Osteoarthritis is a common joint disease, especially in older people. You should always remember the threat of premature wear of joints, and the prevention of this disease should begin in youth; your joints will thank you for this with an unlimited range of movements in old age.
Osteoarthritis or simply arthrosis is a degenerative-dystrophic (the result of tissue drying) disease of the joints. Osteoarthritis is a common disease, its incidence increases with age, while a significant part of arthrosis is asymptomatic.
All osteoarthritis is divided into primary and secondary. Primary forms include those that begin without a noticeable cause after the age of 40 in articular cartilage that has not changed until then and simultaneously affect many joints. Secondary osteoarthritis develops at any age after injuries, vascular disorders, inflammatory changes in the joint, etc. Such osteoarthritis usually affects one or more joints.
Causes of osteoarthritis
In the development of osteoarthritis, static (stationary) loads (prolonged standing on your feet, lifting heavy objects, etc.) are of great importance. excess weight) on joints and minor joint injuries. Changes come with age blood vessels synovium (the sac surrounding the joint), the joint begins to receive less nutrients and oxygen and gradually atrophies (dries out). The same phenomena occur when the function of certain glands is impaired, for example, when the thyroid and gonads are insufficient. Hereditary structural features of joints also play a certain role.
As a result of the influence of all of these factors, the nutritional conditions of joint cartilage are disrupted, its cells in the surface layer are gradually destroyed, the cartilage loses its elasticity, small cracks form on its surface, then this layer acquires a ragged structure. In the later stages, cartilage cells begin to die, forming large foci of necrosis (tissue decay), instead of cartilage tissue, connective tissue and bone tissue grow, and limited joint mobility is formed.
How does osteoarthritis occur?
Any arthrosis develops and proceeds very slowly and never leads to severe dysfunction of the joints. An exception is the hip joint, which has its own anatomical features, due to which limited mobility is formed in it very early, which can later cause disability.
Signs of osteoarthritis are joint pain, a feeling of stiffness, rapid fatigue, stiffness, change in joint shape, crunching in the joints, etc. The pain is usually dull, intermittent, intensifies in cold and damp weather, in the evening (after prolonged exercise) and during initial movements after a state of rest (“starting pain”). In the hip joints, pain radiates to the groin or sciatic region. Very often (especially in old age) instead of pain, there is only aching and a feeling of heaviness in the bones and joints.
True impairment of mobility is rarely observed; rather, we are talking about stiffness and rapid fatigue of the joints. Joint deformities are most noticeable in the joints of the fingers, which become knotty, and in the knee joints. These deformities are caused by bone growths, and not by soft tissue swelling, as with inflammation of the joint. The cause of rough crunching in the joints is unevenness of the articular surfaces of the bones.
Diagnosis of osteoarthritis
Diagnosis is based on typical signs of the disease (pain, changes in the appearance of joints without signs of inflammation), laboratory data (no signs of inflammation in blood tests) and x-ray studies. Asymptomatic arthrosis can only be seen on x-rays.
Radiologically, there are three stages of osteoarthritis. The first stage is characterized by a slight narrowing of the joint space and small growths of bone tissue along the edges of the glenoid cavity. The second stage - the narrowing of the joint space is already clearly visible, the surfaces of the bones become uneven, change their shape, and bone growths reach significant sizes. In the third stage, changes occur in deeper areas of the bones.
Treatment of osteoarthritis
Treatment of osteoarthritis depends on the shape and location of the lesion and the general condition of the patient. To restore joint cartilage, biological stimulators of cartilage tissue formation (for example, Rumalon) are prescribed. Reflex spasm of the muscles located around the affected joint is relieved by muscle relaxants - drugs that relieve muscle spasm (for example, mydocalm). Vasodilators (nicotinic acid) can increase the nutrition of the joints; for the same purpose (as well as for pain relief), thermal procedures (paraffin, warming compresses, etc.) and massage are prescribed.
To eliminate pain, non-steroidal anti-inflammatory drugs (indomethacin, voltaren) are used.
It is very important to give rest to the affected joint several times a day; you cannot stay in the same position for a long time, stand on your feet for a long time, walk for a long time, or lift weights. In advanced stages of the disease, it is advisable to use a cane or crutches when walking.
Osteoarthritis can gradually creep up on each person, but if you do not overload your joints, then these processes can proceed unnoticed.
Galina Romanenko
Pain in the hands may indicate the occurrence of a serious disease - arthrosis. A competent doctor will recognize arthrosis of the fingers by symptoms and select treatment based on the cause of the disease. This is a pathology in which inflammation of the joints occurs. According to statistics, it appears more often in women. This is due hormonal changes(at menopause) in female body and a decrease in collagen synthesis. The disease usually occurs in older people. Among young people, the percentage of patients is small.
Pathology, deforming the joints, can lead to loss of motor activity of the hands, their curvature and severe pain. The joints of the phalanges are usually affected. There is also polyarthrosis, in which inflammation of all joints of the hand occurs and their thickening (Heberden's or Bushard's node).
Causes of the disease and its symptoms
Arthrosis of the hand can appear under the influence of many factors. One such factor is age. With age, cartilage becomes less elastic. The amount of synovial fluid that nourishes and protects them from mechanical damage gradually decreases. Thickening of the joints causes a person to experience terrible pain and difficulty moving.
In addition to age, doctors identify the following causes of arthrosis of the fingers:
- injuries;
- hard physical work;
- presence of chronic diseases (arthritis, diabetes and etc.);
- hereditary factor;
- hormonal changes (menopause in women);
- hypothermia of the finger joints.
The disease has clear symptoms. It is recognized by symptoms such as pain during manual work and at rest, muscle hypertonicity (increased tension) of the hands, the formation of nodules and thickenings. The photo shows what the curvature of the fingers and their shortening look like. Pathology can not only deform the fingers, but also cause their edema (swelling). Another sign is a crunching sound when you move your hands.
Stages and types of disease
Symptoms also depend on the severity of the disease. Arthrosis of the hands at the initial stage is characterized by a gradual loss of elasticity of the joints. The patient complains of discomfort and aching pain, muscle tension in the hands. Painful sensations often worsen at night. At this stage there is no difficulty in moving your fingers.
At the second stage, the pain syndrome intensifies. The pain does not leave the patient even at rest. There is a crunching sound and difficulty moving. The fingers swell and begin to become deformed.
At the last stage, arthrosis of the fingers leads to severe swelling and redness. The patient completely loses the ability to perform manual labor. The deformed joint continues to grow, and cartilage and bone tissue are destroyed. A disease of this severity is called polyosteoarthrosis.
Depending on the location of the lesion, deforming arthrosis of the hands is of 3 types:
- Arthrosis of small joints of the hands. People who work with their hands are highly susceptible to this type of disease. Most often, lesions appear at the junction of the phalanges. This type of disease is dangerous due to its high rate of development. A person may completely lose the ability to move their fingers.
- Arthrosis of the thumb. This type of disease is more rare. In official medicine, this pathology has another name - rhizarthrosis. Inflammation occurs at the junction of the metacarpal joint and the wrist bone. According to statistics, rhizarthrosis occurs in 5% of patients. With this type of disease, the thumb may completely lose mobility.
- Arthrosis of the wrist joint. A very rare type of disease. Damage to this joint occurs due to injury (fracture or dislocation).
Rhizarthrosis (arthrosis of the thumb) manifests itself with signs similar to those of other types of osteoarthritis. Develops in the joint It's a dull pain and crunching. Rhizarthrosis then leads to severe curvature and shortening of the thumb.
The least common type of osteoarthritis is arthrosis of the wrist joint. It is difficult to diagnose. At first, a person does not pay attention to the discomfort in the hand. He turns to a specialist for help when arthrosis of the wrist joint reaches stage 2.
How to treat the disease?
Many older people wonder how to treat arthrosis. The first thing you need to do is see a doctor. He will make the correct diagnosis and prescribe the necessary medicine.
Arthrosis of the fingers can be treated in 2 ways: conservative and surgical. Surgery is usually prescribed in the final stages.
Pathology of 1 or 2 severity is treated conservatively. Such therapy includes:
- taking medications;
- proper nutrition;
- hand exercises;
- physiotherapy;
- treatment folk remedies.
Drug therapy should only be prescribed by the attending physician. A properly selected drug will provide the necessary therapeutic effect. Usually the patient is prescribed NSAIDs (non-steroidal anti-inflammatory drugs) and chondroprotectors.
Among NSAIDs, drugs such as Diclofenac, Nimesulide, Ketoprofen, Meloxicam are often used. They eliminate pain, swelling and suppress the inflammatory process. The course of taking NSAIDs lasts 2 weeks. Chondroprotectors are used for the synthesis (restoration) of damaged cartilage tissue. Drugs such as Chondroxide, Glucosamine and their analogues are used.
Non-drug methods
Gymnastics for the hands plays an important role in the treatment of the disease. The most common exercises are:
- Lightly tap on a hard surface with your fingertips.
- Clenching and unclenching fists.
- Exercises with rosaries.
- Flexion and extension of fingers ( Special attention It is worth paying attention to the thumb if there is rhizarthrosis).
The main rule of nutrition for patients is to exclude salt from the diet and eat alkaline foods. The diet for joint arthrosis consists of foods such as:
- goat milk;
- milk serum;
- bread made from rye flour;
- fresh vegetables.
It is beneficial for the patient to take cabbage juice.
For arthrosis of the fingers, treatment with folk remedies is based on the use of baths of decoctions and herbal infusions. Commonly used plants are:
- birch leaf;
- comfrey;
- thyme;
- horsetail.
They help restore cartilage tissue and restore its former elasticity.
To prepare the decoction you will need 1 tbsp. l. dried medicinal plant per glass of boiling water. This product should be added to baths. It is recommended to carry out the procedure 2 or 3 times a week.
Deforming arthrosis knee joint, the symptoms, causes of development and treatment of which we will consider below, is a fairly common problem. According to statistics, almost every fifth person encounters this disease in one way or another, but it is most common among people over 40 years of age. In addition, this disease is much more common in women.
The difficulty is that this disease progresses gradually, without immediately showing significant symptoms. Thus, people usually perceive minor pain in the knee simply as an annoying misunderstanding that will “go away on its own.” But the pain gradually becomes chronic, intensifies, the mobility of the joint is gradually limited, and after that it begins to gradually change its appearance. Then the person goes to see a doctor, but the problem is that this happens in the later stages of the disease, when treatment is already quite complex and often not very effective. Therefore, it is extremely useful to understand what arthrosis of the knee joint is of 1st and 2nd degree, when the symptoms are not yet too pronounced. But identifying the disease at this moment gives the greatest chance of successful treatment.
What are the reasons for the development of this disease?
Gonarthrosis is a fairly common disease that affects mainly older people. But over the past few years, this disease has become significantly “younger”; now people over 30 years of age fall into the “risk group”.
There are two main types of this disease - primary and secondary arthrosis. Primary is somewhat less common, but it is an independent disease that appears on its own, without being a consequence of the influence of other factors. However, the reasons for the development of this disease are not known, but it is believed that the cause of its development is metabolic disorders.
Thus, it is believed that almost any process in which damage to the articular cartilage occurs can lead to the development of arthrosis of the knee joint. This may be a metabolic disorder, endocrine disorders, various circulatory disorders (atherosclerosis, varicose veins, etc.).
One of the common causes of the disease is physical activity and joint injuries. Thus, post-traumatic arthrosis of the knee joint is a common problem among athletes. But the load on the joint is not always associated with sports - overweight also puts stress on the joints, and trying to “lose weight” by running can be a serious mistake. For this reason, overweight people are advised to stop running and switch to brisk walking.
Secondary gonarthrosis most often occurs due to insufficiently correct or incomplete treatment of permanent microtraumas of the joints, which can occur due to:
- meniscopathies (meniscal injuries that can occur due to unsuccessful movements);
- genetic pathologies (it is believed that there is a genetic predisposition to diseases of this type, and a lack of a certain type of collagen may also be the cause);
- prolonged static loads on the joint (a striking example is squatting, in which the muscles are not too tense, but the joint is overloaded);
- excess weight (which also leads to constant excess load on the joint);
- significant loads on the joints (this occurs when snowboarding and skiing, running, jumping, playing basketball and football).
Also, the cause of the development of the disease can be congenital inferiority of the knee joints, as well as inflammatory processes in these joints.
What are the symptoms at various clinical stages of gonarthrosis?
When discussing how to cure arthrosis of the knee joint, they often talk about the importance of timely diagnosis of the problem. Thus, all experts agree that it is much easier to stop the development of the disease if it was identified at the 1st or 2nd stage of development, but if this disease is diagnosed late, it is quite difficult to achieve any significant results in treatment. But the main problem is that in the early stages the disease manifests itself only slightly, so people often simply ignore such symptoms.
Thus, the only significant symptom of the disease at stage 1 is a dull pain that is localized deep in the joint. It usually appears after prolonged exercise, so people rarely pay attention to it.
Painful sensations in the 2nd stage of this disease are already more intense and prolonged, and “crunching” in the joints may also appear when walking. Some stiffness in the joints appears in the morning, but it disappears after some time of walking. There may be a slight limitation of mobility when extending and flexing the joint. But although there are many symptoms, they are all subtle, which is why most people relieve knee pain with conventional analgesics, and simply do not pay attention to other problems.
At the third stage, the pain becomes constant and intensifies regardless of whether the person moves or is at rest. Sensitivity to changes in weather appears, due to serious restrictions on movement in the joints, the gait changes sharply, the joint increases in size and becomes deformed. All this can be accompanied by frequent inflammation and tension in the muscles that are located near the joint.
Even a very patient person is no longer able to ignore such symptoms, which is why in most cases people turn to the doctor precisely at this stage of the disease. The problem is that the “process” has already been seriously launched, so it will be quite difficult to change the situation for the better.
How is this disease treated?
How to treat arthrosis of the knee joint is a rather complex and extensive question. Typically, the treatment process combines a number of therapeutic measures that should relieve pain, activate blood circulation near the affected joint, stop the destruction of articular cartilage and speed up its recovery, increase the mobility of the joint itself and strengthen the surrounding muscles.
For elimination pain Non-steroidal anti-inflammatory drugs are usually used. Often their use is simply necessary, since the pain is constant and with any impact on the joint it intensifies. Thus, for arthrosis of the knee joint, NSAIDs are usually used before massage, exercise therapy or gymnastics. Various exercises and loads for arthrosis of the knee joint provoke an increase in pain, which is why it is necessary to “dampen” the pain first. But it is worth considering that NSAIDs themselves do not treat the joint, but simply perform the function of pain relief.
The main treatment is taking chondroprotectors. These drugs do not so much eliminate pain as help restore damaged cartilage tissue, as well as better production of joint fluid. Treatment of this disease simply makes no sense without these drugs, since there are essentially no other methods for restoring cartilage tissue.
Also, various ointments and creams, as well as compresses, are actively used in treatment. It should be understood that they cannot save a person from the disease; their main task is to relieve pain.
One common method is the use of intra-articular injections of corticosteroid drugs. They almost instantly relieve pain, which is why they have earned recognition from many doctors who began to prescribe them almost instantly. for preventive purposes. But at the same time, Evdokimenko (a representative of completely traditional medicine, a fairly well-known and respected specialist), as well as a number of other specialists, consider the treatment of arthrosis of the knee joint with the frequent use of such drugs to be unjustified, since in essence their entire effect comes down to pain relief, and often this can be achieved and less “drastic” means. At the same time, this drug itself requires compliance with certain rules, which many specialists simply do not think about, being carried away by the “instant” effect.
Nutrition also plays a significant role in treatment - the diet for arthrosis of the knee joints is not as demanding on the choice of products as on their quality, or more precisely, on the absence of preservatives and other “chemicals” in them.
Treatment of a disease such as arthrosis of the knee joint also involves the use of methods such as manual therapy, physiotherapy and therapeutic exercises. But it can be noted that they are most effective in the early stages of the development of the disease.
Deformation of the facet (facet) joints occurs due to arthrosis - unfortunately, a fairly common disease. This disease is very unpleasant and painful. Most often they suffer in mature age or elderly people, but there are cases of arthrosis being detected in very young people, as a result of some physical injuries or congenital diseases.
- Spondyloarthrosis of the facet joints
- Causes and symptoms
- Arthrosis lumbar region spine
- Diagnostic and treatment methods
- Video on the topic
Spondyloarthrosis of the facet joints
Spondyloarthrosis of the facet joints is an inflammatory process that arises due to the destruction of cartilage tissue and all components of the joints, including bone tissue. Due to the uneven distribution of the load, the cartilage layer that protects the bone tissue from abrasion and deformation is destroyed, which ultimately leads to hypertrophy (deformation) of the facet joints. Such changes cannot allow the joints to function fully, and stiffness of the spine occurs.
There are three types of arthrosis of the facet vertebrae:
- cervicoarthrosis - deformation of the facet joints of the cervical spine;
- dorsarthrosis. The joints of the thoracic region are affected;
- lumboarthrosis, damage to the joints of the lumbar spine.
Causes and symptoms
Deformation of the facet joints most often develops for the following reasons:
- previous spinal injuries;
- excessive stress on the spine (professional sports);
- impaired metabolic processes in the body, as well as excess weight;
- a consequence of old age;
- other diseases (osteochondrosis, flat feet).
Symptoms of spondyloarthrosis of the facet joints may not appear for a long time. Arthrosis is often discovered during examinations related to completely different human complaints. At the very beginning of the disease, they can make themselves known with mild, nagging pain and discomfort during physical activity.
A more advanced stage of the disease can cause acute pain and stiffness of movement, the inability to bend and straighten in the spine.
Typically, people who spend a lot of time at the computer or sit for a long time in an incorrect position experience pain in the neck. Periodically, movements are accompanied by an unpleasant crunching sound. Gradually, a person loses the ability to fully turn or tilt his head.
Arthrosis of the lumbar spine
Arthrosis of the facet joints of the lumbar spine is a disease characteristic of people with a sedentary lifestyle. It occurs as a result of regular static loads on the lumbar region of the spine, often expressed by pain in the sacral area. The pain has pulling character, may radiate in the buttocks. Lumboarthrosis has another striking sign - stiffness of the lower back upon awakening.
With arthrosis of the thoracic joints, back pain is usually a concern. And in case of prolonged illness, difficulty breathing may also appear. But this type of arthrosis is considered the rarest.
If the disease is not treated promptly, it can lead to incapacity.
Diagnostic and treatment methods
If arthrosis is suspected, it is necessary to undergo an examination, which must include an X-ray examination of the spine. The image can determine the stage of the disease and general state spine and cartilage tissue.
Treatment of facet joint deformity is a long and painstaking process. In order to get the effect of the prescribed procedures, you need a comprehensive approach to the problem, including:
- drug treatment;
- wearing orthopedic corsets and collars;
- physiotherapy;
- massage;
- physiotherapy;
- alternative medicine methods;
- traditional methods of treatment.
When starting treatment, you should remember that the result will depend not only on the effect of drugs and prescriptions. It is necessary to reconsider all aspects of your lifestyle - lose excess weight, add useful physical activity and, possibly, adjust your diet.
The essence of drug treatment for joint deformity is to a greater extent in blocking pain, as well as in restoring cartilage tissue. When using this method, injections are used, including intravenous and intervertebral, tablets and various ointments. These can be analgesics, anti-inflammatory drugs, and also chondroprotectors that tend to support cartilage tissue.
Orthopedic correction, that is, wearing corsets and collars, is designed to reduce the load on the spine, apply this method must be under the strict supervision of a physician.
Massage for facet joint deformities is used to normalize muscle tone. To achieve better results, it is recommended to carry it out together with physical therapy.
Physiotherapy is also an important component of proper and effective treatment. For this disease, types of physiotherapy such as electrophoresis, ultrasound treatment and phonphoresis are used. By influencing the affected area, the devices improve blood flow and accelerate metabolic processes.
Alternative medicine methods include procedures such as hirudotherapy, manual therapy, and acupuncture. But only qualified and certified specialists should carry out such procedures. My patients use a proven remedy that allows them to get rid of pain in 2 weeks without much effort.
O.B. Ershova
Department of FPDO Therapy with a Course of Gerontology, Yaroslavl State Medical Academy
Osteoarthritis is a heterogeneous group of diseases of different etiologies with similar biological, morphological and clinical outcomes, which are based on damage to all components of the joint (articular cartilage, subchondral bone, ligaments, capsule, synovial membrane and periarticular muscles). Osteoarthritis is the most common disease of the musculoskeletal system. It is also one of the main causes of premature loss of ability to work and disability. The most important risk factor for developing osteoarthritis is age. There are studies showing that signs of the disease are detected in 90% of people over 50 years of age. It is obvious that people in the older age group, as a rule, suffer from not one, but several diseases at the same time, including gastrointestinal and cardiac diseases. This makes it difficult to select adequate therapy for osteoarthritis, since it becomes necessary to take into account numerous side effects and interactions between a number of drugs.
The causes of osteoarthritis are diverse, they are often combined, and the contribution of many factors to the formation of the disease at the stages of its development may be different. There are mechanical effects, biological (genetic) characteristics of joint structures, and inflammation. The pathological process in osteoarthritis is characterized primarily by the degradation of cartilage. Histological changes in cartilage concern two main components of the matrix - collagen and proteoglycans, and are detected already in the early stages of the disease. Cartilage degradation is caused by changes in the structure of proteoglycans, aggregated proteoglycans and a decrease in the aggregation properties of monomers. Damage to articular tissue is not limited to the destruction of cartilage, but is accompanied by inflammation of the synovial membrane, since as a result of damage to the cartilage matrix by proteolytic enzymes, its degradation products enter the synovial fluid in excess, causing an inflammatory reaction of the synovial membrane, which in turn leads to the synthesis of cytokines: interleukin-1 , tumor necrosis factor-a, etc.
The most striking clinical manifestations and consequences of osteoarthritis are: pain and dysfunction of the joint, which force the patient to reduce physical activity.
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 medications are classified as disease-modifying drugs. Selection of drugs, selection of combinations various methods Treatments remain strictly individual. Knowledge of the mechanisms of action, effectiveness, contraindications when prescribing drugs, and the safety profile of drugs is extremely important.
Chondroprotectors are currently one of the main prescriptions for patients with osteoarthritis. However, the effectiveness of only certain chondroprotectors (chondroitin sulfate and glucosamine) has been proven in multicenter randomized studies, and their use in osteoarthritis has a high (A1) degree of evidence. More often they are classified as symptomatic slow acting drugs for osteoarthritis (SYSADOA).
Chondroitin sulfate is a sulfated glycosaminoglycan, which is found in the extracellular matrix of articular cartilage and is a polyanionic glycosaminoglycan. high degree, which is an integral part of the aggrecan molecule of cartilage and is responsible for its cellular and physicochemical characteristics. In patients with osteoarthritis, the concentration of chondroitin sulfate in the synovial fluid is lower than normal. Chondroitin sulfate therapy is essentially replacement therapy. The results of pharmacokinetic studies indicate that, when taken orally, it is well adsorbed and is found in high concentrations in synovial fluid. In vitro studies have provided evidence that this drug has anti-inflammatory activity, aimed mainly at the cellular component of inflammation, stimulates the synthesis hyaluronic acid and proteoglycans and inhibits the action of proteolytic enzymes. In experimental studies in vivo, it was found that the administration of chondroitin sulfate orally or intramuscularly to rabbits (with artificial chemical degeneration of cartilage) significantly increased the content of cartilage proteoglycans compared to control animals. This indicates that chondroitin sulfate protects cartilage when damaged and has the ability to support resynthesis of matrix proteoglycan.
There is evidence of the ability of chondroitin sulfate to suppress the formation of superoxide radicals and the synthesis of nitric oxide, which explains the analgesic effect that develops quite quickly during treatment with it. Another mechanism that could potentially underlie its structure-modifying effect is associated with the suppression of catabolic (cytokine-dependent cartilage destruction, inactivation of matrix metalloproteinases) and stimulation of anabolic (proteoglycan synthesis) processes in cartilage, as well as slowing down chondrocyte apoptosis.
A published meta-analysis covering studies up to 1999 is devoted to the study of chondroitin sulfate and glucosamine sulfate. The authors conclude that chondroitin and glucosamine have moderate to significant effects on pain and functional joint mobility in OA compared with placebo.
In a randomized controlled comparative study of chondroitin sulfate and diclofenac, conducted in 146 patients, a more rapid reduction in clinical symptoms was observed in patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs), but a return of these symptoms was noted immediately after discontinuation of therapy. Chondroitin sulfate was characterized by a slower onset of therapeutic action, which lasted up to 3 months after the end of treatment.
The level of evidence for the effectiveness of the original glucosamine sulfate was high (1A). In the multifaceted complex mechanism of action of this drug, the anti-inflammatory component is represented by the ability to inhibit the factor activating pro-inflammatory genes - NF-kb. Glucosamine sulfate is a component of articular cartilage. In vitro, this substance, added to cultured chondrocytes, has been shown to stimulate proteoglycan synthesis. Early short-term studies suggest the effectiveness of oral glucosamine sulfate. Glucosamine monosulfate is a substrate for the synthesis of proteoglycans by chondrocytes, participates in the synthesis of glucuronic acid (a substance that ensures the viscosity of intra-articular fluid), and also inhibits the activity of metalloproteinases (collagenase, phospholipase). It is believed that glucosamine monosulfate has a dual effect - anti-inflammatory and chondroprotective. According to available data obtained from randomized multicenter studies, 1500 mg/day of glucosamine sulfate improved the condition of patients when used alone. In cases where the disease occurred with an unexpressed inflammatory component, the effectiveness of glucosamine sulfate was not inferior to that of NSAIDs. Additionally, data were obtained indicating the presence of an additive effect with the combined use of glucosamine sulfate and NSAIDs.
For all chondroprotectors E.L. Nasonov notes the following common features:
- their anti-inflammatory effect is comparable to that of NSAIDs;
- they allow you to reduce the dose of NSAIDs;
- the effect persists after the end of treatment;
- they are combined with paracetamol and NSAIDs;
- there are practically no side effects when using them,
- they slow down the progression of osteoarthritis (?).
And although the last point needs confirmation, a number of studies have shown the ability of some chondroprotectors to slow down structural changes in joints. As for their real analgesic, anti-inflammatory effect and reducing the need for NSAIDs, this study is almost unanimous, and we, taking into account personal experience and the results of clinical trials, also join this opinion.
There are combination drugs containing chondroitin sulfate and glucosamine sulfate). The duration of taking these chondroprotectors is usually up to 3-4 months; Such courses are recommended 2 times a year. New chondroprotectors consisting of these components are appearing on the market. Several clinical studies have evaluated the effectiveness of a combination of glucosamine and chondroitin (often with other components) compared with placebo. These combinations have not been compared with each other, or with monotherapy, so it is impossible to draw conclusions about the advantages or disadvantages of this approach. Drugs from other groups with a chondroprotective effect are appearing, but the data is still insufficient and, accordingly, the degree of evidence for treatment with these drugs is lower than that of chondroitin sulfate and glucosamine. As an example, let us take piascledine 300, a complex of active phytostyrenes (g-tocopherol and b-sitostyrol) and saturated fatty acids (fraction H), obtained by molecular distillation. In the mechanism of its action, three points should be noted:
- stimulation of collagen synthesis through an anabolic effect by increasing the expression of the transforming growth factor TGF-b1;
- inhibition of collagenolytic activity of chondrocytes by increasing the synthesis of an inhibitor of plasminogen activity, which leads to a decrease in the activity of metalloproteinases;
- decreased production of pro-inflammatory cytokines and PGE.
However, the methods used to treat osteoarthritis cannot be considered perfect, so the search continues for new drugs that could not only reduce pain, but also slow down the progression of joint destruction, and thereby prevent or delay joint dysfunction and the development of disability. Along with this, local (local) therapy, including the use of ointments and gels, is of great importance in the treatment of articular syndrome in osteoarthritis.
Let us recall the existence of such a method of treatment as intra-articular injection of lubricants, which has its own history (many rheumatologists remember the use of polyvinylpyridone for this purpose), but this direction has become popular only since the end of the last century. Currently, hyaluronic acid preparations are used as “artificial lubricant” of the joint. They are usually injected into the knee joint once a week, the course is 3-5 injections, the duration of improvement is 4-6 months. It should be borne in mind that a clearer effect is observed only in the early stages of arthrosis. The domestic drug of this group is a synthetic polymer, the allergenicity of which, due to the fact that it does not contain ingredients of animal origin, is negligible; its entry into soft periarticular tissues does not cause reactions and, therefore, it is possible to inject it into different joints, not just the knee . This drug also has certain antibacterial properties due to the silver ions it contains and can be effective for up to 1-2 years at any stage of arthrosis.
Among the domestic products for local therapy, Chondroxide (ointment) has recently gained recognition, the active ingredient of which is chondroitin sulfate, due to which it has a stimulating effect on the regeneration of articular cartilage, which allows this drug to be classified as a replacement restorative agent, identical to mucopolysaccharides and glycosamines. Recommended for external use by applying 2-3 times a day to the skin over the lesion and rubbing for 2-3 minutes until completely absorbed.
Dimethyl sulfoxide has anti-inflammatory, analgesic and fibrinolytic effects, promotes the penetration of chondroitin through cell membranes and its entry into periarticular tissues, muscles and the joint cavity. The active substances of Chondroxide are chondroitin sulfate and dimethyl sulfoxide.
Chondroitin sulfate is a structural modulator that is not only synthesized by the body, but also, after administration, integrates into the structures of cartilage tissue, stimulating its synthesis and inhibiting destruction. Its timely administration and regular use ensure inhibition, stabilization and prevention of development destructive processes in the joint. When applied topically, dimethyl sulfoxide also causes a general anti-inflammatory effect and helps to enhance the direction of other drugs into inflamed organs (tissues).
Thanks to its unique composition, Chondroxide ointment has a rapid and pronounced analgesic and anti-inflammatory effect, and has a chondroprotective and regenerative effect.
With an integrated approach to the treatment of patients with osteoarthritis, physiotherapeutic methods are widely used, the use of which helps to improve microcirculation in the subchondral bone, synovium and periarticular tissues, metabolism, and slow down destructive processes. Techniques such as ultrasound, electrophoresis with drugs, laser therapy, paraffin therapy, magnetic therapy and many others in patients with osteoarthritis lead to a decrease in muscle spasm, increasing lymphatic drainage, improving blood supply to tissues, reducing pain and increasing the functional activity of joints. However, the widespread use of many treatment methods is limited due to the frequent presence of contraindications in patients with this disease due to concomitant pathologies, such as cardiovascular, including arterial hypertension, coronary heart disease, rhythm disturbances, as well as diseases of the thyroid gland, uterine fibroids , mastopathy, etc. Magnetotherapy, including magnetophoresis of drugs, unlike other physiotherapeutic methods, does not have side effects, which makes it possible to use it for different concomitant pathology. An important difference between magnetic therapy is the possibility of using this method in any phase of local inflammation, including in the presence of synovitis. For magnetophoresis, the authors used the Polyus-2 apparatus for low-frequency magnetic therapy. Magnetophoresis was carried out in continuous mode with a frequency of 50 GU (stepped intensity, up to 4, duration of one procedure – 15 minutes).
According to a study conducted by V.N. Sorotskaya et al. , the use of magnetophoresis with Chondroxide ointment in the treatment of patients with osteoarthritis of large joints (knee, hip, shoulder) provided a pronounced analgesic effect. At the same time, against the background of this therapy, there was a significant improvement in the functional state of the joints, as well as a more rapid onset of the positive effect of treatment compared to patients who received only basic therapy. Along with this, magnetophoresis with Chondroxide ointment has proven itself to be not only effective, but also safe method treatment of osteoarthritis, including in patients for whom phonophoresis is contraindicated.
According to the authors from CITO im. N.N. Priorova, for the treatment of arthrogenic pain in osteoarthritis, the use of chondroxide by ultraphonophoresis is more effective. Due to the presence of dimethyl sulfoxide in the composition of the drug, the permeability of the skin increases, which means that the penetration into the body of chondroitin sulfate, which acts in the metabolism of proteoglycans and thereby ensures an increase in the synthesis of cartilage matrix components and inhibition of the processes of cartilage destruction, is improved. This achieves an anti-inflammatory effect in recurrent synovitis, which is one of the causes of arthrogenic pain in osteoarthritis. The course of treatment includes 8-10 daily procedures. Phonophoresis should be carried out as follows: 5% chondroxide ointment is applied around the circumference of the affected joint and rubbed in for 2-3 minutes until completely absorbed (ultrasound intensity - 0.40.6 W/cm 2, technique - labile, mode - continuous, 3- 5 minutes on the field). Chondroxide phonophoresis is safe, does not cause side effects and can be recommended for complex therapy of osteoarthritis.
In general, the main advantage of Chondroxide is the combination of anti-inflammatory, analgesic and chondroprotective effects, which allows, while solving the main problem of treating osteoarthritis - the use of disease-modifying therapy with chondroprotectors, to reduce the use of non-steroidal anti-inflammatory and analgesic drugs that cause a number of serious side effects (gastrointestinal, cardiac, etc. )
Thus, the drugs used for osteoarthritis are numerous and varied. At the same time, the correct choice of the type of therapy and prescription regimen with the mandatory inclusion of drugs that have a chondroprotective effect is extremely important, since in this case not only the effectiveness of treatment increases, but also the quality of life of patients improves.
Literature
Osteoarthritis (OA) is a chronic progressive degenerative joint disease characterized by degradation of articular cartilage with subsequent changes in the subchondral bone and the development of marginal osteophytes, leading to loss of cartilage and concomitant damage to other components of the joint (synovium, ligaments).
During the International Decade of Bone and Joint Diseases (2000–2010), the following diseases were identified as having the most important medical and social significance for society: osteoarthritis, osteoporosis, low back pain, rheumatoid arthritis, traumatic injuries. In terms of its impact on health, OA ranks fourth among all diseases in Western countries in women and eighth in men. The incidence of OA progressively increases with age. Due to the significant aging of the population, including the Ukrainian population, the issues of prevention and treatment of this disease are of particular relevance.
Medical and social significance. Osteoarthritis is the most common form of joint pathology. In Western countries, radiographic evidence of OA occurs in most people over 65 years of age and in approximately 80% of people over 75 years of age. Approximately 11% of people over 60 years of age have symptomatic (clinical) knee OA. Among US residents over 30 years of age, symptomatic knee OA occurs in approximately 6%, and symptomatic knee OA hip joint– approximately 3% of the population.
Because of its prevalence and the frequent disability that accompanies the disease when it is localized in the knee and hip joints, OA causes more problems with walking and climbing stairs than any other disease. OA – the most common reason endoprosthetics of the hip and knee joints.
The prevalence of the disease has been studied through epidemiological studies. The incidence of osteoarthritis increases with age, with obvious sex differences. Before age 50, the prevalence of OA in most joints is higher in men compared to women. After 50 years, women, compared to men, are more likely to experience OA of the knee joints, hand joints, and feet. In most studies, hip OA is more common in men. In population studies, the incidence and prevalence of the disease increases 2-10 times over the period from 30 to 65 years and continues to increase further with age.
OA develops mainly in middle and old age, and at a young age it can occur after joint injuries, inflammatory processes, and in patients with congenital pathology of the musculoskeletal system. With age, the incidence of OA increases significantly. So, if under the age of 29, 8.4 people per 1000 people are sick, at 30–39 years old – 42.1 per 1000 people, 40–49 years old – 191.9 per 1000 people, 50–59 years old – 297.2 per 1000 people, then in 60–69 years old – 879.7 per 1000 people . Gonarthrosis in men occurs more than 2 times less often than in women, while women more often suffer from OA of the knee joint (gonarthrosis), and men more often suffer from OA of the hip joint (coxarthrosis). . Although the development of OA does not affect life prognosis, the disease is one of the main causes of premature loss of ability to work and disability. Osteoarthritis is one of the main causes of chronic pain syndrome, which significantly reduces the quality of life of patients.
The incidence of damage to individual joints in OA varies. Some studies indicate the predominance of arthrosis of the small joints of the hands over other localizations, while others indicate the predominance of arthrosis of the knee joint. A study by the Institute of Rheumatology of the USSR Academy of Medical Sciences found that among patients with OA there was more frequent damage to the knee joints (71.2%) and small joints of the hands (47.7%), followed by joints of the feet, including ankles (23.3%) and the spine .
Figure 1. Prevalence of osteoarthritis depending on age and location
Mechanisms of development of osteoarthritis. Osteoarthritis can be diagnosed based on clinical symptoms or pathological manifestations of the disease. The pathological process of OA involves the entire joint, which includes focal and progressive loss of hyaline articular cartilage with associated changes in subchondral bone, development of marginal growths (osteophytes) and thickening of the endplate of bone (subchondral sclerosis). Soft tissue structures in and around the joint are also affected. They include the synovium, which may exhibit mild inflammatory infiltrates, often altered muscles and ligaments that become “weak.” Many people with radiographic signs of OA have no clinical signs of the disease.
There are two main forms of OA: primary, or idiopathic osteoarthritis, the etiology of which is unknown, and secondary, the occurrence of which is caused by disorders in the joint caused by the influence of known etiological factors ( inflammatory diseases, injuries, congenital or acquired anatomical deformities, metabolic disorders and etc.).
Many factors take part in the development of OA, with some playing a leading role (physical activity, microtrauma, hypoxia and ischemia), while others play a predisposing role (hormonal, metabolic, infectious-allergic factors, age, physical inactivity).
Risk factors that determine the possibility of developing OA are conventionally divided into three main groups (Table 1).
Table 1. Risk factors for developing osteoarthritis
|
Genetic |
Purchased |
Environmental factors |
|
|
|
It should be noted that factors associated with damage to various joints (coxarthrosis, gonarthrosis, etc.) may vary significantly.
The basis of damage in OA is changes in cartilage tissue, the most important function of which is adaptation of the joint to mechanical load. With OA, degeneration and death of chondrocytes occurs, depolymerization of the main substance produced by them develops, and the number of glycosaminoglycans decreases. The loss of proteoglycans leads to a decrease in cartilage strength and degeneration. The response of bone tissue is expressed in its growth and formation of osteophytes.
The state of the endocrine status of the body is important factor possible development of OA. It has now been proven that hormonal influences are significant regulators at the stages of growth and development of cartilage tissue, and chondrocytes have specific receptors for thyroxine , insulin , glucocorticoids, somatotropin , estradiol , testosterone . Under experimental conditions, it has been shown that an imbalance of hormones in the body leads to changes in the metabolism of cartilage tissue, and therefore disorders in the endocrine system can be considered a risk factor for osteoarthritis .
Today, there is a debate in the world literature about the role of sex hormone deficiency and menopause in the development of OA. In 1940, M. Silberberg, N. Silberberg showed that the administration of pituitary gland extract to animals leads to degeneration of articular cartilage, and the administration of estrogens has a beneficial effect on their metabolism. In 1966, S. Seze and A. Ryskewaert expressed the view that disorders in the hypothalamic-pituitary-ovarian system, especially those occurring in the postmenopausal period, may be a pathogenetic link in the development of OA. More recent work has shown that estrogen receptors exist in joint tissues, namely in synoviocytes, chondrocytes, fibroblasts, synovial epithelium, articular vascular walls, and articular stroma.
Immune disorders are of great importance in the development of OA. The destruction of cartilage proteoglycans is accompanied by the development of immune reactions of cellular and humoral immunity. Sensitization of the breakdown products of T- and B-lymphocytes is manifested by increased production of lymphokines and the formation of immune complexes, as well as, possibly, the formation of autoantibodies to cartilage tissue and synovial tissue. This leads to progressive fibrosis of the synovial membrane, pathological changes in the synovial fluid, and impaired lubrication and nutrition of the cartilage. The production of defective synovial fluid supports the progression of degenerative changes in articular cartilage .
An important role in the development of catabolic processes in cartilage in OA is played by “pro-inflammatory” cytokines, especially interleukin I (IL-I) and tumor necrotizing factor α (TNF-α), which activate enzymes involved in proteolytic damage to cartilage tissue. OA develops when the catabolism (destruction) of cartilage tissue exceeds its synthesis. It is believed that collagenolytic enzymes (metalloproteinase -1, 8, 13) contribute to the destruction of cartilage.
Another important factor leading to the more frequent development of OA is excessive stress on the joints. Thus, it has been established that people who are engaged in heavy work are more likely to get sick. physical labor and with work experience of more than 5 years. In addition, most often with OA, the process involves weight-bearing joints (knees, hips), small joints of the hands (distal and proximal interphalangeal joints of the hands) and the spine . Occupational stress associated with bending the knee joints, squatting and walking on stairs are associated with a higher risk of developing knee OA, while heavy lifting and heavy physical work are associated with a risk of developing coxarthrosis. However, health physical exercise exercises, such as running, do not increase the risk of developing OA in the absence of biomechanical disorders in the joints.
Overweight people have a high incidence of knee OA. Weight loss in obesity may reduce the risk of developing OA. In the Freemanheim Study, women who lost an average of 11 pounds reduced their risk of developing knee OA by 50%. The relationship between increased body weight and osteoarthritis of the hip joints is less pronounced than with OA of the knee joints. In this case, unilateral damage to the hip joint is not associated with excess weight, in contrast to bilateral localization.
Overload of the knee and hip joints leads to damage to cartilage tissue and disorders in the ligamentous apparatus, as well as other supporting structures. For every 1 pound increase in mass, the total force acting on the knee joint while standing on one lower limb increases by 2 to 3 pounds. This effect of overuse explains most of the increased risk of developing knee and hip OA among overweight individuals. Some, but not most, studies have reported an association between excess weight and hand OA, suggesting that metabolic disorders may act as a mediator (eg, diabetes or lipid disorders), but such a mediator has not been conclusively identified.
Classification of osteoarthritis. In accordance with the International Classification of Diseases, X revision, the following are distinguished:
M15. Polyarthrosis. Included: arthrosis of more than one joint.
M16. Coxarthrosis (arthrosis of the hip joint).
M17. Gonarthrosis (arthrosis of the knee joint).
M18. Arthrosis of the first carpometacarpal joint.
M19. Other arthrosis.
There are two main forms of OA: primary, or idiopathic osteoarthritis, the etiology of which is unknown, and secondary, the occurrence of which is caused by disorders in the joint caused by the influence of known etiological factors (Table 2).
Table 2. Classification of osteoarthritis
| Primary osteoarthritis |
Secondary osteoarthritis and its causes |
|
The degenerative process develops in healthy articular cartilage, for example, under the influence of excessive functional load |
Degenerative processes develop in altered articular cartilage as a consequence of: · inflammatory diseases connective tissue; · injuries (fractures, meniscus damage, repeated microtraumas); joint overload (professional or sports overload); metabolic disorders (acromegaly, hyperparathyroidism, hemochromatosis, etc.); · congenital or acquired anatomical deformities (hip dysplasia, epiphyseal dysplasia); · some diseases of bones and joints (aseptic necrosis, Paget's disease, etc.) |
The following specific subclasses of secondary osteoarthritis are distinguished:
· erosive OA of the hand;
Monoarticular synovitis of the knee joint;
chondrocalcinosis and osteoarthritis.
Based on localization, the following types of secondary osteoarthritis are distinguished: monoarticular, oligoarticular, polyarticular.
Clinical manifestations of osteoarthritis. The main clinical symptoms of OA are pain and joint deformation, leading to dysfunction of the joint. . Variants of pain syndrome in osteoarthritis of the knee joint are shown in Table 1. Pain occurs when the affected joint is loaded, when walking, and decreases with rest. Evening and night pain is typical after daytime exercise. Sometimes joint pain intensifies under the influence of meteorological factors (low temperature, high humidity and atmospheric pressure etc.), causing an increase in pressure in the joint cavity. Stiffness in OA lasts up to 30 minutes, unlike rheumatoid arthritis(more than an hour).
Table 3. Variants of pain syndrome in osteoarthritis (Mazurov V.I., Onushchenko I.A., 2000)
|
Variant of pain syndrome |
Clinical features |
Mechanical pain |
Occurs when there is a load on the joint, more in the evening, subside after a night's rest |
Starting pains |
Occurs in the presence of reactive synovitis at the beginning of walking, then quickly disappears and resumes with continued physical activity |
|
Pain associated with the presence of tendobursitis and periarthrosis |
Occurs only during movements that involve the affected tendons |
|
Pain associated with venous hyperemia and blood stasis in the subchondral bone against the background of intraosseous hypertension |
Appears at night and disappears in the morning when walking |
Reflex pains |
Caused by reactive synovitis |
Referred pain |
Associated with the involvement of the joint capsule in the inflammatory-degenerative process |
|
"Blockade pain" |
Caused by infringement of the sequester of cartilage (articular “mouse”) between the articular surfaces |
According to the course, OA is divided into slowly and rapidly progressing. OA may be accompanied at certain stages of its course by reactive synovitis. The clinical course of OA is characterized by waves, when short periods of exacerbation are followed by spontaneous remission.
When interviewing the patient, the reasons for the development of the disease and the presence of risk factors for the development and progression of the pathological process are clarified. The examination makes it possible to identify joint deformations in the frontal and sagittal planes, gait disturbances, its features, the ability to move independently or with the use of additional means (cane, crutches), and to compare the patient’s movement across terrain and on stairs (up and down). The localization of pain, the presence of synovitis, loose intra-articular bodies are determined, damage to the menisci is identified, the range of motion in the joint, and the magnitude of flexion and extension contractures are measured.
The formation of nodules in the area of the proximal (Bouchard's nodes) and distal (Heberden's nodes) interphalangeal joints is also characteristic. Severe swelling and a local increase in temperature over the joints are not typical, but can occur with the development of secondary synovitis.
Diagnosis of osteoarthritis. Classification criteria help to distribute patients into various categories according to etiopathogenetic principles, but do not reflect individual characteristics and differences in the clinical manifestations of OA. Classification criteria differ from diagnostic criteria, which describe the symptoms of the disease. This is reflected in the classification criteria for OA of the knee, hip joints and OA of the hand joints developed by the American College of Rheumatology (Table 4).
Table 4. Classification criteria for osteoarthritis of the knee and hip joints (American College of Rheumatology).
Clinical criteria |
Clinical, laboratory and radiological criteria |
|
|
Knee-joint |
||
|
1. Knee pain on most days of the previous month |
||
|
2. Crepitation |
2. Presence of osteophytes |
|
|
3. Morning stiffness< 30 мин |
3. Synovial fluid typical for OA |
|
|
4. Age > 38 years |
4. Age > 40 years |
|
|
5. Increase in bone size |
5. Morning stiffness< 30 мин |
|
|
6. Crepitus |
||
|
|
The diagnosis is reliable with such sets of criteria |
|
|
Hip joint |
||
|
1. Hip pain on most days of the previous month |
||
|
2. Internal rotation< 15 0 |
2.ESR< 20 мм/час |
|
|
3.ESR< 45 мм/час |
3. Osteophytes (x-ray) |
|
|
4. Hip flexion< 115 0 |
4. Narrowing of the joint space (x-ray) |
|
|
5. Internal rotation > 15 0 |
||
|
6. Morning stiffness< 60 мин. |
||
|
7. Age > 50 years |
||
|
8. Pain during internal rotation |
||
|
The diagnosis is reliable with such sets of criteria |
The diagnosis is reliable with such sets of criteria |
|
Currently, diagnostic approaches and classification criteria have been developed for the most common localizations of OA (knee, hip and hand joints); however, there may be difficulties in establishing the initial manifestations of OA of various localizations.
The diagnostic process involves a thorough history taking, a detailed analysis of complaints, a clinical examination, an analysis of the causes of pain and the presence of deformities. When making a diagnosis, it should be taken into account that pain and joint deformities are not always a consequence of OA, even if the patient is elderly age groups and signs of OA were confirmed radiographically. It should be borne in mind that with OA, the patient’s main complaints may be related to the pathology concomitant with the disease (for example, enthesopathy or tendinopathy), and the most effective treatment methods will be physiotherapy, as well as local injection therapy. A timely diagnosis of OA is the key to successful treatment.
To establish a correct diagnosis, the following criteria must be taken into account:
· certain symptoms, such as pain of a mechanical type (occurs when walking and especially when going up and down stairs and goes away at rest);
· clinical signs of deformity;
· X-ray signs of narrowing of the joint space.
Laboratory tests usually show no changes in the blood; examination of the synovial fluid reveals slight turbidity, the absence of crystals, leukocytes - less than 2000 cells/mm 3 and neutrophils - less than 25%.
X-ray criteria for osteoarthritis. The following main radiological signs of OA are distinguished:
· osteophytes – bone marginal growths that increase the area of contact, changing the congruence of the articular surfaces;
· narrowing of the joint space, more pronounced in segments experiencing greater load (in the knee joints - in the medial sections, in the hip joints - in the lateral sections);
· subchondral sclerosis (hardening of bone tissue).
Optional radiological signs of OA are:
cysts (usually located along the axis heaviest load);
· subluxations and dislocations;
· erosion.
To determine radiological changes and the severity of OA, the classification proposed by J. Kellgren and J. Lawrence is most often used, which identifies 4 stages of the main radiological signs of OA.
Stages of osteoarthritis according to J. Kellgren and J. Lawrence:
Stage 0 – absence of radiological signs;
Stage I – doubtful;
Stage II – minimal;
Stage III – middle;
Stage IV – pronounced.
N.S. Kosinskaya proposed to distinguish 3 clinical and radiological stages of OA.
Stage I – slight restriction of mobility in the joint, mainly in any specific direction. The radiograph reveals small bone growths along the edges of the articular cavity, as well as islands of ossification of the articular cartilage that subsequently merge with the epiphysis, the joint space is slightly narrowed.
Stage II – general limitation of joint mobility, rough crunching when moving, moderate atrophy of regional muscles. The x-ray shows significant bone growths, narrowing of the joint space by 2-3 times compared to normal, subchondral sclerosis.
Stage III – significant joint deformation with severe limitation his mobility. The radiograph shows almost complete disappearance of the joint space, pronounced deformation and compaction of the articular surfaces of the epiphyses, and extensive marginal growths.
Mistakes in diagnosing osteoarthritis. The most important causes of errors in the diagnosis of osteoarthritis are listed below.
I. Incorrect interpretation of pain syndrome
1. The cause of the pain syndrome is not OA, but another pathological process:
arthritis of another origin;
· pathological changes in the bones that form the joint (tumor, osteomyelitis, metabolic bone diseases, etc.);
· mechanical damage, pathological fractures;
· irritative pain syndrome (for example, radiculopathy of the L 4 spinal root can cause pain in the knee joint or in the area of the greater trochanter);
· other neurological diseases causing immobility in the joint (parkinsonism, damage to central motor neurons, etc.);
· soft tissue disorders independent of OA (for example, tendinopathy of the pes anserine region, Querwen's disease, etc.).
2. The cause of the pain syndrome is OA of a different localization:
· pain in the knee joint with OA of the hip joint;
pain in shoulder joint with osteochondrosis of the spinal motion segment C 4 – C 5;
· pain due to osteochondrosis of the lumbosacral spine, causing pain in the hip, knee or ankle joints.
3. The cause of pain is secondary changes in periarticular soft tissues in OA:
· ligamentitis (especially with OA of the knee joint);
· enthesopathies, tendinopathies as a result of joint contractures;
· bursitis (for example, Baker's cyst).
II. Incorrect interpretation of joint deformities:
Pseudohypertrophic arthropathy;
· psoriatic arthritis (distal type);
· flexion contracture of joints;
mucopolysaccharidosis;
· neurogenic arthropathy;
· crystalline arthropathy;
· varus or valgus deformity of joints not associated with OA.
III. Incorrect interpretation of x-ray images:
· arthritis due to previous OA;
· initial manifestations of OA (radiological signs of OA may be absent);
idiopathic widespread hyperostosis syndrome;
· flexion contracture, causing an apparent narrowing of the joint space.
IV. Neurogenic and metabolic arthropathy:
· pyrophosphate arthropathy;
· hydroxyapatite arthropathy;
arthropathy due to hemochromatosis;
alkaptonuria.
To avoid mistakes when making a diagnosis of osteoarthritis, a thorough medical history should be taken, a qualified neuro-orthopedic examination (determination of pain, identification of contractures and deformities, examination of joint function), laboratory and X-ray studies, and, if necessary, use other diagnostic methods (computed tomography, magnetic resonance imaging) -nuclear resonance, etc.).
Differential diagnosis of pain syndrome in osteoarthritis of the knee joint. Pain syndrome in OA of the knee joint is mainly mechanical in nature, i.e. occurs when physical activity and decreases at rest. Its nature depends on various pathogenetic mechanisms.
The most common cause of pain in knee OA is reactive synovitis. The causes of its occurrence are most often trauma, mechanical overload of the joints, and inflammatory changes. Synovitis is often accompanied by the phenomenon of tendobursitis, in which pain occurs during certain movements in the knee joint, associated with contraction of the affected tendon. These phenomena, unlike synovitis in arthritis, quickly disappear with bed rest.
Reactive synovitis is characterized by so-called starting pains that occur during the patient’s first steps; they then quickly disappear and may recur after continued physical activity. Initial pain occurs when the affected cartilages rub against each other, on the surface of which cartilaginous detritus (fragments of necrotic cartilage) settles. With the first movements in the knee joint, detritus is pushed into the joint cavity and the pain stops. The occurrence of initial pain is facilitated by the discrepancy between the rapid increase in the need for tissue respiration and the ability of the microvasculature to provide blood to the tissues.
The occurrence of synovitis may be associated with the precipitation of calcium pyrophosphate or hydroxyapatite crystals into the joint cavity with their subsequent phagocytosis, release of lysosomal enzymes and the development of an inflammatory reaction.
Venous hyperemia, stasis in the subchondral bone, and increased intraosseous venous pressure cause dull, continuous pain at night, which disappears with walking. These pains are figuratively called “articular migraine,” which emphasizes the leading role of venous disorders in their pathogenesis. It should be borne in mind that ischemic pain can also occur with avascular necrosis and in patients with sickle cell anemia.
Pain during prolonged stay vertical position or prolonged walking (with mechanical load), usually occur due to a decrease in the ability to bear the load of the subchondral bone. They are caused by the development of osteosclerosis and osteoporosis of the epiphyses.
Patients with knee OA often experience tissue tenderness in the immediate vicinity of the joints, i.e. periarticular tissues (muscle tendons, their sheaths, mucous bursae, ligaments, fascia and aponeuroses), as well as tissues located at some distance from the joints (muscles, neurovascular formations, subcutaneous fatty tissue).
With OA of the knee joint, soft tissue changes are observed both in the periarticular area (mainly in the places of attachment of the muscles of the sartorius, tender, semitendinosus, semimembranosus and biceps femoris muscles), interpreted as periarthritis of the knee joint, and in areas associated with the joint functionally. At the same time, zones of painful trigger activity are formed in the proximal parts of the rectus muscle, the muscle that tenses the fascia lata, the gluteus maximus muscle, as well as in the area of the iliotibial tract, which is regarded as myofascial syndromes in OA of the knee joint. These changes lead to the formation of painful contractures and limitation of movements in the knee joints.
The pain syndrome that occurs when walking down stairs in the later stages of the pathological process is caused by damage to the ligamentous apparatus and regional muscles. Constant pain with any movement of the joint is associated with a reflex spasm of nearby muscles. Sudden acute pain and the appearance of a block in the joint, forcing the patient to stop, are associated with the pinching of a relatively large bone or cartilaginous fragment, the so-called articular mouse, between the articular surfaces. The source of the formation of loose articular bodies in OA of the knee joints can be fragments of altered cartilage, bone fragments, and meniscal tissue. After several successful movements in the joint, the “joint mouse” slips out, the pain suddenly stops, and movement in the joint is restored.
Degenerative changes or rupture (full or partial) of the meniscus lead to joint instability and pain.
The most common causes of pain in OA of the knee joint are reactive synovitis, periarthritis and spasm of nearby muscles.
Incorrect interpretation of the pain syndrome when diagnosing OA of the knee joint can occur with arthritis of other origins, mechanical damage and other processes in soft tissues not associated with OA, with pain in the knee joints of an irritating nature caused by OA of the hip joint or clinical manifestations of osteochondrosis of the lumbosacral region spine.
Differential diagnosis should also be carried out for diseases in the clinical picture of which pain syndrome of the knee joint is observed:
· osteochondropathy of the tibial tuberosity (Osgood–Schlatter disease);
osteochondropathy articular surface femoral condyle (König disease);
· post-traumatic calcification of soft tissues in the area of the internal femoral condyle (Pelligrini–Stieda disease);
· post-traumatic damage to the pterygoid folds and hyperplasia of the articular fatty tissue of the knee joint (Hoffa disease).
Treatment of osteoarthritis. The famous specialist John Kent Spender (1829–1916) wrote more than a hundred years ago that “few topics can cause drowsiness and despair like a conference devoted to the problem of discussing osteoarthritis. The area is so barren. The result is minimal...” Note that in foreign literature osteoarthritis is an analogue of osteoarthritis, so researchers emphasize the role of the inflammatory process in the pathogenesis of the disease. However, the most commonly used group of drugs used in the treatment of OA are non-steroidal anti-inflammatory drugs (NSAIDs).
The mechanism of action of NSAIDs is due to inhibition of the conversion of arachidonic acid into prostaglandins by inhibiting the enzyme cyclooxygenase (COX). Two COX isoenzymes have been identified: COX-1 and COX-2. COX-1 exists normally in the body and catalyzes the synthesis of prostaglandins (PGs), which are involved in numerous physiological functions, including the normal functioning of the mucous membrane gastrointestinal tract and aggregation properties of thromboxane 2 in platelets. COX-2 is synthesized only when tissue is damaged, induces the production of cytokines and other inflammatory mediators in a number of tissues, including endothelial cells, and is thought to play a role in the development of pain, inflammation and fever. COX-2 production increases significantly under inflammatory conditions. PGs formed under the influence of COX-2 take part in the development and progression of acute and chronic inflammation. Thus, PG E2, expanding the arterioles, increases blood flow to the area of inflammation, and PG F2a narrows the venules and impedes the outflow of blood, which contributes to the development of exudation. In addition, PGs cause hyperalgesia and potentiate the action of other inflammatory mediators.
The central mechanism of action of NSAIDs is associated with inhibition of the synthesis of prostaglandins, which are formed in the central nervous system and contribute to the transmission of pain signals. NSAIDs reduce the sensitivity of pain receptors, reduce tissue swelling at the site of inflammation, weakening the mechanical pressure on nociceptors. Additional mechanisms of the anti-inflammatory activity of NSAIDs that are not related to COX inhibition are discussed: inhibition of neutrophil function and interaction of leukocytes with the vascular endothelium, activation of the NF-kB transcription factor, which regulates the synthesis of proinflammatory mediators, or even opioid-like effects.
In providing an adequate level of pain relief great attention is given to traditional NSAIDs, which have a powerful analgesic effect, but have a number of side effects. According to the literature, the prevalence of gastric and duodenal ulcers in patients with long-term use of NSAIDs is about 20%, and the annual incidence serious complications from these ulcers – 1–4%. Therefore, choosing an adequate pain reliever with minimal risk of developing side effects remains a challenge.
Among COX-2 selective drugs, nimesulide (4-nitro-2-phenoxymethanesulfonamide) remains the most studied - a unique anti-inflammatory drug that differs from most NSAIDs.
Nimesulide is the first representative of a new class of selective COX-2 inhibitors presented on the world market. It has been used in clinical practice since 1985, when it first appeared on the Italian pharmaceutical market, and is currently registered in more than 50 countries around the world. Nimesulide is the most commonly prescribed NSAID in Italy, Portugal, and France. The drug was developed in Switzerland by Helsinn Healthcare in 1980; in 1994, the predominant effect of nimesulide on COX-2 was proven, and was subsequently confirmed by numerous studies. The effect on COX-1 is carried out primarily at the site of inflammation, which provides an additional anti-inflammatory effect, and the lack of effect on COX-1 in the stomach and kidneys, in turn, determines a high safety profile [Barskova V.G., 2011].
The effect of nimesulide is due to class-specific mechanisms characteristic of most NSAIDs and the effects of nimesulide specifically. Like all representatives of the class, nimesulide has anti-inflammatory, analgesic and antipyretic effects. The drug reduces the concentration of short-lived PG H2, from which PG E2 is formed under the action of PG isomerase. A decrease in the concentration of PG E2 leads to a decrease in the degree of activation of EP-type prostanoid receptors, which is realized in analgesic and anti-inflammatory effects. The drug reversibly suppresses the formation of PG E2 not only at the site of inflammation, but also in the ascending pathways of the nociceptive system, including the pathways of pain impulses in the spinal cord. Nimesulide has little effect on COX-1 and practically does not interfere with the formation of PG E2 from arachidonic acid under physiological conditions, thereby reducing the number of side effects of the drug (Fig. 2).
Figure 2. Mechanisms of action of nimesulide
Nimesulide suppresses platelet aggregation by inhibiting the synthesis of endoperoxides and thromboxane A2, suppresses the synthesis of platelet aggregation factor, suppresses the release of histamine, and also reduces the degree of bronchospasm caused by exposure to histamine and acetaldehyde [Kosarev V.V., Babanov S.A., 2011].
Nimesulide inhibits the release of tumor necrosis factor α, which causes the formation of cytokines. It has been shown that nimesulide is able to suppress the synthesis of interleukin-6 and urokinase, metalloproteinases (elastase, collagenase), slowing down the destruction of proteoglycans and collagen of cartilage tissue. In addition, nimesulide suppresses interleukin-1b and chondrocyte apoptosis factor [Vorobeva O.V., 2010].
Nimesulide has antioxidant properties, inhibits the formation of toxic oxygen breakdown products by reducing the activity of myeloperoxidase, affects the production and action of oxidative radicals, as well as other components of neutrophil activation, which enhances the anti-inflammatory and analgesic effects and reduces the likelihood of gastrointestinal ulcerogenicity. The interaction of nimesulide with GCS receptors and their activation by phosphorylation enhances the anti-inflammatory effect of the drug [Kosarev V.V., Babanov S.A., 2011].
The gastrointestinal safety of nimesulide is due to the lack of effect on COX-1 and the chemical properties of the drug. Most traditional NSAIDs have a chemical structure that is acidic and increases permeability small intestine. This is an additional mechanism for the development of gastropathy, not related to inhibition of PG synthesis. Nimesulide, on the contrary, has weak acidic properties and does not accumulate in the mucous membrane of the stomach and intestines. In addition, nimesulide reduces the production of oxidative radicals and leukotrienes, as well as the release of histamine from mast cells, thereby creating additional protection for the gastrointestinal mucosa. In numerous clinical studies with various diseases musculoskeletal system it has been proven that the vast majority adverse reactions for nimesulide, side effects from the gastrointestinal tract are transient, weakly expressed and weakly correlate with the ulcerogenic effect. A double-blind study using gastroduodenoscopy showed that the use of nimesulide at a dose of 100 or 200 mg for 7 days did not lead to changes in the mucous membrane compared with placebo. Thus, it can be stated that nimesulide extremely rarely causes severe gastrointestinal complications, which is especially important for people in older age groups.
Experience with its long-term use is of fundamental importance for assessing the safety of nimesulide. Thus, in the work of P. Locker et al. 199 patients with OA received nimesulide (200 mg) or etodolac (600 mg) for 3 months. The therapeutic potential of nimesulide turned out to be higher: its effect was rated as “good” or “excellent” by 80% of patients, while the comparison drug was given a similar rating by only 68% of patients. Moreover, although etodolac is a selective NSAID and is considered a very well-tolerated drug, the number of side effects in both treatment groups did not differ. In a large study by Huskisson et al. nimesulide (200 mg/day) or diclofenac (150 mg/day) were prescribed to 279 patients with OA, and the duration of therapy was 6 months. The effectiveness of the drugs, which was assessed by the dynamics of the patients’ well-being and the Lequesne functional index, turned out to be virtually the same. However, nimesulide was significantly superior to diclofenac in tolerability: the occurrence of side effects from the gastrointestinal tract was recorded in 36 and 47% of patients, respectively (p<0,05) . В настоящее время наиболее длительным и большим рандомизированным двойным слепым исследованием нимесулида остается работа W. Kriegel et al. В этом исследовании определялись эффективность и безопасность нимесулида (200 мг) и напроксена (750 мг) у 370 больных с ОА в течение 12 мес. Как и в работе Huskisson, эффективность обоих препаратов оказалась сопоставимой. Количество медикаментозных осложнений при использовании нимесулида также оказалось меньшим: суммарно 47,5% (54,5 % – у пациентов, получавших напроксен) [Каратеев А.Е., 2009]. Очень важно, что ни в одной из трех представленных работ не зафиксировано значимого повышения частоты кардиоваскулярных осложнений на фоне длительного приема нимесулида.
In a study by N. A. da Silva et al. A comparative assessment of the effectiveness and tolerability of nimesulide and celecoxib in the treatment of osteoarthritis was carried out. Fifty-seven patients aged 40 and 80 years with osteoarthritis of the knee and hip took part and were randomly assigned to receive either nimesulide or celecoxib for 30 days. The patients' condition was assessed before the start of therapy, after 10, 20 and 30 days of treatment. Significant reductions in pain at rest and with movement were similar in both groups at all follow-up visits. The average duration of morning stiffness decreased significantly with nimesulide throughout the study. In patients receiving celecoxib, a significant reduction in stiffness was noted at the third visit. When assessing functional abilities using the HAQ scale in patients taking nimesulide, a significant improvement in the indicator was observed throughout the entire study period, and in patients receiving celecoxib, only at the 4th visit. The Lesquesne & Samson’s (1991) knee osteoarthritis severity index significantly decreased when taking nimesulide at the 3rd visit; when taking celecoxib, no significant changes in the index were established. Side effects were detected in 21% of patients receiving nimesulide and 25% receiving celecoxib. Thus, although this study showed similar reductions in knee and hip osteoarthritis pain with both nimesulide and celecoxib, there was a significantly greater reduction in morning stiffness, the Lesquesne & Samson's Knee Osteoarthritis Severity Index, and patient functional ability. established in a group of patients receiving nimesulide.
The chondroprotective properties of nimesulide were studied in a randomized, double-blind, controlled clinical trial by H. Ergün et al., the purpose of which was to comparatively evaluate the effectiveness, tolerability and chondroprotection of nimesulide and piroxicam. The study involved 90 patients suffering from osteoarthritis of the knee joint. As a result of treatment, a significant improvement in the osteoarthritis severity index was noted after 2 weeks (p<0,01) и улучшение глобальной оценки артрита врачом через 4 недели (р <0,01) терапии в обоих группах наблюдения. Достоверное снижение суставного индекса болезненности суставов (р <0,05) через 8 недель и самостоятельной оценки нетрудоспособности – через 4 недели (р <0,05) по сравнению с исходным показателем, наблюдалось только в группе пациентов, получающих нимесулид. При проведении магнитно-резонансной томографии с целью оценки изменений в суставном хряще после 6 месяцев терапии не было выявлено достоверных отличий между двумя группами обследуемых пациентов. Побочные эффекты наблюдались у 6 пациентов при приеме нимесулида и 9 пациентов, получавших пироксикам. Таким образом, учитывая клиническую эффективность, результаты визуализирующих методов исследования, меньшую частоту побочных явлений препаратом выбора в лечении остеоартрита коленных суставов является нимесулид .
Have you ever wondered why cats and dogs don't live long? The whole point turns out to be in the structure of the skull, or rather, one might even say so - how the bones of the skull are connected to each other.
And they are connected primarily by special bone tissue, forming sutures. It is these sutures that are very important in the connecting process, as they are shock absorbers and areas for bone growth.
But there is one sad “BUT” - after forty years, these seams heal.
Cervical osteochondrosis is a disease of the cervical spine with degenerative-dystrophic changes in the vertebrae and intervertebral discs.
This type of osteochondrosis is the most common due to the mobility of the cervical spine and the heavy load placed on it.
Osteochondrosis of the cervical spine - symptoms
The sooner you notice signs of cervical osteochondrosis, the greater your chances of stopping this disease.
All symptoms of cervical osteochondrosis can be grouped into three groups:
- neurological group;
- group of movement disorders;
- group of brain symptoms.
The neurological group of symptoms of cervical osteochondrosis includes: discomfort and pain in the neck, tingling and numbness in the neck, upper limbs, shoulder blades and upper chest.
Osteochondrosis is dangerous not only due to constant pain, but also to the risk of complications. Therefore, if you have prolonged and intense pain in the neck area, you should definitely consult a specialist.
In the initial stages of the disease, you will only be recommended exercises for the neck for osteochondrosis. In an advanced state, the disease requires drug therapy to eliminate inflammation and restore vascular patency.
In some cases, it is necessary to wear a special corset to support the head.
If you want to learn all the secrets of treating cervical osteochondrosis, we recommend that you familiarize yourself with this free course. A very effective technique!
Below is an example of several exercises.
- The patient lies down on the floor. Place one palm on your stomach and the other on your chest. Slow, smooth inhalation (the stomach and then the chest rise), then exhale. Repeat 8-10 times. It is necessary to consciously relax the body. The exercise is repeated 3-4 times during the day.
- Position on the floor, but this time on your stomach. Slowly raise your head and torso, placing your hands in front of you on the floor. You need to stay in this position for 1 - 1.5 minutes, then smoothly return to the original position. Important! You need to make sure that your shoulders don’t “sag” - keep your posture under control! The exercise is performed 3-4 times a day.
- Position - lying on your stomach. The arms are extended along the body. The head slowly turns to the right. You must try to press your ear to the floor. Then in the opposite direction. Important! Pain should not accompany exercise! Perform 5-6 times. You can perform this exercise 3-4 times during the day.
- Sitting position. Slowly, as you exhale, bend forward, bringing your chin as close to your chest as possible. Then, as you inhale, slowly tilt your head back, trying to look as far as possible. Repeat 10-15 times. The exercise itself is repeated 2-3 times a day.
- Without changing position, you need to press your forehead to your own palms. Applying as much pressure as possible. The exercise is done while exhaling - this is important! Repeat 5-6 times. Perform 3-4 times during the day.
- If the violation is not severe, you can perform a gentle rotation of the head in both directions.
