Therapy for peripheral joint damage in psoriatic arthritis

What it is

Chronic arthritis is an inflammatory disease of the joints that lasts more than three months. In this case, exacerbations are replaced by remissions. After exacerbations, the inflammatory process gradually turns into a degenerative-dystrophic process with the destruction of cartilage, the proliferation of bone tissue and the gradual formation of ankylosis (immobility).

Initially, rheumatoid, psoriatic, gouty, and juvenile arthritis last for a long time. Whereas infectious and reactive arthritis, with proper, timely treatment, is acute with complete recovery. But these forms can gradually become chronic if the prescribed treatment is not timely or if the patient’s immunity sharply decreases.

Patients with this disease should be observed by a doctor and receive courses of anti-relapse therapy. This tactic is needed to suppress the progression of the disease. It is possible to achieve this with the current state of medicine. But the result will depend not only on the doctor, but also on the patient’s strict compliance with his instructions.

Codes according to the International Classification of Diseases, 10th revision:

• ICD code for rheumatoid seropositive arthritis - M05.8; seronegative – M06.0;
• ICD code for chronic juvenile arthritis – M0.8;
• ICD code for gouty arthritis – M10.0;
• psoriatic arthritis – M07.0;
• unspecified arthritis - M13.0.

Causes of chronic arthritis

Chronic arthritis is a multifactorial disease. Its different clinical forms have different causes. Today, most experts agree that the main reason for the long course of the disease is burdened heredity in combination with the influence of unfavorable factors, which are trigger points.

Predisposing factors include:

• hypothermia, damp cold climate;
• a sedentary lifestyle, leading to excess weight (increased stress on the joints), poor circulation and metabolism;
• abuse of artificial (solarium) and natural (sunlight) tanning;
• professional (loaders, pianists, tennis players) and sports (heavy lifting) hazards associated with increased load on the skeleton;
• the presence of chronic foci of infection (chronic tonsillitis, sinusitis, cholecystitis, etc.);
• frequent colds and acute infections;
• endocrine disorders, primarily diabetes mellitus, leading to disruption of blood supply and innervation of articular joints; thyroid function disorders, female and male sexual disorders are also important;
• vaccination - the introduction of a foreign protein into the body can provoke the development of an autoimmune process in individuals with a family history.

The most common causes of long-term joint inflammatory processes are infection, autoimmune processes and metabolic disorders.

Infectious causes

Infection can enter the joint cavity in different ways: through open injuries, through the blood in the presence of distant foci of infection (carious teeth, tonsillitis, sinusitis, etc.), as a complication of various general infections (gonorrhea, syphilis, tuberculosis).

The causes of chronic arthritis can be infectious, autoimmune or metabolic in nature

In most cases, the body copes with the infection and after an acute inflammatory process, complete recovery occurs. If treatment is not prescribed in a timely manner, the process may become chronic with gradual destruction of the joint. Initially, tuberculous arthritis can become chronic, which is due to the nature of this infection.

Autoimmune causes

Arthritis such as rheumatoid, juvenile, psoriatic are of autoimmune origin. Their development is associated with an allergic reaction to the body’s own tissues. It mainly affects people with a hereditary predisposition.

The disease begins with exposure to a provoking factor. This could be a past infection, exacerbation of sinusitis, hypothermia, etc. In response to infection, the body produces antibodies, first to the infectious pathogen, and then to the patient’s own tissues. They are deposited on target tissues. Taking into account hereditary predisposition, these will be articular tissues, where a long-term inflammatory process develops. The causes and mechanism of development of the disease according to the type of autoimmune process have not been fully established; currently, their study is one of the main tasks of medicine.

Metabolic causes

Metabolic disorders are another reason for the development of chronic inflammatory process in the joints. Thus, a violation of purine metabolism leads to the development of gout with the deposition of urate salts in the joints in the form of nodules - tophi. Tophi appear under the skin and in the joint cavity, leading to long-term inflammation and gradual loss of joint function.

Chronic arthritis can be caused by various reasons, they are worth knowing, especially for people who have relatives with this disease.

Causes of rheumatoid arthritis

Currently, there is no reliable data on the causes of the disease. There are several most likely versions supported by most of the medical community. The most popular of them is that RA is caused by several factors present in the patient’s medical history at the same time.

• Genetic predisposition to autoimmune disorders.
• Presence of MHC class II antigen (noted in most patients).
• Infectious agents: paramyxoviruses, hepatoviruses, retroviruses.
• The presence of antibody titers to the Epstein-Barr virus (found in 80% of patients).

Thus, the risk of developing rheumatoid arthritis is higher in women aged 35 - 40 years and older. Increases the chances of having close relatives with a similar diagnosis, as well as previous diseases such as measles, hepatitis B, lichen, herpes, mumps.

Any changes in the immune system, which begin an attack on one’s own connective tissue, can activate the pathological process. Among the triggering factors are frequent hypothermia, hyperinsolation (sunstroke), prolonged intoxication, viral and bacterial infections. May be affected by medications, disruption of the endocrine glands, long-term stress and depression.

Symptoms of chronic arthritis

The signs of primary arthritis, which initially proceed for a long time and imperceptibly, differ from the primary manifestations of arthritis, which only become chronic under unfavorable conditions.

First signs

Initial symptoms are characterized by smoothness and inconspicuousness. At first there is slight soreness and mild morning stiffness after sleep. In a few minutes everything goes away. Over time (usually after a few weeks), the period of stiffness lengthens. It is difficult to completely clench your hand into a fist. There is some swelling in the joint area, but there is no redness, so the swelling is not always noticeable.

Sometimes the lesion begins with damage to one or two large joints (hip, knee). Symptoms also develop unnoticed: pain in the knees appears, worsening with movement, slight stiffness after sleep, and a slight, almost imperceptible swelling. At the same time, weakness, malaise, and a slight increase in body temperature may appear. All these symptoms can be regarded as overfatigue, so in the initial stages, patients rarely consult a doctor.

Sometimes the disease is acute, with fever, severe swelling in the articular area, and a disturbance in the general condition. All symptoms then go away (sometimes without treatment) and then return as typical manifestations of chronic arthritis.

Obvious symptoms

These are increasing pain and severe stiffness in the morning. It will no longer be possible to ignore this. The pain becomes constant, intensifies with movement, and is debilitating. Overt symptoms of arthritis include changes in the appearance of the joints: they become larger and take on a knobby appearance. With rheumatoid arthritis, the hand can change its appearance: it seems to deviate to the ulnar side, its appearance over time resembles the fins of a walrus.

Fingers are deformed due to contracture due to persistent flexion or hyperextension in the proximal (located closer to the hand) interphalangeal joints. They take on the appearance of a “boutonniere” and “swan neck”.

In the area of ​​large joints (for example, knees), deformation is clearly visible with outward deviation of the joint and incomplete extension. A dense formation is often felt on the back of the knee - a Baker's cyst. The feet are also deformed, deviate outward, and with rheumatoid and gouty arthritis, the big toe is deformed.

Increasing joint pain and severe stiffness in the morning are clear symptoms of chronic arthritis.

Disorders in the area of ​​the cricothyroid and cricoarytenoid joints of the larynx lead to difficulty swallowing, deepening of the voice, shortness of breath and a tendency to frequent bronchopulmonary diseases.

Subluxations, especially of small joints, are characteristic. They are especially dangerous in the area of ​​the cervical spine, as they can lead to compression of the vertebral artery supplying the brain.

With rheumatoid arthritis, small, dense, painless nodules can be felt on the surface of the skin, located mainly in the area of ​​the elbow and fingers. The same nodules often appear in the lungs, which leads to the development of pulmonary pathology.

Joint symptoms are accompanied by signs of general intoxication: weakness, malaise, weight loss, and periodic occurrences of fever. The appearance of shortness of breath may indicate damage to the cardiovascular system.

Compression of nerve endings in the joint area leads to the appearance of chronic neuropathic pain. It underlies the pain syndrome. Often the inflammatory process affects muscles, followed by their atrophy (decrease in volume) and blood vessels (vasculitis). Severe vasculitis can lead to impaired renal function.

Such patients develop anemia, a tendency to increased thrombosis, and decreased immunity.

But you shouldn’t despair: you can help a patient at any stage of the disease, you just need to see a doctor.

When to see a doctor

You should not wait for the most pronounced symptoms to appear. You should contact your doctor if you notice the following changes:

• joint pain and stiffness that occurs in the morning;
• inability to completely clench the hand into a fist;
• a feeling of creaking in the joints when moving;
• slight swelling of the joint area;
• weakness and slight malaise, sometimes a slight increase in temperature;
• hoarseness, difficulty swallowing;
• shortness of breath with mild physical exertion;
• frequent colds complicated by bronchitis;
• the appearance of painless dense nodules on the extensor surface of the elbow and in the area of ​​the fingers.

Identification of these symptoms should be a signal to seek medical help.

Arthritis symptoms

Manifestations of the disease depend on its clinical form and severity of the process. The main symptoms of arthritis include local manifestations of inflammation in the joint - pain, redness and swelling of surrounding tissues, limited mobility, deformation as pathological changes progress. There is also a local increase in temperature, the affected area becomes hot when touched.

Infectious

The course of the disease depends on the type of pathogen. Often there is a sharp increase in temperature, chills, headache, and weakness. Tuberculous arthritis occurs in a chronic form, is difficult to treat and leads to severe dysfunction of the affected joint. With gonorrhea, as a rule, acute serous inflammation develops. Viral lesions go away after the infection is cured.

Gouty

Gout is a metabolic disorder that is accompanied by the deposition of uric acid salts - urates - in the joints. They penetrate the tissues, forming gouty nodes or tophas. The metatarsophalangeal joints of the thumbs are usually affected first, followed by arthritis in other areas. During an exacerbation of the disease, acute inflammation develops with tissue swelling and severe pain. After several attacks of gout, the joint becomes deformed and its function is impaired.

Rheumatoid

An autoimmune reaction develops with damage to the body’s own tissues, including joints. The causes of the disease have not been precisely established, but it is known that inflammation is triggered by infection in the body. At the onset of the disease, there is an increase in body temperature, the patient is worried about morning stiffness - a gradually passing limitation of mobility after waking up, pain and swelling at the site of inflammation. Symptoms may spontaneously disappear for several months, followed by exacerbation and progression of the disease. Damage to the hand and fingers is typical, but there are cases of atypical reactive arthritis with inflammation of the knee or shoulder joint. Gradually, without treatment, articular cartilage is destroyed, connective tissue grows, subluxations and dislocations occur, leading to disability of the patient.

Traumatic

Develops after injury to large joints - hip, knee, shoulder and others. There is pain, swelling and crunching when moving. With a closed injury and aseptic inflammation, spontaneous recovery is possible. With an open wound, the infection penetrates deep into the tissue and can cause purulent inflammation.

Psoriatic

It is characterized by damage to the terminal interphalangeal joints of the fingers and nails with simultaneous asymmetric damage to several other areas. The course of the disease occurs with relapses and remissions.

Reactive

This form is associated with a toxic-allergic reaction to an infection that develops within a week after a bacterial, viral or fungal infection. It occurs acutely, affecting 1-3 large joints. Characterized by pain at the site of inflammation, redness, swelling of surrounding tissues, and limited mobility. Other symptoms of inflammatory damage to the eye mucosa and urinary tract may also be present.

Juvenile idiopathic

Arthritis of unknown cause in children under sixteen years of age. It is believed that the basis is the genetic predisposition of the child. Prolonged exacerbations alternate with remissions and lead to early disability of the patient.

How dangerous is the disease?

Chronic arthritis is dangerous because it slowly but steadily progresses, destroying the joint. As the disease passes from stage to stage, a gradual and sometimes imperceptible loss of joint function occurs.

Any form of arthritis has serious complications, so you should not delay treatment.
See how easily the disease can be cured in 10-12 sessions.

Stages of chronic arthritis

During the course of the disease there are 4 stages:

1. I
   – very early, lasting about six months. Symptoms: transient joint pain and stiffness of movement. The general condition suffers slightly; changes in the joint can only be seen on x-rays.
2. II
   – early (from six months to a year). Inflammatory processes are gradually replaced by proliferative processes - the growth of connective tissue, under which the slow destruction of articular cartilage occurs. The periarticular tissues become denser, motor activity decreases, and any movements are accompanied by pain. Weakness increases, the patient loses weight.
3. III
   – extensive (from one to two years or more). There is destruction of articular cartilage and fusion of connective tissue with bone tissue with the formation of fibrous ankylosis (incomplete joint immobility). The joint is deformed, its function is impaired, but it is still supported by the muscular system. I am concerned about constant debilitating pain; during an exacerbation, inflammation develops, followed by degenerative-dystrophic processes during remission.
4. IV
   – late (lasts more than two years). Bone tissue replaces connective tissue, and ankylosis becomes complete (osseous ankylosis). At the same time, disorders of other organs and systems develop: cardiovascular, respiratory, etc.

Possible complications

The disease can cause complications, both from the affected joints and from other organs and systems. Joint complications include:

• articular deformation, subluxations, dislocations, necrosis (death) of cartilage and bone tissue; subluxation of the cervical vertebrae leads to severe complications in the brain;
• ankylosis with loss of joint function;
• development of tunnel syndromes due to compression of nerves in narrow anatomical spaces during inflammation and swelling of articular and periarticular tissues; most often found in the area of ​​the carpal, ulnar, and tibial nerves, manifested by pain and movement disorders.

Common complications of chronic arthritis are osteoporosis and atherosclerosis with the formation of cardiovascular complications

Complications from other organs and systems include:

• osteoporosis
  – loss of calcium from bone tissue, which leads to brittle bones and frequent fractures;
• accelerated development of atherosclerosis with the formation of cardiovascular complications
  - coronary heart disease and arterial hypertension;
• amyloidosis
  – in response to long-term inflammation, a protein-polysaccharide complex (amyloid) is deposited in the tissues, disrupting the function of internal organs; Amyloidosis is especially dangerous for the kidneys.

You should not wait for complications; it is better to immediately consult a doctor at the first signs of illness. But there is no need to panic: all this can be treated.

Exacerbation of chronic arthritis - what to do

If a relapse occurs, the joint should be kept motionless and, if possible, in an elevated position. This will promote blood flow and reduce swelling and pain.

As a pain reliever, you can take orally any drug from the group of NSAIDs (non-steroidal anti-inflammatory drugs) - Nise, Diclofenac, Ibuprofen, etc. Apply gel or ointment with NSAIDs - Voltaren, Fastum-lel, etc. to the skin over the affected joint.

After this, you need to call a doctor at home.

Chondroprotectors: what are they, how to choose, how effective are they?

Joint pain at rest

Inflammatory bowel diseases (IBD) are often accompanied by a variety of systemic extraintestinal manifestations in various organs and systems. Rheumatological manifestations, primarily lesions of the musculoskeletal system (MSA), occupy an important place among them. This is due to their wide prevalence (up to 50%), diversity and variability of the course (from asymptomatic to severely disabling), as well as the possibility of appearing long before the first symptoms of IBD [1–4].

The origin of extraintestinal manifestations of IBD remains unclear. The involvement of intraintestinal bacteria, increased permeability of the intestinal wall in nonspecific ulcerative colitis (UC) and Crohn's disease (CD), as well as the genetic characteristics of the organism is assumed [5, 6]. As a result of damage to the intestinal wall, components of the bacterial cell membrane enter the bloodstream, which can lead to the development of arthritis through the induction of immunological mechanisms. By binding to molecules of the major histocompatibility complex (HLA B27) and subsequently activating T-lymphocytes, peptides cause inflammation of the joints. In this case, during the process of recirculation between the intestine and the synovium, adhesion of activated T cells of the intestinal mucosa occurs to the endothelium of the synovial venules, which leads to synovitis [7, 8].

Internists first paid attention to the problem of the combination of arthritis and IBD at the beginning of the 20th century, when the idea of ​​extraintestinal manifestations of UC and B.C. was put forward. Several decades later, V. Wright and J. Moll [9] formulated the concept of seronegative spondyloarthritis, the group of which, in addition to ankylosing spondylitis (AS), psoriatic and reactive arthritis, also included arthritis due to IBD.

Since that time, interest in the problem of extraintestinal manifestations of IBD, including rheumatological syndromes, has grown, since for a long time arthritis of large joints, sacroiliitis, and AS were interpreted in IBD as manifestations of concomitant diseases not related to intestinal pathology. Many scientific works carried out subsequently refuted this idea, since they proved that the course of some variants of the musculoskeletal system is closely related to exacerbations and remissions of IBD [10, 11].

Currently, the presence of extraintestinal manifestations is considered as one of the signs of UC and B.C. activity. Rheumatological manifestations, primarily symptoms of damage to the musculoskeletal system, are almost the same in UC and CD [12, 13]. The frequency of their development is quite high - from 21.4 to 62%, with most researchers pointing to an interval of 30-40% [14-16].

When studying the relationship between the pathology of the musculoskeletal system and the severity and nature of the course of intestinal inflammation, data were obtained on the development of rheumatological manifestations with a more severe course of IBD and a larger area of ​​​​damage to the gastrointestinal tract, although variants of a mild course of IBD with limited intestinal damage cannot be excluded [17, 18]. For example, E.A. Dorofeev et al. [19] in a study of 319 UC patients found that arthritis developed significantly more often with more widespread intestinal lesions (left-sided colitis and pancolitis) than with distal colitis. In addition, there is information in the literature indicating an increase in the number of rheumatological manifestations with increasing duration of IBD [20–22]. When comparing the chronology of the onset of IBD and arthritis, the majority of patients (up to 50%) first note the onset of UC or CD, and later lesions of the musculoskeletal system appear [23, 24]. The simultaneous appearance of clinical symptoms of IBD and arthritis or spondylitis is detected in 30-40% of patients [22].

There are several options for the development of articular syndrome in UC and B.C. A fundamentally important point is the division of musculoskeletal pathology into damage to peripheral joints or the axial skeleton. Most often, the clinician deals with the development of peripheral arthritis (PA). Prevalence of P.A. Among patients with IBD, it most often accounts for 10–22% [25–27]. In most cases, arthritis is asymmetrical and often migratory in nature [28, 29]. Symptoms usually stop within 4-6 weeks [10, 30], while relapses of PA associated with exacerbation of IBD are noted in 10-20% of patients, and in 20-40% at least single repeated episodes of articular syndrome are observed [15, thirty]. In patients with CD, a more frequent development of PA with involvement of the colon in the inflammatory process was noted [31, 32]. This fact is well illustrated by the well-known study by A. Greenstein et al. [29] with the participation of 700 patients with CD: rheumatological manifestations occurred significantly more often in the case of involvement of the large intestine in the inflammatory process (with colitis and ileocolitis) than in cases where only the small intestine was affected. An attempt to classify patients with PA was made by T. Orchard et al. [14], based on an analysis of data from 1459 patients with IBD and reliable P.A. The authors identified two types of peripheral arthritis: in type 1, arthritis develops predominantly in the knee and ankle joints, associated with an exacerbation of the underlying disease; in type 2, small joints of the hands are affected (metacarpophalangeal, proximal interphalangeal joints), which can make it difficult carrying out differential diagnosis with rheumatoid arthritis. A distinctive feature of type 2 PA is the absence of a chronological connection between exacerbations of IBD and the development of arthritis: intestinal and articular syndromes exist almost independently of each other. Both types of PA also differ in the number of joints involved: with the 1st, oligoarthritis is observed, while the 2nd is characterized by a polyarticular nature of the articular syndrome. X-ray examination of the affected joints of patients with PA in most cases fails to detect any changes, and laboratory parameters show a negative rheumatoid factor [33]. Only in a small number of patients with a chronic inflammatory process in the joints, periarticular osteoporosis and single cyst-like clearings of bone tissue near the affected joints are detected over time, but even with torpid chronic synovitis, erosion of the articular surfaces cannot be detected [34].

As mentioned above, inflammatory changes in the spine (axial spondyloarthropathy) in IBD can be presented in two variants [11]. In the first case, we are talking about isolated sacroiliitis (SI), often asymptomatic, affecting only the sacroiliac joints without involving the higher parts of the spine [35]. Another option is AS, in which, in addition to sacroiliitis, there is damage to other parts of the spine with the development of typical symptoms [5]. In this case, patients meet the New York modified criteria for AS. In a number of patients, spinal damage may be accompanied by the development of inflammatory pain in the spine [36, 37]. Unlike PA, the course of forms of axial spondyloarthropathy practically does not depend on the activity of IBD [38].

In IBD, it is possible to develop both SI and sacroiliitis with A.S. In addition, sacroiliitis can be combined with inflammatory pain in the lower back, PA [39].

The frequency of detection of SI in IBD depends on the methods of examination of the sacroiliac joints. Traditionally, pelvic radiography is used to diagnose SI. From the literature it is known that SI, detected by radiography, occurs in 15-27% of patients with IBD [40-42]. However, the main disadvantage of radiography is the impossibility of early detection of inflammatory changes in the SIJ, and this is important for timely diagnosis and adequate therapy. Computed tomography is superior to radiography in diagnosing SI [43], but for the early detection of SI, great hopes are currently placed on magnetic resonance imaging [44]. Clinical symptoms in most patients are mild, so the detection of sacroiliitis often becomes a finding during examination [45, 46]. Interesting data regarding asymptomatic sacroiliitis were obtained in the work of W. Scott et al. [47], when in a group of 64 patients with IBD, computed tomography revealed SI in 29% of patients, while clinical symptoms of SI were present in only 3% of cases. The genetic predisposition for SI is less understood than for AS.

SI most often occurs with minimal clinical symptoms and is often asymptomatic; the process is often bilateral, although the development of unilateral lesions is possible. The clinical significance of AS has not been sufficiently studied; large long-term studies are apparently needed to identify patients progressing to AS [48]. Prevalence of A.S. in patients with IBD it is 2-12% [18, 39]. Clinical manifestations of AS in IBD are practically indistinguishable from idiopathic AS (Bechterew’s disease) [10, 11]. The leading symptoms are inflammatory pain in the spine, including in the lower back, morning stiffness, and pain in the buttocks [49]. With a long course of AS, there is a restriction or loss of movements in various parts of the spine with the formation in some cases of forced positions of the body [20, 50]. Symptoms A.S. may significantly precede the appearance of the first signs of IBD [51]. In contrast to idiopathic AS, the frequency of detection of the HLA B27 histocompatibility complex in IBD and AS is lower and amounts to 40-60%. X-ray changes in the spinal column are indistinguishable from idiopathic A.S. It is possible to develop radiological symptoms typical of AS, such as spondylitis (anterior and posterior), spondylodiscitis, syndesmophytes. Unlike PA, the course of AS is isolated and practically does not depend on the activity of IBD [52–54]. To confirm this fact, we can cite literature data on the lack of influence of surgical treatment of IBD (excision of the affected intestine) on the course of AS [11].

In recent years, descriptions of damage to soft periarticular tissues in IBD have appeared in the literature - enthesitis (inflammation of the attachment sites of tendons, ligaments, aponeuroses to the bone), tendonitis, dactylitis, bursitis [55]. Epidemiological studies of periarticular pathology in IBD have been rare, but its prevalence is reported to be 1.5–5.4% [50, 56]. Pain and, in some cases, local swelling are typical clinical manifestations of soft periarticular tissue damage in IBD, which can be either associated with the activity of the underlying disease or present independently. The localization of enthesopathies is varied, although the Achilles tendon and heel area are most often affected [38].

In addition to the types of lesions described above, it is possible to develop rare conditions that are also related to lesions of the musculoskeletal system in IBD, but are not related to spondyloarthritis: for example, hypertrophic osteoarthropathy, periostitis and aseptic bone necrosis, and extremely rarely, granulomas of bones and joints [10, 11].

In some cases, along with damage to the musculoskeletal system, other rheumatological manifestations of IBD develop. The most significant include damage to the skin (erythema nodosum, pyoderma gangrenosum) and eyes (conjunctivitis, uveitis). Erythema nodosum occurs in 10% of patients and is often associated with the activity of IBD and PsA [14].

Uveitis in most cases is associated with spinal lesions and practically does not correlate with IBD activity [51].

Treatment of musculoskeletal pathology is a challenging task due to the limited use of nonsteroidal anti-inflammatory drugs (NSAIDs). The effectiveness of sulfasalazine (at a dose of 2 g per day) in patients with PsA is well known. At the same time, its use in isolated lesions of the axial skeleton turned out to be ineffective. The management of this particular category of patients is the most difficult. The impossibility of long-term administration of NSAIDs in therapeutic doses and the ineffectiveness of sulfasalazine dictate the advisability of early use of biological agents belonging to the group of antibodies to tumor necrosis factor-α [57]. In the presence of torpid synovitis or enthesitis, intra-articular or periarticular administration of glucocorticoids is possible. In addition, physiotherapeutic treatment and physical therapy are used in the complex treatment of articular syndrome in IBD. Determining treatment tactics for rheumatological manifestations of IBD should be carried out jointly by gastroenterologists and rheumatologists.

Classification

Chronic arthritis is a collective concept; it includes different forms of the disease that have different causes and symptoms that differ from other forms. The most common forms are rheumatoid, juvenile, psoriatic and gouty arthritis.

Rheumatoid chronic arthritis

RA - rheumatoid arthritis - is a chronic disease of an autoimmune nature. It mainly affects people with a genetic predisposition. The onset of the disease is associated with some triggering factor, in most cases it is a previous infection, after which an autoimmune process begins with damage to the joints. Women get sick more often.

The disease begins gradually with moderate joint pain and mild stiffness in the morning. At first, these symptoms are not given any importance, but then they gradually increase and are constantly disturbing. Initially, several symmetrically located small joints of the hand are affected. But sometimes the disease begins with damage to one or two large joints (hip, knee, elbow) and only after some time the inflammatory process spreads to the small joints of the hand and foot.

Externally, the joints are initially almost unchanged, only a slight dense swelling is noted, without redness and constant pain. After six months, the pain becomes constant, swelling is more pronounced, but redness almost never occurs. On x-rays at this time you can see signs of inflammation and the beginning of destruction of cartilage tissue.

Chronic rheumatoid arthritis

In later stages, the shape of the affected limbs gradually changes. The joints increase in volume, the fingers acquire a peculiar shape of a “swan neck”, “button loop”, and the hand - “walrus fins”. The toes are hammer-shaped, the foot deviates outward, and flat feet develop. Subluxations of small joints are characteristic.

The pain syndrome in chronic rheumatoid arthritis is severe, the pain is constant, often associated with pinched nerve endings in anatomical tunnels (tunnel syndromes).

If left untreated, the joints gradually become completely destroyed, deformed, immobilized and disabled. Proper treatment can stop this process.

Juvenile chronic arthritis

Juvenile chronic arthritis (JCA) is a disease that develops in children under 16 years of age, has a different origin and a long progressive course with a gradual loss of joint function. JCA is a heterogeneous concept, but various clinical forms of inflammatory joint diseases in children and adolescents.

More often than not, no more than four joints are affected (wrist, hip, knee, etc.). Initially, the disease proceeds unnoticed in the form of minor pain and stiffness of movement in the morning, so JCA is rarely detected in the first 3 to 6 months. Gradually the disease progresses, pain increases, movements are increasingly limited. The process often involves the joints of the cervical spine and the temporomandibular joint with fairly rapid formation of immobility.

Juvenile rheumatoid arthritis develops in children under 16 years of age

Among the general (systemic) lesions noted: periodically rising body temperature, weakness. Often, especially in girls, eye lesions (uevitis) and heart lesions are detected.

Juvenile chronic arthritis is a serious disease that often leads to disability. Therefore, it requires the earliest possible detection, appropriate treatment and long-term observation by a rheumatologist.

Psoriatic chronic arthritis

Psoriatic arthritis is a chronic disease that develops against the background of psoriasis. The causes are not fully established, but it is believed to be of autoimmune origin. It mainly affects people with a genetic predisposition.

The first symptoms of the disease appear several years after the onset of skin manifestations. But sometimes they appear before skin symptoms. The lesion begins asymmetrically, from one or several (no more than 4) large joints. But sometimes it has a rheumatoid-like symmetrical character. The small end joints of the fingers are affected, with inflammation and swelling spreading over the entire length of the finger. Sometimes the inflammation spreads to the lumbosacral spine.

Only continuous maintenance therapy can prevent progression of the disease.

Gouty chronic arthritis

Psoriatic and gouty chronic arthritis

The cause of chronic gouty arthritis is an imbalance of purine metabolism, the accumulation of urates in the joint cavity. The initial attack is inflammation of the first metatarsophalangeal joint of the foot. The disease develops mainly in men after 40 years of age.

Chronic gouty arthritis begins acutely, but then disappears completely. Repeated attacks at first also do not affect the condition of the joints involved, but over time, accumulations of uric acid salts form in the joints in the form of nodules - tophi. They periodically become inflamed and destroy joints according to the same principle as in all other chronic arthritis.

The progression of the disease can only be suppressed with continuous maintenance treatment.

How does it manifest itself?

The inflammatory process first affects small joints - hands and feet, and over time affects large ones. The joints are damaged symmetrically. Unlike arthrosis of the knee, shoulder or elbow, pain after exercise does not intensify, but rather subsides. Symptoms appear in waves: acute pain attacks are followed by a lull. The disease begins with morning stiffness, and without treatment ends with joint deformation.

Characteristic symptoms of the disease are redness and swelling in the joint area, local fever. A person experiences general weakness and malaise, internal organs are affected, and other complications develop.

Is the joint swelling? Contact a rheumatologist

Localizations

Different clinical forms of the disease have their own favorite localization and other features.

Crunching in joints - when to worry

Intra-articular injections of hyaluronic acid

Inflammation of the joints of the lower extremities

Chronic arthritis of the leg joints has the following localizations:

• joints of the foot
  - in the gouty form there is severe inflammation, hyperemia, pain, in the rheumatoid form - all symptoms are initially mild, there is no redness of the tissues, the tips of the fingers thicken and look like hammers; when the ligamentous apparatus is inflamed, the heel hurts;
• ankle
  - affected in all forms of arthritis, but especially often in JCA; swelling and pain are not pronounced, all symptoms increase gradually;
• the knee
  is one of the most common locations for all forms of the disease; pronounced manifestations in gout and psoriasis, erased in RA and JCA;
• hip
  – inflamed with JCA; manifested by painful movements.

Read more about hip arthritis here.

Inflammation of the joints of the upper extremities

Localizations for chronic arthritis of the joints of the hands:

• joints of the hand
  - in RA, the interphalangeal joints are affected, in PsA - distal joints with necrosis and involvement of the nail plates;
• fingers
  – affected by gout, swell and have a characteristic sausage appearance;
• elbow
  – with psoriasis, signs of inflammation are clearly expressed; with JCA, the elbow is painful when moving, but there are no external changes for a long time;
• Shoulder
  – often involved in the pathological process in JCA and psoriasis.

Read our articles on inflammation of the joints of the upper extremities, “Elbow Arthritis” and “Arthritis of the Joints of the Hand and Fingers.”

Temporomandibular arthritis

In JCA, especially often in girls, it is combined with characteristic ocular symptoms (uevitis). Sometimes the same symptom occurs in RA. Chronic arthritis of the temporomandibular joint is manifested by pain and impaired movement when chewing.

Arthritis of the joints of the spine

In JCA and RA, chronic arthritis of the spinal joints sometimes develops, mainly in the cervical region. Gout may be accompanied by involvement of the cervical and lumbosacral spine. This manifests itself as pain and impaired mobility (difficulty turning the neck, bending).

Diagnostics

If chronic arthritis is suspected, the patient is carefully examined: it is advisable to establish the cause and clinical form of the disease. This is not always possible, so the diagnosis is often “chronic unspecified arthritis.” To clarify the diagnosis, the following studies are carried out:

• Laboratory
  :
  general blood test - signs of inflammation are detected;
• biochemical blood test - metabolic disorders;
• immunological studies - the presence of antibodies to various patient tissues is detected; detection of rheumatoid factor (RF) indicates the presence of RA, the presence of antinuclear factor (ANF) indicates the presence of JCA;
• examination of fluid taken from the joint cavity.
• Instrumental
  :
  Ultrasound – detection of early changes in the joint;
• X-ray examinations – bone changes;
• computed tomography (CT) - a more detailed examination of the condition of the osteoarticular system;
• diagnostic arthroscopy - identifying any changes in the articular cavity.

Treatment of chronic arthritis

Treatment of chronic arthritis is selected individually based on clinical observation and additional examination data.

Drug therapy

Drugs for the treatment of chronic arthritis

For chronic arthritis, the following medications are prescribed:

1. Analgesics
   . Acetylsalicylic acid, Pentalgin, Analgin, as well as drugs from the NSAID group - Nise, Ketanov, Movalis, etc. They are prescribed orally in tablets, as well as in injections 1 - 2 times a day. If necessary, stronger prescription painkillers are prescribed - Promedol, Tramal, etc. Ointments and gels containing NSAIDs, as well as capsaicin, a substance that causes tissue irritation, are prescribed externally; after using ointments with capsaicin, tissues become less sensitive to pain.
2. Glucocorticoid hormones
   are prescribed in short courses to eliminate swelling, pain and prevent proliferative processes (the growth of connective tissue in the joint cavity).
3. Antirheumatic drugs
   . Basic anti-inflammatory drugs (DMARDs) - Metatrexate, Sulfasalazine, Plaquenil, etc. - are prescribed in long courses to suppress inflammation and joint destruction. The most effective drug in this group is Metatrexate. It is prescribed in separate independent courses, as well as in combination with other DMARDs or biological agents.
4. Medicines from the group of biological agents or biological response modifiers
   . This is a new group of drugs whose action is associated with the suppression of the action of pro-inflammatory cytokines - information proteins that support inflammation. This group includes: Mabthera (active substance rituximab), Enbrel (etanercept), Kineret (anakinra), etc.
5. For gout, long-term courses are prescribed medications that reduce the level of urate in the blood
   - Allopurinol, Adenuric (febuxostat).

Non-drug treatments

Non-drug methods of treating chronic arthritis include: fixing bandages, physiotherapeutic procedures, reflexology courses, diet:

1. Fixation of joints using special orthopedic devices
   - splints, orthoses, etc. Not always applied. Usually, fixation is necessary during exacerbations with severe pain that worsens with movement. The patient wears the fixation device throughout the day. Most often, due to high load, the knee is fixed.
2. Physiotherapeutic procedures
   . Depending on the clinical form of arthritis, the presence or absence of exacerbation, electrophoresis with painkillers, magnetic and laser therapy and other procedures are prescribed.
3. Reflexology
   . Reflexology courses with specially selected points of influence perfectly relieve pain and suppress the progression of the disease.
4. Folk remedies
   . Prescribed to enhance the effectiveness of treatment and reduce the drug load on the patient’s body. Courses include pumpkin seeds, sesame seeds, ginger, rose hips, etc.
5. Diet
   . There is no special diet. The only exception is gouty arthritis. A dairy-vegetable diet is recommended with the exception of fatty, fried, smoked foods, alcohol, sweets, and sweet carbonated drinks. If you have gout, avoid high-calorie foods: red meat, offal, seafood, alcohol.

Surgery

In some cases, when significant articular destruction occurs, surgical intervention cannot be avoided. The following surgical operations are performed:

1. Therapeutic arthroscopy
   - the operation is performed using an arthroscope through small incisions. Everything that happens is reflected on the monitor screen. Using micro-instruments, the doctor performs minor operations, removing areas of necrosis, overgrown tissue, etc. This improves the patient's condition and relieves pain.
2. Arthrodesis
   is the immobilization of one or more small joints that cannot be treated. In this case, parts of the destroyed joints are connected to each other. This eliminates the pain, but the joint remains immobile for life.
3. Endoprosthetics
   is the replacement of a destroyed joint with an artificial one.

Modern medicine has a wide range of treatment methods that allow you to maintain a decent standard of living at any stage of chronic arthritis.

Treatment

Treatment of arthritis is aimed at eliminating the cause of the disease and risk factors that contribute to the development of inflammation, relieving symptoms, improving metabolism in the affected joint, and preserving its function.
This can be achieved through the use of medications, physiotherapy, physical therapy and massage. In advanced cases, with purulent processes, dislocations and subluxations, surgical intervention may be required. If the joint is completely destroyed, it can be replaced with an artificial one - endoprosthetics.

Conservative therapy, depending on the form of arthritis, includes the use of tablets, ointments and injections of various groups of drugs:

• antibiotics for bacterial infections;
• non-steroidal anti-inflammatory drugs and hormones;
• chondroprotectors – agents that improve the quality of joint tissue;
• painkillers;
• vitamins, microelements and amino acids.

Author:

Pugonina Tatyana Alekseevna, Therapist

Approach to treating the disease in our clinic

Many years of practice have allowed specialists from the Moscow Paramita clinic to develop their own approach to the treatment of chronic arthritis. It includes:

• thorough preliminary examination of the patient using all modern laboratory and instrumental diagnostic methods;
• prescribing a comprehensive course of treatment, including the most modern methods of drug and non-drug therapy, affecting directly the source of inflammation;
• application of a complex of individually selected procedures developed by ancient doctors in China and Tibet; treatment is aimed at general improvement of the body, leading to a gradual restoration of joint function; More information about these methods can be found here.

The clinic’s specialists will provide assistance to patients with chronic arthritis at any stage of the disease. They will relieve you of pain and restore the joy of life. Contact us!

Reflexology and electrophoresis are used to treat chronic arthritis

Clinical recommendations for patients with chronic arthritis

To avoid exacerbations and loss of joint function, the patient must be constantly under the supervision of the attending physician and follow all his recommendations:

• regularly conduct examinations and courses of preventive treatment prescribed by a doctor;
• monitor your health, promptly treat all acute and chronic diseases, foci of infection;
• lead an active lifestyle, do therapeutic exercises, swimming;
• avoid heavy physical activity, long periods of driving, stress, exposure to the sun;
• follow the rules of a healthy diet, monitor your weight; if you have gout, follow a diet;
• get rid of bad habits: smoking and alcohol abuse.

We combine proven techniques of the East and innovative methods of Western medicine.
Read more about our unique method of treating arthritis

Disease prevention

Preventive measures are especially relevant for people who have close relatives suffering from chronic arthritis. To avoid the disease, they should, as far as possible, eliminate exposure to provoking factors on the body. Recommendations for preventing the disease are no different from recommendations for preventing relapses of chronic arthritis.

Persons suffering from chronic arthritis should be very careful about their health. Self-medication should be completely excluded. Only an experienced specialist from a clinic with an impeccable reputation can help, improve the quality of life and stop the progression of the disease. Clinic "Paramita" is waiting for its patients!

FAQ

Is it possible to get disability?

It is possible if there is significant dysfunction of the joint.

Which doctor treats you?

Rheumatologist. For psoriatic arthritis, consultation with a dermatovenerologist is also required, and for gout, an endocrinologist.

What prognosis do doctors usually give?

It is possible to stop the progression of the disease and improve the quality of life at any stage.

Bibliography:

1. Comparative assessment of the information content of ultrasound markers of joint damage in chronic arthritis in children [Electronic resource] / Lukinskaya, Zharov, Sinelnikova // Ultrasound and functional diagnostics, 2015. - No. 5. - P. 59-59.
2. Nicola J. Kalk, Petra Schweinhardt et al. 'Functional magnetic resonance imaging of central processing of clinical and experimental pain in rheumatoid arthritis. Abstracts 11th world congress on pain August 21–26, 2005. Sydney, Australia 502-P108.
3. Schaible HG, Ebersberger A., ​​von Banchet GS Mechanisms of pain in arthritis // Ann NY Acad Sci. 2002: 966: 343–354.

Themes

Arthritis, Joints, Pain, Treatment without surgery Date of publication: 02/19/2021 Date of update: 03/15/2021

Reader rating

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Psoriatic arthritis

Psoriatic arthritis (PsA) is a multifactorial disease that develops as a result of complex interactions between genetic, immunological and environmental factors. There is a hereditary predisposition to the development of both psoriasis and PsA: more than 40% of patients with PsA have first-degree relatives suffering from these diseases. External factors include trauma, infections, nervous and physical stress [1].

PsA is considered a T-cell-mediated disease in which activation of cellular immunity occurs in the skin and synovium with subsequent overproduction and imbalance of key pro- and anti-inflammatory cytokines, such as tumor necrosis factor α (TNFα), interleukins (IL) 1β, 6, 12, 17, 23 and chemokines [1].

The development of synovitis in PsA is characterized by increased vascularization and infiltration of the synovium by immune cells. Activated immune cells produce cytokines that support the inflammatory process. Under the influence of proinflammatory cytokines, the proliferation of fibroblast-like synoviocytes leads to the formation of pannus and the spread of the pathological process to cartilage and bone tissue. Activation of osteoclastogenesis further promotes bone resorption, leading to joint deformation and loss of function. Synovitis and erosive changes in bone tissue are important manifestations of PsA; radiological changes are observed in 47% of patients during the first 2 years of the disease [2]. Activation of immune cells of innate and acquired immunity leads to activation of endothelial cells and immune infiltration of synovial tissues in PsA. Dendritic cells play a key role in activating and coordinating the inflammatory response in PsA by activating T cell subsets (Th1, Th2, Th17, Th9, Th22 and Tregs) that secrete proinflammatory or anti-inflammatory cytokines. In addition, macrophages, innate lymphoid cells (ILCs), mucosal associated invariant T cells (MAIT), natural killer cells, and mast cells are potential producers of predominantly proinflammatory cytokines. In this case, IL-23, TNF, IL-17 and IL-22 are key cytokines involved in inflammation and activation of resident cells in the joint and periarticular tissues. Resident cells (synovial fibroblasts, chondrocytes, osteoblasts and osteoclasts) secrete matrix-degrading enzymes and RANKL, which leads to cartilage degradation, bone erosion, and also secrete pro-inflammatory mediators to attract more immune cells, maintaining the inflammatory response [3].

Among the proinflammatory cytokines involved in the development of spondyloarthritis, special attention is paid to the IL-12/23 and IL-17A axis. The main producers of IL-17—resident populations of FLV type 3 and γδ T cells—have been identified in enthesitis. IL-17 is a key cytokine in the development of enthesitis, which, in turn, is the earliest pathological element in spondyloarthritis. It is assumed that enthesitis precedes clinical joint damage (arthritis), as evidenced by MRI studies. In this case, the pathogenesis of enthesitis may differ from the pathology of the skin and synovial inflammation. Signs of inflammation of the entheses, according to MRI, were also noted in dactylitis [3].

The role of a special subpopulation of T cells—T helper type 17 (Th17)—in the development of spondyloarthritis is well known. Increased levels of Th17 and IL-17A are found in the skin and blood of patients with psoriasis, as well as the blood and synovial fluid of patients with PsA [4–8]. IL-17A triggers several feedback mechanisms in spondyloarthritis and leads to Th17 proliferation and, consequently, further synthesis of IL-17A [9].

The cytokine profile in the pathogenesis of arthritis in different immunoinflammatory diseases differs, which probably determines the different effectiveness of anti-cytokine therapy in these diseases. Thus, in rheumatoid arthritis, CD8 + T cells producing IL-17A are not found in the synovial fluid, but in PsA, they are present in the synovial fluid of inflamed joints, and their levels correlate with disease activity [10–12]. In psoriatic arthritis, pathological changes in bone tissue in the form of destruction (formation of joint erosions) and osteoproliferation can occur simultaneously in different anatomical sites, while IL-17A plays a complex role in these processes [13].

Bone erosion in PsA

Numerous preclinical studies have demonstrated the involvement of IL-17A in bone resorption in experimental arthritis. IL-17A activates receptor activator of nuclear factor kappa-β ligand (RANKL), which is expressed on osteoblasts and inhibits Wnt signaling, thereby leading to decreased osteoblast activity and activation of osteoclastogenesis with subsequent bone resorption [14–17].

Osteoproliferation in PsA

There is evidence suggesting a role for IL-17A in excessive osteoproliferation in spondyloarthritis. IL-17A stimulates the differentiation of local populations of mesenchymal stem cells into osteoblasts. Osteoblast differentiation and new bone formation are enhanced by bone morphogenetic protein (BMP) and Wnt protein. Increased amounts of BMP and Wnt have been associated with excessive new bone formation and osteophyte formation. Wnt proteins and their inhibitors, DKK1 and sclerostin, are key effector molecules for the activation of osteoblasts and allow an increase in the amount of bone tissue in the enthesis. The balance between Wnt proteins and their inhibitors also determines the amount of new bone formed at the enthesis. For example, blockade of the Wnt inhibitor DKK1 is associated with increased differentiation of mesenchymal stem cells into hypertrophic chondrocytes, which leads to bone spur formation in peripheral joints, as well as ankylosis of the sacroiliac joints [18].

There is no doubt about the immune-mediated mechanism of PsA development. Despite the fact that the cause of PsA is not understood and there is no etiotropic treatment, understanding the genetic, cellular and molecular factors involved in the pathogenesis of PsA allows the development of new approaches to therapy. Studying the role of CD8+ T lymphocytes, TNFα, and the IL-32–Th17 axis has led to the successful development of targeted drugs that are highly effective against the main manifestations of PsA.

Sources

• Mease PJ Psoriatic Arthritis: update on pathophysiology, assessment and management. Ann Rheum Dis. 2011 Mar;70 Suppl 1:i77-84. doi: 10.1136/ard.2010.140582
• Kane D., Stafford L., Bresnihan B., FitzGerald O. A prospective, clinical and radiological study of early psoriatic arthritis: an early synovitis clinic experience. Rheumatology (Oxford) 2003; 42:1460–68
• Veale DJ, Fearon U. The pathogenesis of psoriatic arthritis. Lancet. 2021 Jun 2;391(10136):2273-2284. doi: 10.1016/S0140-6736(18)30830-4.
• Lynde CW, Poulin Y, Vender R, et al. Interleukin 17A: towards a new understanding of psoriasis pathogenesis. J Am Acad Dermatol 2014;71:141–50.
• Lowes MA, Kikuchi T, Fuentes-Duculan J, et al. Psoriasis vulgaris lesions contain Discrete populations of Th1 and Th17 T cells. J Invest Dermatol 2008;128:1207–11.
• Menon B., Gullick NJ, Walter GJ, et al. Interleukin-17+CD8+ T cells are enriched in the joints of patients with psoriatic arthritis and correlate with disease activity and joint damage progression. Arthritis Rheumatol 2014;66:1272–81.
• Jandus C., Bioley G., Rivals JP., et al. Increased numbers of circulating polyfunctional Th17 memory cells in patients with seronegative spondylarthritis. Arthritis Rheum 2008;58:2307–17.
• Shen H., Goodall JC, HILL Gaston JS Frequency and phenotype of peripheral blood Th17 cells in ankylosing spondylitis and rheumatoid arthritis. Arthritis Rheum 2009;60:1647–56.
• Benedetti G., Miossec P. Interleukin 17 contributes to the chronicity of inflammatory diseases such as rheumatoid arthritis. Eur J Immunol 2014;44:339–47.
• Menon B., Gullick NJ, Walter GJ, et al. Interleukin-17+CD8+ T cells are enriched in the joints of patients with psoriatic arthritis and correlate with disease activity and joint damage progression. Arthritis Rheumatol 2014;66:1272–81.
• Jandus C., Bioley G., Rivals JP., et al. Increased numbers of circulating polyfunctional Th17 memory cells in patients with seronegative spondylarthritis. Arthritis Rheum 2008;58:2307–17
• Wang C., Liao Q., Hu Y., et al. T lymphocyte subset imbalances in patients contribute to ankylosing spondylitis. Exp Ther Med 2015;9:250–6.
• McGonagle DG, et al. The role of IL-17A in axial spondyloarthritis and psoriatic arthritis: recent advances and controversies. Ann Rheum Dis 2019;78:1167–1178. doi:10.1136/annrheumdis-2019-215356
• Chabaud M., Lubberts E., Joosten L, et al. IL-17 derived from juxta-articular bone and synovium contributes to joint degradation in rheumatoid arthritis. Arthritis Res 2001;3:168–77.
• Chabaud M., Miossec P. The combination of tumor necrosis factor? blockade with interleukin-1 and interleukin-17 blockade is more effective for controlling synovial inflammation and bone resorption in an ex vivo model. Arthritis & Rheumatism 2001;44:1293–303.
• Lubberts E., van den Bersselaar L., Oppers-Walgreen B., et al. IL-17 promotes bone erosion in murine collagen-induced arthritis through loss of the receptor activator of NF-kappa B ligand/osteoprotegerin balance. J Immunol 2003;170:2655–62.
• Adamopoulos IE, Chao C-chi, Geissler R., et al. Interleukin-17A upregulates receptor activator of NF-κB on osteoclast precursors. Arthritis Research & Therapy 2010;12
• Georg Schett et al. Enthesitis: from pathophysiology to treatment. Nature Reviews Rheumatology volume 13, pages 731–741 (2017) doi:10.1038/nrrheum.2017.188