Rheumatic soft tissue lesions: symptoms and treatment

Causes Symptoms

Rheumatic soft tissue lesions are pathological changes in the tissues surrounding the joint, that is, periarticular tissues. The pathology can occur independently or develop against the background of joint diseases. This category includes inflammatory processes or degenerative changes not caused by a tumor, infection or injury that occur in:

synovial membrane of the joint capsule (bursitis);
ligaments (ligamentitis) and tendons (tendinitis and tendovaginitis), places of their attachment to the bones (enthesopathy);
tendon plates - aponeuroses (aponeurosis);
covering the muscles - fascia (fasciitis).

This pathology is a fairly common condition. It can affect representatives of both sexes at any age, but more often it occurs in people 34-54 years old whose work involves physical activity.

Causes of pathology

The most common causes of soft tissue damage include joint diseases and inadequate physical activity. Often, problems also arise among office workers who, due to the nature of their work, have to remain in one position for a long time while working.

When walking, pain in the popliteal area, around the heel and ankle can occur due to flat feet, on the outer side of the thigh - due to incorrect foot placement. The following can also provoke pathology:

Osteoarthritis (osteoarthritis) is the most common joint disease in which degradation of joint cartilage occurs. Osteoarthritis is accompanied by pain, stiffness in the joints, and signs of inflammation. In this case, all joint tissues and periarticular structures are involved in the pathological process;
periodic minor and serious injuries resulting from bruises, awkward movements, significant stress (observed among professional athletes and people engaged in physical labor);
some infectious diseases; however, as a rule, the symptoms are varied and are not limited to periarticular tissues;
diabetes;
menopause;
congenital features of the development of tendons and ligaments (for example, joint hypermobility syndrome);
obesity;
previous myocardial infarction.

Pathology of soft tissues of the shoulder and hip joints - diagnosis and treatment

Periarticular pathology is widespread and includes a huge range of changes from syndromes divided into separate nosological units to symptoms accompanying rheumatological diseases.

When describing soft tissue pathology, the following concepts are usually used:

tendonitis - inflammation of tendon tissue;
tenosynovitis/tenosynovitis - inflammation of the tendon tissue and tendon sheath;
enthesitis/enthesopathy - inflammation of the tendon tissue at the site of its attachment to the bone;
Bursitis is an inflammation of the bursae, thin-walled cavities lined with synovium that facilitate the movement of tendons and muscles over bony prominences.

Periarticular diseases of the shoulder joint are represented by several nosological forms:

1) isolated damage to the tendons of the muscles surrounding the joint:

rotator cuff tendonitis (specifying the specific muscle);
biceps tendinitis;
calcific tendinitis;
rupture (partial or complete) of the tendons of the muscles of the shoulder joint;

2) diffuse non-inflammatory damage to the capsule of the shoulder joint (retractile capsulitis);

3) subacromial syndrome (complex damage to the structures surrounding the subacromial bursa).

The spherical structure of the shoulder joint allows it to perform a variety of movements: flexion, extension, abduction, adduction and rotation. It should be remembered that the angle of movement in the shoulder joint without the participation of the scapula characterizes the true range of movements in it, and with their participation - the full range. When testing shoulder abduction, pain in the joint may only appear when it reaches 70–90°. In this case, the greater tubercle of the humerus rises close to the acromion process and can compress the structures passing here (the supraspinatus tendon and the subacromial bursa). As you continue to raise your arm, the greater tubercle moves away from the acromion process and the pain decreases significantly. This painful arch is characteristic of supraspinatus tendinitis or subacromial bursitis. The appearance of pain at the moment of maximum abduction of the arm in the shoulder joint (up to 160–180°) indicates damage to the acromioclavicular joint. With an anterior dislocation, there is a displacement of the head of the humerus anteriorly and downward, which leads to a characteristic change in the contours of the shoulder and a sharp limitation of mobility due to pain (Table 1).

For shoulder tendinitis, the following is recommended:

avoid movements that cause pain for 2–3 weeks;
prescribing non-steroidal anti-inflammatory drugs (NSAIDs) for the duration of severe pain and inflammation;
local application of ointments and gels with NSAIDs 3 times a day for 14 days (in the acute period), as well as irritating ointments that increase blood flow (with capsaicin) - in the chronic course;
periarticular administration of glucocorticoids (GC) (avoid in case of biceps tendinitis);
physiotherapeutic methods: phonophoresis, electrophoresis, cryotherapy, magnetic currents, balneotherapy.

Treatment for calcific rotator cuff tendinitis follows the same principles as for normal tendinitis. However, calcific tendinitis is rarely cured completely and often recurs. There is evidence of the effectiveness in a number of cases of extracorporeal shock wave therapy in relation to both the pain syndrome and the calcifications themselves.

Retractile capsulitis should be considered as one of the variants of the syndrome of reflex sympathetic dystrophy (isolated or as part of the “shoulder-hand” syndrome), which differs from tendinitis in the absence of a degenerative component in the pathogenesis, diffuse damage to the capsule of the shoulder joint, manifested by fibrosis, involvement of bone structures in the form of regional osteoporosis.

Treatment of retractile capsulitis is aimed at physical rehabilitation with restoration of the original range of motion in the shoulder joint, and follows the principles of treatment of reflex sympathetic dystrophy.

Subacromial syndrome (subacromial collision syndrome) develops as a result of an imbalance between the muscles - stabilizers and depressors of the head of the humerus (supraspinatus, infraspinatus, subscapularis and biceps brachii), which leads to a decrease in the space between the head of the humerus and the acromion, to chronic injury to the tendons of the rotator cuff muscles shoulder cuffs during movements.

There are stages of subacromial syndrome.

I. Swelling and hemorrhages in the tendons. II. Fibrosis, thickening of the tendons, the appearance of partial tears in them. III. Complete tendon ruptures, degenerative bone changes involving the inferior surface of the acromion and the greater tubercle of the humerus.

Treatment of subacromial syndrome depends on the severity of clinical manifestations and the stage of the process. In stage I - avoid raising the arm above the head, trial therapy with full doses of NSAIDs for two weeks, subacromial administration of glucocorticosteroids (GCS) (repeated injection no earlier than after 6 weeks), physiotherapeutic treatment in the presence of weakness of the muscles of the shoulder girdle (after 1-2 weeks). At stage II - drug treatment (see above), if ineffective within a year - subacromial decompression (intersection of the coracoacromial ligament with anterior acromionoplasty), at stage III - arthroscopic revision of the subacromial space, removal of osteophytes, restoration of tendon integrity.

Damage to the periarticular tissues of the hip joint

The hip joint is a large ball-and-socket joint that has a significant range of motion: flexion/extension, abduction/adduction, pronation/supination. The mobility of the hip joint is determined by the elongated neck of the femur, which forms an angle of 130° with the axis of the limb. The most common causes of pain in the hip joints are injuries, arthritis (osteoarthritis (OA), rheumatoid arthritis), aseptic necrosis of the femoral head, osteochondritis dissecans (Perthes disease), infections (for example, osteomyelitis, tuberculous coxitis). However, pathology of the soft tissues surrounding the joint is also common (Table 2).

The most difficult diagnostic situation arises when the patient complains of pain in the hip joint, but no changes are detected during X-ray examination. In these cases it matters:

well-collected medical history;
physical examination: a combination of pain with extreme abduction and internal rotation suggests arthritis or osteonecrosis; restriction of movements in the direct projection in patients with diabetes mellitus will allow one to suspect adhesive capsulitis;
the presence of general signs such as weakness, fever, weight loss or increased pain at night requires special laboratory testing to exclude a tumor or hidden infectious processes.

The most common cause of pain is bursitis in the area of the greater trochanters, which is characterized by:

the pain is deep, sometimes burning, mainly along the lateral surface of the joint and thigh. The pain increases when walking on a flat surface and stairs, squatting, and is combined with lameness in 15% of patients;
pain decreases with rest, but can periodically intensify at night, especially when lying on the sore side;
upon palpation, tension is noted in the area of the greater trochanter;
resistance is felt when the hip is abducted while the patient is lying down in the opposite direction, and a feeling of discomfort may occur.

Treatment of periarticular pathology of the hip joint area should take into account the underlying disease (for example, OA - the prescription of “chondroprotective” drugs, body weight control; seronegative spondyloarthritis - the prescription of disease-modifying drugs (sulfasalazine, methotrexate, etc.), tuberculous coxitis - specific anti-tuberculosis drugs, etc. .d.). Often the main methods of treatment are local administration of GC, electrophoresis and iontophoresis, and the administration of muscle relaxants.

One of the main directions in the treatment of periarticular soft tissue pathology is the prescription of various forms of NSAIDs. The anti-inflammatory and analgesic activity of NSAIDs is associated with a decrease in the production of prostaglandins. The anti-inflammatory effect of NSAIDs is due to the suppression of the activity of cyclooxygenase (COX), the main enzyme in the metabolism of arachidonic acid on the path of its conversion into prostaglandins. The mechanisms of action of NSAIDs are quite well studied, and the main side effects of this group of drugs are also described, limiting their use in patients at risk. An alternative to oral and parenteral use of NSAIDs, as well as an important auxiliary component of the complex treatment of pain syndrome in periarticular pathology, is local therapy with NSAIDs. Currently, the basic requirements for local therapy have been formulated: the drug must be highly effective, must not cause local toxic and allergic reactions, and also have the ability to penetrate the skin, reaching the target tissue; the concentration of drugs in the blood serum should not reach a level leading to side effects. The most successful form for local therapy is the use of a gel, in which alcohol as a solvent ensures rapid absorption of the active substance into the superficial structures of the joint. Therefore, the use of gel is justified compared to ointments or creams and is more economical. All these requirements are met by Deep Relief - a two-component gel for external use based on ibuprofen 5.0% and menthol 3.0% of natural origin, in which the analgesic and anti-inflammatory effects of ibuprofen are complemented and enhanced by the therapeutic properties of levomenthol (optical isomer of menthol) due to the reflex reaction associated with irritation of the nerve endings of the skin, stimulation of nociceptors. Thanks to the components of the gel base, ibuprofen molecules in a bound state penetrate the surface layer of the skin. Menthol causes the release of vasodilating peptides, which leads to additional distracting, analgesic effects, causing a feeling of slight coolness. To enhance the local anti-inflammatory effect, the product should be applied multiple times throughout the day. Clinical studies in recent years have shown that the minimum is 4 times the application of a local product during the day. In case of active inflammation with the most severe pain, the application of the drug should be increased to 6 times a day.

Literature

William J. Koopman (editor) et al. Arthritis and Allied Conditioins: A Textbook of Rheumatology, 13th edition. Williams & Wilkins, 1997.
Hakim A., Clunie G., Hag I. Oxford Handbook of Rheumatology, 2nd edition. Oxford University Press, 2008. 606 p.
John H. Klippel. Primer on the Rheumatic Diseases, 12th edition. In: Leslie J. Grofford, John H. Stone, Cornelia M. Weyand. Atlanta, Georgia, 2001.
R. Watts et al. Oxford Desk Reference: Rheumatology. Oxford University Press, 2009.

N. A. Shostak, Doctor of Medical Sciences, Professor N. G. Pravdyuk, Candidate of Medical Sciences A. A. Klimenko, Candidate of Medical Sciences, Associate Professor

GBOU VPO RNIMU im. N. I. Pirogova Ministry of Health and Social Development, Moscow

Contact information for authors for correspondence

Hypermobility syndrome (HS, M35.7 according to the International Classification of Diseases, 10th revision) combines the phenomenon of joint hypermobility (HMS), associated with joint dysfunction, and phenotypic signs of connective tissue dysplasia (CTD).

The clinical manifestations of HS are diverse and include both articular and extra-articular signs, reflected in the HS criteria (Table 1) [1].

.Diagnostic criteria for HS (Brighton, 1998).

For an objective assessment of HMS, the Beighton criteria are used [1]:

Passive flexion of the metacarpophalangeal joint of the 5th finger in both directions.
Passive flexion of the 1st finger towards the forearm while flexing at the wrist joint.
Hyperextension of the elbow joint over 10 degrees.
Hyperextension of the knee joint over 10 degrees.
Bend forward with fixed knee joints, while palms reach the floor.

To establish hypermobility, a generally accepted score is: 1 point means pathological hyperextension in one joint on one side. The maximum value of the indicator, taking into account bilateral localization, is 9 points (8 for the first 4 points and 1 for the 5th point). An indicator from 4 to 9 points is regarded as a state of hypermobility.

HS is diagnosed if two major criteria are present, or one major and two minor criteria, or four minor criteria. Two small criteria are sufficient if a first-degree relative has signs of DTD.

The pathogenesis of HS is based on a hereditary defect in collagen, which causes its hyperextensibility and a decrease in the mechanical strength of connective tissue structures (ligaments, entheses, tendons). The latter leads to an increased risk of macro- and microtraumatization of the articular apparatus in the absence of obvious physical overload.

The main clinical manifestation of HS is damage to the musculoskeletal system in the form of arthralgia associated with physical activity. The knee and ankle joints are most often involved in the process. The cause of the pain syndrome in this case is the sensitivity of the supporting joints to load and moderate orthopedic anomalies (hip dysplasia, longitudinal and transverse flatfoot), which are often found in people with HS. The onset of arthralgia occurs at a young age and is observed mainly in females. Joint subluxations (mainly ankles and knees) are typical in patients with HS. Recurrent joint effusion as a manifestation of HMS is an uncommon, but most difficult diagnostic situation. A characteristic feature of synovitis with HMS is a direct connection with injury, the non-inflammatory nature of the synovial fluid and rapid reverse development. Subsequently, these patients may develop persistent arthralgia of the injured knee joint associated with post-traumatic meniscopathy. Dorsalgia, often combined with scoliosis and spondylolisthesis, occurs in patients with HS at any age.

Various lesions of periarticular soft tissues (tendinitis, epicondylitis, other enthesopathies, bursitis) are typical for patients with HS in the second half of life. At this age, involutive processes in the tendon-ligament apparatus are superimposed on the existing systemic connective tissue defect. Periarticular lesions in HS occur in response to unusual (unusual) load or minimal trauma. The presence of multiple (more than two localizations) periarticular lesions during life is one of the minor diagnostic criteria for HS. Treatment of this pathology in HS is not fundamentally different from the general tactics known for this group of diseases. However, within the framework of HS, soft tissue pathology is often more persistent and recurrent.

Damage to soft tissues in the upper extremities

Lesions of the periarticular apparatus in the area of the shoulder joint are represented by damage to the tendons of the muscles surrounding the joint - tendonitis (inflammation of the tendon tissue) of the rotator cuff muscles (indicating the specific muscle) and tendinitis of the biceps brachii muscle. Tendinitis of a specific muscle is characterized by pain and limitations in performing certain movements, which underlies the clinical assessment of the disease (Table 2) [2–4].

.Diagnostics of tendinitis of the muscles of the shoulder joint.

Pain in the shoulder joint when trying to maximally raise the arm up (up to 160–180 degrees) indicates damage to the acromiocleidoid joint. If there is pain and restriction of all movements in the shoulder joint, it is necessary to think about damage to the capsule or the shoulder joint itself. If there is pain in the shoulder area that is not associated with movement, it is necessary to differentiate it from plexitis and thoracic outlet syndrome. Imaging methods include ultrasound, radiography, and magnetic resonance imaging (including intravenous magnetic resonance arthrography).

For tendonitis of the shoulder muscles, it is recommended:

Avoiding movements that cause pain for 2-3 weeks.
The use of non-steroidal anti-inflammatory drugs (NSAIDs) during severe pain and inflammation.
Local application of ointments and gels with NSAIDs 3 times a day for 14 days, as well as irritating ointments that increase blood flow (with capsaicin).
Periarticular administration of glucocorticosteroids (GCS).
Physiotherapeutic methods: phono-, electrophoresis, cryotherapy, magnetic currents, balneotherapy.

Damage to the periarticular tissues of the elbow joint is represented by enthesitis - inflammation of the tendon tissue at the site of its attachment to the bone (epicondylitis). There are medial (“golfer’s elbow”) and lateral (“tennis elbow”) epicondylitis (inflammation of the epicondyles of the humerus at the attachment points of the flexor and extensor tendons of the fingers) (Table 3).

Damage to the periarticular tissues of the elbow joint.

Medial epicondylitis is characterized by increased pain during flexion (medial epicondylitis) and extension (lateral epicondylitis) of the wrist joint when resisting this movement.

A frequent manifestation of periarticular lesions of the elbow joint is olecranon bursitis (inflammation of the synovial bursa - a thin-walled cavity lined with a synovial membrane that facilitates the movement of tendons and muscles over bone protrusions), which occurs against the background of trauma to the posterior surface of the elbow (for example, in car drivers resting their elbow on the door ).

Upon examination, a mildly painful tumor is revealed on the posterior surface of the joint in the area of the olecranon, while movements in the joint are preserved. However, olecranon bursitis can be infectious and observed with gout, rheumatoid arthritis, psoriatic arthritis, and osteoarthritis.

Treatment of epicondylitis is often conservative with the use of NSAIDs and local administration of corticosteroids, ultrasound therapy, and resting the elbow joint during the period of acute pain. In the case of olecranon bursitis, the bursa is punctured at the site of the greatest fluctuation; if an infectious etiology of bursitis is excluded, GCS is administered after evacuation of the effusion [1, 2].

Damage to the periarticular tissues of the wrist joint and hand. Among periarticular lesions of the wrist joint and hand, de Quervain's disease (stenotic tenosynovitis of the long abductor and short extensor of the first finger) is of greatest importance. The disease manifests itself with severe pain and swelling in the area of the “anatomical snuffbox” (2 cm proximal to the base of the first finger). Characterized by local pain, which intensifies when the thumb is abducted, especially when resisting this movement. Among many methods of treating soft tissue pathology of the wrist joint and hand (NSAIDs, physiotherapeutic methods of treatment), the most effective is local injection of corticosteroids into the affected area (into the tendon sheath of the abductor longus and extensor digitorum brevis) [1].

Pathology of soft tissues of the ankle and foot area

Pain when the periarticular tissues of the ankle and foot are affected usually has a clear localization. Periarticular pathology is listed in Table. 4.

.Periarticular pathology of the ankle and foot area.

The most common causes of chronic Achilles tendon pain are Achilles tendonitis, partial rupture, or Achilles tendon bursitis.

Achilles tendonitis (Achilles tendonitis) is accompanied by swelling and pain when loading the tendon or where the tendon attaches to the heel bone. The main clinical symptoms characteristic of Achilles tendonitis:

pain in the heel, sometimes along the back of the shin;
increased pain when bending the foot;
pain on palpation (2–3 cm proximal to the junction of the tendon with the heel bone);
swelling and thickening of the tendon.

Cases of spontaneous tendon rupture have been described, when sudden severe pain appears during dorsal flexion of the foot, a click or other sound heard in the ear during the rupture, a positive Thompson test (the patient is kneeling in a chair and his feet hang over the edge of the chair; the doctor squeezes the calf muscle and moves it towards the knee joint; normally, plantar flexion of the foot occurs, but with a rupture of the Achilles tendon this does not happen).

It should be remembered that the causes of spontaneous tendon rupture can be not only Achilles tendonitis itself, but also the introduction of corticosteroids into the thickness of the tendon, hypothyroidism, as well as the use of fluoroquinolones in patients over 60 years of age with kidney disease, who have undergone a heart or lung transplant, or during corticosteroid therapy .

Retrocalcaneal bursitis is clinically similar to Achilles tendinitis, but the pain often becomes excruciating and intensifies significantly with walking and prolonged standing, and often there is swelling or swelling proximal to the site of attachment of the tendon to the heel bone. Ultrasound examination of this area helps differentiate the disease.

Plantar fasciitis is inflammation in the area of attachment of the flexor digitorum brevis muscle to the anteromedial edge of the calcaneal tuberosity. The main symptom of plantar fasciitis is pain along the entire plantar surface of the foot when walking. Usually this pain appears during the first steps - after the patient gets out of bed in the morning or after sitting for a long time. Overstrain and traction of the tendon and fascia lead to reactive inflammatory production of bone tissue with the formation of a heel spur. Diagnosis is based on clinical data; X-ray examination is performed to clarify the diagnosis.

Periarticular foot pathology also occurs with seronegative spondyloarthritis and flat feet, which must be taken into account when making a diagnosis. Pain associated with the ankle joint itself is usually localized at the front between the two ankles and worsens with movement or standing. When the subtalar joint is affected, the pain is localized in the area between the heel and ankle joint, and intensifies when walking and rocking the foot to the sides [2, 3].

In the treatment of periarticular pathology of the foot, it is important to exclude chronic trauma to this area, rest during the acute period of the disease, and the use of NSAIDs. If you have flat feet, correct them using therapeutic insoles, shoes, or orthoses.

Taking into account the contribution of DST to the development of periarticular pathology in HS, the prescription of magnesium preparations that improve the metabolism of connective tissue is pathogenetically justified.

Thus, the clinical manifestations of HS are varied. Often they are the background for the development of serious pathology. The doctor’s task can be called identifying the leading clinical manifestation and determining treatment tactics, as well as preventing complications of HS that have a defined somatic framework.

Rheumatic diseases of periarticular soft tissues

Pathological changes first affect the tendons that are subject to the greatest load and mechanical stress. This leads to the appearance of fibril defects, foci of necrosis, the development of post-inflammatory sclerosis, hyalinosis and calcification. Primary changes are localized in the places of fixation of tendons to bone tissue (entheses) and are called enthesopathy. In the future, the process may involve tendon sheaths (tenosynovitis), synovial membranes (bursitis), fibrous capsules (capsulitis), joint ligaments (ligamentitis), etc.

Common symptoms of extra-articular rheumatism include pain and limited joint mobility. Pain is associated with certain active movements in the joint; local painful areas are determined in the areas of tendon fixation. With tendovaginitis and bursitis, swelling is clearly detected along the tendons or in the projection of the synovial membrane.

Humeroscapular periarthritis

It predominantly develops in women over 40-45 years of age. Humeroscapular periarthritis is caused by dystrophic changes in the tendons of the supraspinatus muscle, the rotator muscles of the shoulder (subscapularis, infraspinatus, teres minor and major), tendons of the head of the biceps muscle (biceps) and the subacromial bursa. Involvement of the supraspinatus tendon can result in simple tendonitis, calcific tendonitis, or a tear (or rupture) of the tendon.

Simple tendinitis is characterized by pain in the supraspinatus muscle during active abduction of the arm (Dauborn's sign), with the greatest pain observed when the amplitude of abduction of the limb is 70-90°. A sharp increase in pain is associated with temporary compression of the tendon between the epiphysis of the humerus and the acromion. The calcific form of tendinitis is diagnosed after radiographs of the shoulder joint are taken. Painful symptoms are more pronounced, and the motor function of the joint is more significantly impaired.

A tear or complete rupture of the tendon that anchors the supraspinatus muscle is usually caused by heavy lifting or an unfortunate fall on the arm. It differs from other forms of glenohumeral periarthritis by the typical symptom of a “falling arm,” i.e., the inability to keep the arm in an abducted position. This condition requires arthrography of the shoulder joint and, if a tendon rupture is detected, surgical intervention.

With tendinitis of the head of the biceps, persistent pain and palpation tenderness are noted when trying to strain the biceps muscle. The clinical picture of subacromial bursitis usually develops secondarily, following damage to the supraspinatus muscle or biceps. It is characterized by pain, limitation of rotation and abduction of the limb (symptom of a blocked shoulder). It can occur in the form of calcific bursitis with the deposition of calcium salts in the subacromial bursa.

Periarthritis of the elbow joint

Variants of damage to the periarticular tissues of the elbow joint include enthesopathies in the area of the epicondyles of the humerus and ulnar bursitis. Enthesopathies of the tendons that attach to the epicondyle of the shoulder constitute the pathogenetic basis of the syndrome called “tennis elbow.” Pain is noted in the area of the external and medial epicondyles of the humerus, which intensify at the slightest tension of the extensors and flexors of the hand and fingers.

In the case of olecranon bursitis, a voting protrusion in the projection of the olecranon is determined by palpation.

Periarthritis of the hip joint

It develops when the tendons of the gluteus minimus and medius muscles are damaged, as well as the joint capsules in the area of the greater trochanter of the femur. For the clinic of hip periarthrosis, the occurrence of pain in the upper outer thigh when walking and absence at rest is typical. Palpation of the soft tissues in the area of the greater trochanter is painful, and x-rays reveal tendon calcification and osteophytes along the contour of the apophysis of the femur.

Periarthritis of the knee joint

Caused by damage to the tendon apparatus, which provides fixation of the semitendinosus, sartorius, gracilis, semimembranosus muscles to the medial condyle of the tibia. Pain accompanies both active and passive movements (extension, flexion, rotation of the leg), sometimes local hyperthermia and swelling of soft tissue structures are noted.