factors, including genetic, developmental disorders, metabolic and traumatic, but in any case, all tissues of the joint are involved in the pathological process. Ultimately, OA is manifested by morphological, biochemical, molecular and biomechanical abnormalities in both cells and matrix, which leads to softening, fiberization, ulceration and loss of articular cartilage, sclerosis and eburnation of subchondral bone, the formation of osteophytes and subchondral cysts. Clinically, OA is manifested by pain in the joints, limited mobility, crunching in the joints when moving, the periodic appearance of effusion (swelling?) and inflammation of varying severity without any systemic manifestations. According to the classification adopted by the American Association of Rheumatology

, primary and secondary OA are distinguished (Table 1); Criteria have been developed to distinguish OA of the joints of the hands, hip and knee joints. Most often, these criteria are used when conducting scientific clinical studies, mainly at the stage of inclusion in clinical trials, and not in epidemiological studies.

In most epidemiological studies, the diagnosis of OA was based on the presence of typical radiological signs. Radiological signs of OA of at least one group of peripheral joints (most often the hands, then the feet, knees and hips) are detected in approximately 1/3 of the white population of North America and Northern Europe aged 25 to 74 years.

Numerous risk factors for radiographically confirmed OA (Table 2; Fig. 1) vary not only depending on the location of the OA, but even within the same joint (for example, the femoropatellar and femorotibial joints, which are components of the knee joint, each have their own risk factors OA). In addition, the main risk factors for radiographically confirmed OA (age, female gender, obesity and joint trauma) differ from the risk factors for knee pain (psychosocial factors, general health).

Age is the most significant risk factor for OA; With increasing age, the prevalence of OA of all localizations increases. The incidence of OA also increases with age and reaches a plateau after age 70. It is likely that biomechanical changes associated with aging of articular cartilage contribute to its damage and destruction. However, there is no clear evidence for this assumption. Women, especially menopausal women, are at greater risk of OA than men. Although data on the biochemical effects of sex hormones on cartilage metabolism are inconsistent, epidemiological studies have shown a protective effect of hormone replacement therapy on the development of OA of the knee and hip joints. Fig 1. Etiopathogenesis of OA

Prospective cross-sectional studies have shown a significant effect of obesity on the risk of knee OA and, to a lesser extent, hip OA. Obesity leads to increased stress on weight-bearing joints and thus contributes to the development of OA. However, since women are more likely to be obese, and obesity may also be a risk factor for hand OA, systemic factors may also play a role in the development of OA. Work involving prolonged periods of kneeling, squatting, and stair climbing is associated with a higher prevalence of knee OA, and work involving heavy lifting (eg, in agriculture) is associated with a higher risk of hip OA. Sports activity is also associated with the risk of OA of the joints of the lower extremities. However, active recreation with physical exercise, such as recreational jogging, does not lead to an increased risk of OA, since in this case there is a normal biomechanical load on the joints. In the development of OA, especially generalized with Heberden's nodes, hereditary factors play a role. A study conducted among female twins showed the role of hereditary factors in radiographically confirmed OA of the knee and hip joints. Although mutations in the collagen type II gene (COL2A1) lead to the development of early advanced OA with mild chondrodysplasia, it is likely not the only gene responsible for the structural components of cartilage, completely mediating the influence of genetic factors on the development of OA.

Pathogenesis

OA is generally considered a disease of the articular cartilage, although changes affecting the subchondral bone also play a role. It is unknown where the initial abnormalities in idiopathic OA occur - in articular cartilage or subchondral bone. Articular cartilage performs two functions: weakening the load when exposed to mechanical factors and ensuring the sliding of articular surfaces during movement. This is possible due to the unique structure of cartilage tissue, in which chondrocytes are embedded in a matrix consisting of collagen and proteoglycans. The main structural protein of the matrix is ​​type II collagen. The importance of this protein is supported by the fact that COL2A1 mutations occur in OA; in addition, type II collagen binds to other matrix macromolecules (types IX and XI collagen), which are present in small quantities but are necessary to ensure the stability of cartilage. Another important component of cartilage is proteoglycans, mainly represented by aggrecan. Normally, the processes of synthesis and degradation in articular cartilage are balanced. The cause of OA may be insufficient formation or increased catabolism of cartilage tissue, see (Fig. 1). Thus, the content of matrix metalloproteinases (enzymes that catalyze the degradation of collagen and proteoglycans) in OA cartilage is increased. Their synthesis by chondrocytes is stimulated by the action of interleukin 1. In addition, blockade of these enzymes with doxycycline or reformulated tetracycline, at least in animal models, leads to a reduction in OA lesions. At the same time, the synthesis of cartilage components depends on numerous growth factors. In OA, radiographic changes in the subchondral bone are often detected, which may be considered a cause rather than a consequence of cartilage damage. The importance of changes in bone is demonstrated by the inverse relationship between OA and diseases associated with decreased bone density, including osteoporosis. Bone mineral density in radiographically confirmed OA of the hip joints is higher than normal, even adjusted for body weight, not only in the areas of bones adjacent to the affected joints, but also in other, distant areas. The role of inflammation in the pathogenesis of OA is controversial.

Clinical manifestations

Clinical manifestations of OA are presented in table. 3. Pain is the most common symptom for which a patient seeks medical help; pain occurs suddenly, its intensity can vary from mild to moderate, increases with movement in the affected joint and decreases with rest. Pain at rest or at night indicates severe damage. The source of pain in OA can be the synovium, joint capsule, periarticular ligaments, periarticular muscles (with their spasm), periosteum and subchondral bone. Although pain is often observed in radiographically confirmed OA, the correlation between pain and radiographic changes characteristic of OA is weak. However, pain severity is used as an outcome measure in clinical trials. As a rule, the clinical diagnosis of OA is confirmed by a typical x-ray picture, characterized by the presence of marginal osteophytes, asymmetrical narrowing of the joint space, subchondral osteosclerosis, the formation of subchondral cysts and, in severe cases, deformation of the epiphyses of the bones. Periarticular osteoporosis and marginal erosions characteristic of rheumatoid arthritis are not observed in OA. A routine laboratory examination, including general clinical and biochemical tests, as a rule, does not reveal any abnormalities. Laboratory tests should be carried out before starting non-steroidal anti-inflammatory drugs (NSAIDs), as well as between courses of taking these drugs during long-term treatment.

Rice. 2. Approach to treatment of OA

The natural history of OA is highly variable. Although radiographic changes usually progress, in some cases the condition of patients remains stable for many years. For example, in a prospective observational study of 188 outpatients with knee OA, no progression of radiographic changes was observed over 1 to 5 years. In some joints, there was even an improvement, manifested by restoration of the joint space, although this may have been due to the error of the x-ray examination. The severity of pain may also decrease and, less commonly, joint function may improve. X-ray changes do not correspond to fluctuations in the severity of pain, and therefore the use of X-ray signs in studies as a criterion for assessing the outcome of treatment for OA is inappropriate. Prognostic factors for the progression of radiological changes may include pathological abnormalities according to bone scintigraphy, obesity, generalized OA with Heberden's nodes, chondrocalcinosis and increased levels of C-reactive protein and hyaluronate.

Therapy

At present, OA is difficult to treat, since there are no drugs that affect the course of the disease. The main criterion for the effectiveness of treatment is usually the intensity of pain, although some clinical trials take into account the effect on joint function and quality of life. The approach to treating OA is presented in Fig. 2. Treatment with drugs listed at the bottom of the pyramid can be supplemented with drugs at higher levels (for example, low-dose NSAIDs can complement paracetamol therapy; intra-articular corticosteroids are possible while taking paracetamol, NSAIDs, or both). Treatment is selected individually depending on the location and severity of the joint lesion, as well as concomitant diseases. Exercise is important in the treatment of OA

, including muscle strengthening exercises and aerobics.
Studies have found that quadriceps strengthening exercises and aerobics reduce pain and improve function in knee OA, with effects lasting up to 6 months. It is necessary to lie on your back, bend one leg at the knee, and straighten the other, bringing the ankle joint to a dorsiflexion position of 90 degrees. The quadriceps muscle of the thigh of the straightened leg is tense, the leg is raised to a height of 25 - 50 cm. Hold the leg in this position for 10 s, then lower it, relax the muscle. Repeat the exercise at least 10 times for each leg. Learning how to behave in everyday life helps to adapt to the limitations associated with impaired joint function. Losing body weight reduces the risk of clinically manifested knee OA. One study showed a positive effect of weight loss on both pain and function in obese postmenopausal women with knee OA. Pain is the main indication for drug treatment for OA. is currently considered the drug of choice .
In the absence of sufficient effect from non-drug treatment and taking paracetamol, it is advisable to try using
NSAIDs
.
No clear advantages of any drug from the NSAID group have been identified, however, due to greater toxicity, the use of indomethacin is not recommended. With the use of piroxicam, ketoprofen, there is a greater risk of complications from the gastrointestinal tract (perforation, ulceration, bleeding) than with the use of other NSAIDs, especially low-dose ibuprofen. The basic principles of using NSAIDs for OA are to use the minimum effective dose and avoid simultaneous use of two drugs from the NSAID group. The effect of treatment is assessed after about 1 month and if it is absent, the drug is changed. NSAID
ointments may be effective either as monotherapy or when combined with oral pain medications, especially when a small number of joints are affected.
Ointments allow patients to independently control treatment. In OA, especially with damage to the knee joints, intra-articular injection of corticosteroids is widely used,
but their effect lasts only 1–3 weeks.
Triamcinalone is the most effective. For OA of the knee joints, intra-articular injection of hyaluronic acid
.
Weekly injections over 3 to 5 weeks are more effective than a single intra-articular injection of corticosteroids .
If treatment with the above methods is unsuccessful, it is possible to use narcotic analgesics, but controlled studies on this problem have not been conducted.
In some cases of OA of the knee joints, if there are contraindications or refusal of surgical intervention, lavage of the articular surfaces with saline solution is effective. The positive effect of this procedure may be due to the removal of pathological fragments, decay products and inflammatory mediators from the joint cavity. Joint transplantation
gives the best results.
In moderate and severe cases of OA affecting the joints of the lower extremities, transplantation leads to a noticeable improvement in the quality of life. With the improvement of the quality of joint prostheses, the frequency of re-interventions due to the appearance of “looseness” of the prosthetic joint has decreased. Thus, the understanding of OA has expanded over the past 10 years. The study of selective cyclooxygenase-2 inhibitors
may lead to safer NSAIDs and improved treatment of OA. Several new drugs are being studied—reformulated tetracycline and other metalloproteinase inhibitors, as well as interleukin 1 antagonists—that could potentially reverse the structural and biochemical abnormalities inherent in OA. In addition, autologous cartilage transplantation may be effective in the early stage of the disease and in cases of focal cartilage damage. Perhaps these advances will change the prognosis and improve the quality of life of OA patients in the next century.

Literature:

Caremer P, Hochberg MC. Osteoarthritis. Lancet 1997;350:503–8.