Double punch. What to do if arthrosis is combined with osteoporosis | Healthy Life

Not so different from each other

People who are far from medicine believe that osteoporosis is a disease of the musculoskeletal system.
This is partly correct, because with this disease, bone density decreases, they become fragile, which increases the risk of fractures. However, doctors never tire of emphasizing: osteoporosis is primarily a metabolic disorder. Article on the topic Smart Home. How to equip an apartment for a patient with arthrosis

Bone tissue is constantly renewed: some of its cells are destroyed, others are formed. As long as these processes are in balance, bones remain strong. But if, for one reason or another, destruction begins to prevail over formation, they become more porous and brittle.

The mechanism for the development of arthrosis is the same, only the process occurs not in the bones, but in the cartilage tissue of the joints. As long as the breakdown and synthesis of its cells are balanced, cartilage is strong and elastic. If wear and tear occurs faster than renewal, it cracks, becomes thinner, and pain appears in the joint.

The relationship between osteoporosis and osteoarthritis

Questions regarding the relationship between osteoarthritis (OA) and osteoporosis (OP) have been addressed since the late 1960s. Thus, surgeons during operations for hip fractures in patients with AP noted that they had virtually no signs of coxarthrosis [1]. The presence of OA protected against the occurrence of fractures in the proximal femur and spine. In clinical practice, the presence of these two diseases in one patient was considered rare [2]. Scientists have not yet come to a consensus as to whether in this case we are talking about two mutually exclusive diagnoses or not. Is the presence of OA really a protective sign for the development of AP? Today it is known that OA and AP are very common diseases of the musculoskeletal system in older people. Thus, OA accounts for more than 75% of all rheumatic diseases; it is observed in more than 50% of people aged 65 years and older, and more than 1/3 of them develop impairment of various types of physical activity. The prevalence of AP in Russia among patients aged 50 years and older is 30–33% among women and 22–24% among men. Both diseases occur in both women and men, but are more often reported in women, especially after menopause. Thus, OA is detected in every tenth woman over the age of 50, and by the age of 75 - in every second. One in three menopausal women and more than half of those aged 75–80 years suffer from AP. The social significance of AP is determined by its consequences - fractures of the vertebrae and bones of the peripheral skeleton. Among the urban population of Russia, 24% of women and 13% of men aged 50 years and older have at least one clinically significant fracture. The incidence of osteoporotic fractures increases significantly with age, and the prevalence of proximal femur fractures increases exponentially.

The number of AP and OA increases with age, therefore, the increase in life expectancy observed in recent decades in developed countries and, accordingly, the increase in the proportion of older people, especially women, in the population, leads to an increase in the frequency of these diseases, turning them into one of the most important health problems worldwide world.

Although both OA and OP are more common among people of older age groups, nevertheless, patients with these diseases have significant anthropometric differences (for example, OA usually occurs in people with increased body weight, and OP, on the contrary, in frail women), indicating that these two diseases are caused by different processes (Table) [3, 4].

Over the past 30 years, more than 40 studies have been published using various measurement techniques to examine the effects of OA on bone mineral density (BMD) in various skeletal regions. The authors of most of these studies revealed significantly higher BMD rates in patients with OA compared to the control group. However, there are studies in which no increase in BMD was found and even a decrease was noted. Contradictions in the data obtained can be attributed to differences in the selection of individuals for examination, measurement of BMD in different areas of the skeleton, the use of different measuring techniques and different methods for assessing results [2].

In 1995, the first large cross-sectional epidemiological study [5] assessed the association between radiological signs of coxarthrosis and BMD of the proximal femur and spine, measured using dual X-ray absorptiometry, in 4855 women aged 65 years and older. It was found that older white women with moderate to severe forms of radiographically evident coxarthrosis had higher BMD in all parameters compared with women without coxarthrosis, and there was a correlation of a generalized increase in BMD with bilateral coxarthrosis and severe osteophytosis.

The Rotterdam prospective study (1996) was the first to examine the relationship between radiographic OA, assessed according to the Kellgren and Lawrence criteria, BMD in the femoral neck and its dynamics, adjusted for age and body mass index (BMI). A study that involved 1,723 people who were observed for 2 years demonstrated a significant association of coxarthrosis with high BMD and an increase in BMD with disease progression [6].

In addition, studies conducted on twin women confirmed the inverse relationship between OA and OP in the proximal femur. Severe osteophytosis in the hip joint was associated with a 5–6% increase in BMD in this joint [7].

In patients with OA of the knee joints, increased BMD in the proximal femur and spine was also determined, compared with the values observed in individuals without OA [8, 9]. At the same time, a significant increase in BMD of the spine and femoral neck was shown with an increase in the stage of gonarthrosis from 1st to 4th. In addition, a prospective study demonstrated that higher BMD values increase the risk of developing radiographic knee OA [10]. In people with OA of the knee and hip joints, BMD was 3–8% higher compared to healthy study participants [6].

In case of OA of the hands, data on BMD in various areas of the skeleton are contradictory; significant deviations in BMD were not always detected, especially in the presence of isolated lesions.

According to L.I. Alekseeva and co-authors [11], in women with OP of the lumbar spine, the incidence of OA of the knee joints and nodular form was lower than in patients with normal BMD values (53.3 and 38.9%; 78.6 and 53.6%, respectively, p < 0.05). In women with OP of the femoral neck, the nodular form of OA was less frequently diagnosed compared to women with normal BMD (25.9 and 47.8%, respectively, p < 0.05). Thus, these data support the hypothesis that higher BMD is associated with OA.

Interpretation of densitometry results in spinal OA is often difficult due to the presence of osteophytes, narrowing of intervertebral discs, and sclerosis of facet joints. Thus, according to Peel et al [12], in women with spinal OA, BMD of the lumbar spine was increased by 7.9%, in the femoral neck by 6.4%, and in the whole body by 8.4%. In addition, a study of markers of bone turnover showed that in women with spinal OA aged 50–85 years, the levels of markers of both bone formation and resorption decrease, i.e., bone turnover is reduced, and therefore, the loss of BMD is less than in women of the same age without OA.

Other studies demonstrate increased bone formation, which also explains increased BMD in individuals with OA. The inconsistency of the results obtained may be due to the study of different stages of the disease. Thus, the early stages are characterized by rapid formation processes, and in the later stages there is a slowdown in bone turnover in the subchondral part of the bone, which can be considered as a secondary process in relation to the destruction of cartilage and a decrease in static load.

The social significance of AP is determined by its consequences - fractures of the vertebrae and bones of the peripheral skeleton, causing a significant increase in morbidity, disability and mortality among the elderly and, accordingly, large material costs in the field of healthcare. Therefore, the question of particular interest is: does increased BMD associated with the presence of OA lead to a reduced risk of fractures? Two population-based controlled studies of hip fractures [13, 14] showed that OA was associated with a reduced risk of hip fracture. Another study demonstrated that severe hip OA was negatively correlated with vertebral compression fractures. On the other hand, according to some data, despite a 5% increase in BMD in people with coxarthrosis, such patients have a significantly higher risk of fractures compared to the control group. The authors suggested that the increased risk of fractures in people with OA of the hip joints was most likely associated with an increased risk of falls in these patients due to impaired locomotor function of these joints. Individuals with spinal OA, however, had a lower risk of fractures, while no significant associations were found between knee OA and hand OA and fractures [15].

Subsequently, observation of a sample of elderly women, carried out for more than 7 years, showed that despite higher BMD in people with OA of the hip joints and OA of the hands, the risk of both vertebral and non-vertebral fractures, including femoral neck fractures, was not observed in such patients. decreases.

Possible mechanisms of the relationship between OA and BMD

In many clinical studies that revealed a negative relationship between OA and AP, the formation of the pathological process was influenced by obesity, race, excessive physical activity, i.e. factors that in one way or another contribute to the growth or maintenance of bone mass, but at the same time they increase the risk of developing OA. For example, obesity, a risk factor for knee OA, is associated with increased BMD. Exercise at a young age is important for achieving peak bone mass, but excessive exercise and excess weight predispose to the development of OA in later life. As is known, bone, to a greater extent than cartilage, weakens the load experienced by the joint; under increased loads it becomes denser, which creates the preconditions for the development of OA. Epidemiological studies have shown that OA is more common among Africans and people of African descent than among white people, and the prevalence of OP, on the contrary, appears to be higher among Caucasians. The reasons for these racial differences are unclear, but black individuals have higher bone mass and slower bone turnover, resulting in a higher average age of skeletal tissue.

OA is based on damage to all components of the joint, primarily cartilage, as well as subchondral bone, synovial membrane, ligaments, capsule, and periarticular muscles. In recent years, a theory has emerged that changes occurring in the subchondral bone may initiate cartilage degradation. One hypothesis is the ability of subchondral bone to produce large amounts of proinflammatory cytokines and growth factors, which can penetrate into the overlying cartilage and lead to degradation of cartilage tissue.

Little information has been accumulated on normal remodeling and turnover rates in human subchondral bone due to the difficulty of obtaining healthy bone samples. The rate of remodeling has been shown to decrease at sites subject to stress because high levels of bone tension inhibit the formation of new sites of bone turnover. A lower rate of remodeling leads to an increase in the average age of tissue in load-bearing areas and accumulation of mineral in them.

One of the main pathogenetic mechanisms for the development of primary AP is estrogen deficiency. However, some epidemiological data suggest the possible involvement of estrogens in the development of OA. Thus, OA occurs with approximately the same frequency in men and women under the age of 50, while after the onset of natural or surgical menopause there is an increase in incidence among women. There is also an association of OA with overweight and obesity, which lead to increased production of endogenous estrogens. Estrogens regulate bone turnover, and the increase in bone mass resulting from their excess creates additional mechanical stress on the cartilage during forceful impact on the joint. In addition, estrogens can cause the development of OA through cytokines and growth factors. For example, the cytokines interleukin-1 (IL-1) and tumor necrosis factor-a increase the production of enzymes that degrade the cartilage matrix. Insulin-like growth factor-1 (IGF-1) stimulates bone formation by enhancing bone cell proliferation and differentiation. Transforming growth factor-β (TGF-β) can lead to increased collagen synthesis due to its ability to stimulate the formation of osteoblasts from their precursors [16]. Since estrogens increase the concentrations of IGF-1 and TGF-β in bone tissue, increased bone formation under the influence of these factors may determine the relationship between excess weight, increased mineral density of subchondral bone tissue and the development of OA.

In addition, it has been suggested that increased bone density in OA may be achieved by reducing the level of colony-stimulating growth factor-1 (CSF-1), which stimulates osteoclastogenesis and regulates osteoclast activity. The absence of CSF-1 leads to the development of osteopetrosis in mice, and its elevated levels in the blood serum were found in individuals with AP.

In recent years, evidence has emerged that vitamin D takes part in the metabolism of not only bone, but also cartilage tissue. In particular, it has been shown that vitamin D stimulates the synthesis of proteoglycan by chondrocytes and modulates the activity of metalloproteinases involved in the destruction of cartilage. For example, a decrease in the level of 24,25(OH)2- and 1,25(OH)2-vitamin D is associated with an increase in the activity of metalloproteinases, and normalization of their level reduces the activity of these enzymes in vitro. It should also be emphasized that in the early stages of OA, vitamin D-dependent disruption of cartilage metabolism may be accompanied by remodeling and thickening of subchondral bone tissue. This leads to a decrease in the shock-absorbing capacity of the subchondral bone and acceleration of degenerative changes in the cartilage. It has been demonstrated that in patients with gonarthrosis, reduced vitamin D intake and low serum levels of 25(OH) vitamin D are associated with a 3-fold increase in the risk of progression of radiological signs of OA [3].

Vitamin D deficiency entails an increase in the synthesis of parathyroid hormone, which leads to stimulation of osteoclast activity and increased bone resorption. In addition to its effect on bone cells, in vitro studies have shown that parathyroid hormone is able to enhance the proliferation of chondrocytes in the growth plate, as well as have a dose-dependent stimulating effect on the synthesis of collagen and proteoglycans.

The above data indicate the contribution of various factors to the formation of bone tissue and the development of OA. In recent years, interest in studying the role of genetic factors in the development of OA and AP has increased. Thus, it was found that up to 80% of peak bone mass is determined genetically. The most studied gene is the vitamin D receptor (VDR) gene. Currently, there is evidence of the association of its polymorphism not only with OP, but also with OA, especially in the development of osteophytes. TGF-β gene polymorphism is also associated with AP and spinal osteophytosis. The most likely reason for the “alternative relationship” between OP and OA appears to be gene polymorphism. A study of a sample of twins showed that BMD and OA are determined mainly by genetic factors, the variability of which can determine a number of anthropometric characteristics, an increase in the synthesis of growth factors by osteoblasts and a local acceleration of bone turnover in the joint [4].

Treatment of AP is not an easy task: it must be long-term, since the effect of its use can appear after a long time. The goal of treatment is to slow down and, if possible, stop bone loss, prevent bone fractures, as well as improve the patient’s condition, reduce pain and generally improve the quality of life of patients. Pathogenetic therapy for AP includes drugs that slow down bone resorption - bisphosphonates, calcitonin, estrogens.

The drug alendronate (Fosamax), which is a nitrogen-containing bisphosphonate, is registered in Russia. In multicenter randomized, double-blind, placebo-controlled studies, alendronate at a dose of 10 mg/day showed high efficacy: increasing BMD in all areas of measurement from 5.4 to 13.7%, it significantly reduced the incidence of fractures in the spine by 47%, hip - by 51–56%, forearm - by 48%, and in 64% of patients the progression of vertebral deformities decreased. In a study of the effectiveness of alendronate at a dose of 70 mg once a week compared with 10 mg daily, it was shown that the increase in BMD was 6.8 and 7.4%, respectively, in the spine, and 4.1 and 4.3%, respectively, in the hip. However, it has been clearly shown that the tolerability of alendronate at a dose of 70 mg once a week is equivalent to taking 10 mg per day, and bone biopsy material did not reveal signs of osteomalacia at both doses of the drug. Contraindications for alendronate therapy are hypersensitivity to the drug, hypocalcemia, and the presence of esophageal diseases.

Alendronate showed a consistent therapeutic effect over 10 years of treatment. After discontinuation of alendronate therapy, patients did not experience an increase in bone density loss compared with placebo.

Alendronate is prescribed 70 mg once a week or 10 mg daily for a long time, for 3–5 years, but the exact duration has not been determined.

Positive results were also obtained in experimental studies using bisphosphonates for OA. Thus, in an experiment on a model of OA in rats with dissection of the anterior cruciate ligament, the chondroprotective effect of alendronate was confirmed, as well as its modeling effect on the subchondral bone: a decrease in resorption in the early stages after surgery and prevention of a subsequent increase in bone formation starting from the 10th week after surgery. In addition, a decrease in vascular invasion into the area of calcified cartilage and a dose-dependent inhibition of osteophyte growth were noted.

Salmon calcitonin (miacalcic) is another drug used to treat AP and prevent fractures and is available in two forms: 100 IU injection ampoules and 200 IU nasal spray bottles in 1 dose.

In accordance with the recommendations for intranasal use, the drug at a dose of 200 IU per day can be administered continuously for 3–5 years, taking into account its effectiveness, or in cyclic courses (2–3 months of treatment, 2–3 months break).

The only absolute contraindication to the use of salmon calcitonin preparations is individual hypersensitivity to the drug or its method of administration. The most common side effect of calcitonin nasal spray is irritation of the nasal mucosa. Minor nosebleeds and other nasal symptoms are less common. In most cases, these adverse reactions are mild or moderate and do not require discontinuation of the drug. With parenteral administration of calcitonin preparations, side effects are observed more often: nausea or vomiting, hot flashes to the face and skin rash at the injection site. Serious complications when using nasal or parenteral forms of calcitonin are observed in less than 1% of patients.

In recent years, work has begun to study the effect of calcitonin on the course of OA, which is associated with the possibility of interfering with the metabolism of subchondral bone, as well as the presence of chondroprotective effects.

An important component in the mechanism of action of calcitonin is its ability to exert an analgesic effect through both direct central and peripheral actions.

The positive effect of hormone replacement therapy (HRT) on the risk of fractures in postmenopausal AP has been proven. The use of HRT not only prevents bone loss in postmenopausal women, but also increases BMD in 95% of women. The increase in bone mass in the lumbar spine averages from 2 to 6% over 12 months. It was noted that the effect of HRT is higher in women with lower initial BMD and in those who had an additional risk factor for the development of AP, for example, long-term smoking. A series of multicenter studies in the United States were conducted in this direction, and in particular the WHI study (Women's Health Initiative, 2003), which included more than 16,600 postmenopausal women who received HRT for more than 5 years (8506 people) and were observed in the group placebo (8102 people). Reductions in the risk of hip fractures were observed in 34%, spine fractures in 34%, and total fractures in 24% of the treatment group. However, in the group receiving HRT, there was an increased risk of coronary heart disease, stroke, breast cancer (the maximum risk was obtained between the 4th and 5th year of the study), and thromboembolism. Due to these side effects of HRT, their long-term use for the treatment of AP is limited; the question of the prescription and duration of HRT is decided individually for each patient, depending on contraindications and the possible risk of complications.

The effect of HRT on the risk of occurrence and course of OA remains not fully understood. Thus, data from epidemiological prospective studies showed the effect of HRT in relation to the radiographic progression of OA, while their effectiveness in manifest OA of the knee and hip joints was less significant.

The preliminary results obtained on the use of anti-osteoporotic drugs for the treatment of OA indicate the need for further research to study the mechanisms of action of these drugs and develop schemes for their use.

Thus, an analysis of works devoted to the study of OA and AP showed that in OA of large joints there is an increase in BMD in all parameters, but in other forms of OA this relationship with BMD is less pronounced. There has been no reliable evidence of a reduction in the risk of fractures in patients with OA. Prospective studies have shown that higher BMD increases the risk of developing knee OA, and the mechanisms leading to the progression of OA may vary. The presence of elevated levels of growth factors in bone predisposes to cartilage degradation and protects against loss of BMD. As with AP, the development of OA depends on a whole set of genes, and the association of these diseases with different alleles of the same genes may be one of the reasons that the combined occurrence of AP and OA is quite rare.

Further study of these two widespread diseases will make it possible to carry out preventive measures aimed at reducing the risk of developing both the diseases themselves and their complications, which, in turn, lead to a decrease in both the quality and life expectancy.

Literature

Byer PD, Contepomi CA, Farkas TA A post mortem study of the hip joint. Including the prevalence of the features of the right side//Ann. Rheum. Dis. 1970; 29(1): 15-31.
Dequeker J. Inverse relationship osteoarthritis-osteoporosis: what is the evidence? What are the consequences?//Br. J. Rheumatol. 1996; 35: 813-820.
Nasonov E. L. Osteoporosis and osteoarthrosis: mutually exclusive or complementary diseases? // Consilium medicum. 2000. No. 2(6). pp. 248-250.
Alekseeva L. I. Osteoarthrosis and osteoporosis/guide to osteoporosis/ed. L. I. Benevolenskaya. M.: Binom, 2003. pp. 482-502.
Nevitt MC, Lane NE, Scott JC, Hochberg MC, Pressman AR, Genant HK et al. Radiographic osteoarthritis of the hip and bone mineral density. The Study of Osteoporoti Fractures. Research Group//Arthritis Rheum. 1995; 38(7): 907-916.
Burger H., van Daele PL, Odding E., Valkenburg HA, Hofman A., Grobbee DE et al. Association of radiographically evident osteoarthritis with higher bone mineral density and increased bone loss with age. The Rotterdam Study//Arthritis Rheum. 1996; 39(1): 81-86.
Antoniades L., Macgregor A J., Matson M., Spector TD A cotwin control study of the relationship between hip osteoarthritis and bone mineral density//Arthritis Rheum 2000; 43(7): 1450-1455
Hannan MT, Anderson JJ, Zhang Y., Levy D., Felson DT Bone mineral density and knee osteoarthritis in elderly men and women. The Framingham Study//Arthritis Rheum 1993; 36(12): 1671-1680.
Hart DJ, Mootoosamy I., Doyle DV, Spector TD The relationship between osteoarthritis and osteoporosis in the general population: the Chigford Study//Ann. Rheum. Dis. 1994; 53(3): 158-162.
Zhang Y., Hannan M T., Chaisson CE, McAlindon TE, Evans SR, Aliabadi P. et al. Bone mineral density and risk of incident and progressive radiographic knee osteoarthritis in women: the Framingham Study//J. Rheumatol. 2000; 27(4): 1032-1037.
Alekseeva L. I., Benevolenskaya L. I., Mikhailov E. E., Smirnov A. V. Prevalence of osteoarthritis of the knee joints and joints of the hands among individuals with different indicators of bone mass density: Abstracts of the Third Russian Symposium on Osteoporosis. St. Petersburg, 2000. P. 78.
Peel NFA, Barrington JA, Blumsohn A. et al. Bone mineral density ans bone turnover in spinal osteoarthritis//Ann. Rheum. Dis. 1995; 54: 867-871.
Dequeker J., Johnell O. Osteoarthritis protects against femoral neck fracture: MEDOS study experience//Bone. 1993; 14: 51-56.
Cumming RG, Klineberg RJ Epidemiological study of the relationship between arthritis of the hip and hip fractures//Ann. Rheum. Dis. 1993; 52: 707-710.
Arden NK, Nevitt MC, Lane NE, Gore LR, Hochberg MC, Scott JC et al. Osteoarthritis and risk of falls, rates of bone loss, and osteoporotic fractures. Study of Osteoporotic Fractures Research Group//Arthritis. Rheum. 1999; 42(7): 1378-1385.
Mansell JP, Bailey AJ Abnormal cancellous bone collagen metabolism in osteoarthritis//J. Clin. Invest. 1998; 101(8): 1596-1603.

N. V. Toroptsova, Candidate of Medical Sciences Institute of Rheumatology, Moscow

Companions of Aging

At first glance, typical portraits of patients with arthrosis and osteoporosis do not coincide. Osteoarthritis usually occurs in obese people, and osteoporosis in frail people. Osteoporosis affects women much more often than men, but arthrosis does not have such a dependence.

Shall we do it our way? Why do we violate doctors’ orders for arthrosis?

But the diseases also have common risk factors. The main one is old age. Back in the 90s of the last century, the US National Academy of Sciences proposed the term “inevitable accompaniments of aging,” which included a number of diseases, including osteoporosis and arthrosis. Over the years, metabolism in all tissues slows down. For some, the cartilage suffers first, for others, the bones, for others, both cartilage and bones. This does not mean that everyone will experience severe arthrosis or osteoporosis, but initial changes can be found in most people over 50–55 years of age.

Article on the topic

A fracture out of the blue. Why do bones become brittle?

Another common risk factor is a sedentary lifestyle. With a lack of physical activity, blood circulation slows down, so that the cartilage does not receive sufficient nutrition and the resources for its timely restoration are reduced. And bone density strongly depends on the pressure that adjacent muscles exert on them. If we don't move enough, this pressure remains minimal and the likelihood of osteoporosis increases.

What is osteoporosis of the joints?

Osteoporosis is a serious pathological disease of the human body's skeleton, involving a pathological change in the structure of bone tissue.

As the disease progresses, the mass of bone tissue is noticeably reduced, which leads to a loss of strength. According to the World Health Organization (WHO), osteoporosis is the fourth most common disease of non-infectious etiology in the world.

The disease is diagnosed in predominantly elderly people, especially often in women during the last stage of changes in the female reproductive system (postmenopause).

Complex "relationships"

Even separately, arthrosis and osteoporosis are serious diseases. If they are combined, one disease worsens the course of the other. When the bones that make up a joint become less dense, the stress on the joint cartilage increases, causing it to wear out faster. If a person experiences pain in a joint due to arthrosis, he involuntarily begins to move less. And this, as we already know, helps reduce bone density.

The vicious circle can only be broken with the help of well-chosen treatment. And the sooner it starts, the better. Be sure to consult a doctor if you feel even slight discomfort in your joints. Pain appears when the destruction of cartilage is already pronounced. In the earlier stages, morning stiffness occurs and this is the time to seek medical help.

Is it time to worry? What does joint discomfort indicate?

Osteoporosis cannot be detected on its own in the early stages. Therefore, all women after 45 years of age need to undergo densitometry every two years - a study that allows you to assess bone density.

Degree of development of osteoporosis

The disease can occur from the first to the fourth degree, let's look in detail at how this happens and what features exist in the various degrees.

1st degree

Despite the presence of the first degree, most patients do not observe any symptoms or special manifestations of pathology. At this stage, there is a slight decrease in bone density, which can only be determined through specialized medical research.

2nd degree

Although the disease progresses, it remains difficult to detect.

The bone tissue material undergoes thinning, the density decreases even more, but at the same time maintains the strength of the structure for the normal functioning of the patient.

3rd degree

The progress of pathological changes causes deformation of individual vertebrae, which is manifested by pronounced symptoms of the disease.

It is at the 3rd stage of development that the first bone fractures occur, indicating the presence of the disease.

4th degree

The bone tissues are severely destroyed; X-ray examination shows that their structure is almost “transparent”.

Minor loads cause severe pain in the patient. The risks of fractures and serious spinal injuries are maximum.

Is the nature of arthritis and arthrosis the same or different?

Arthritis is an inflammatory process, most often associated with autoimmune diseases, previous infections, hormonal imbalances and metabolic factors that affect the general condition of the body. In this case, pathological changes occur in the joint fluid (whereas with arthrosis there is insufficient production of it) and connective tissue.

Inflammation usually manifests itself against the background of rheumatoid arthritis, starting from 25-30 years, or genitourinary, intestinal bacterial infections. The changes mainly affect the synovial membrane of the joint, where the blood vessels are concentrated.

Arthritis often causes complications in the heart, kidneys and liver, not limited to damage to the joints.

Arthrosis is a non-inflammatory degenerative disease that is associated with natural wear and tear of the joint surfaces. Thinning of cartilage can be caused by excessive loads, changes in hormonal levels, age-related changes in the patient's body, and disturbances in axial load (for example, with curvature of posture or improperly healed fractures).

Osteoarthritis is accompanied by decreased mobility in the joint and the formation of osteophytes. Unlike arthritis, it leads to mechanical local deformation of the joint capsule and bones, but does not affect other organs and systems. The disease attacks the entire cartilage. With arthrosis, inflammatory processes can also be observed, but they are not permanent and usually occur in the second and third stages of the disease.

Where the difference between arthritis and arthrosis is especially noticeable is the age of onset of the disease. The overwhelming number of patients with osteoarthritis are in the age category of 65 years or more, but the first symptoms can be observed at the age of 45 years. Arthritis affects young, able-bodied people under 55 years of age and can even occur in children and adolescents.

Diagnostic methods

In order to make an accurate diagnosis, you need to contact an orthopedic traumatologist. Diagnosis of osteoporosis involves a combination of several methods:

taking an anamnesis, visual examination - during the process, the specialist finds out the duration of existence of the existing symptomatic picture, as well as characteristic anamnestic signs;
densitometry – makes it possible to fully assess bone density;
X-ray examination - despite the low information content, the method is widely used in diagnostics and allows one to determine existing signs of the development of the disease;
laboratory tests - a set of tests that involve determining the level of essential vitamins and minerals.

Symptoms of osteoporosis

There is a list of common symptoms of osteoporosis, which may differ depending on the type observed and the characteristics of the clinical picture in a particular patient.

Among the main symptoms of osteoporosis are:

aching, dull pain;
decreased patient growth;
increased level of fatigue;
poor posture;
the formation of a large amount of plaque, the development of periodontal disease;
earlier appearance of gray hair;
increased heart rate;
disturbance of the general emotional background of the patient.

The presence of at least one or more symptoms of osteoporosis indicates the need to seek qualified medical help.