Gout

Benign synovial neoplasms

For a long time, these pathologies were considered exclusively inflammatory; however, modern data confirm their neoplastic nature. Histologically, synoviocytes form strands, with numerous macrophages, multinucleated giant cells, and hemosiderin accumulations being detected. Cellular atypia is absent, but the neoplasm is capable of destroying the adjacent bone (erosion) and growing into soft tissues.

• Localized nodular synovitis. Most commonly affects the tendon sheaths of the wrist and fingers. Macroscopically, it presents as a painless node resembling a walnut. Microscopically, cells merge into a single solid conglomerate.
• Giant cell tumor of the tendon sheath. An isolated lesion located in the same area, but achieving larger sizes. The tumor stroma frequently undergoes fibrosis and hyalinosis. The prognosis is generally favorable, but the risk of recurrence remains.

Tumor-like joint lesions (cysts)

Among tumor-like formations, two main types associated with joint capsules and tendons are distinguished:

1. Tendon sheath cyst (ganglion). This is a cavity 1–1.5 cm in diameter filled with fluid. Externally, it resembles a firm-elastic pea. It is formed from connective tissue that has undergone cystic or myxoid alteration. Small elements may coalesce. If the ganglion is located in the popliteal fossa, it is called a Baker's cyst. Sometimes the cyst grows subchondrally (intraosseous ganglion), causing erosion of the cortical layer and bone deformation.
2. Synovial cyst. Represents a herniation of the synovial membrane itself through defects in the joint capsule. The membrane becomes edematous, thickened, and an infiltrate (lymphocytes, macrophages, leukocytes, fibrin) is found within it.

Bone injuries: pathogenesis of fracture healing

A fracture is a mechanical or pathological disruption of bone integrity. Healing represents a complex cascade of reactions:

• Initial stage: vascular rupture leads to hemorrhage and hematoma formation, triggering acute inflammation.
• 2–3 days: the hematoma organizes, being replaced by granulation tissue. A primary fibrous connection emerges.
• 2–3 weeks: osteoblast precursors migrate from the periosteum and endosteum. Granulation tissue transforms into woven bone — primary callus forms.
• Subsequent 3 weeks: the primary callus is resorbed and replaced by strong lamellar bone (forming the secondary callus).

A critical factor is blood supply: with good blood flow, bone trabeculae are formed; with poor blood flow, cartilaginous tissue (which then undergoes endochondral ossification). Ultimately, osteoclasts remove excess tissue, and newly formed osteons grow through the fracture line, restoring normal structure.

Fracture outcomes

Bone tissue repair can proceed through several scenarios:

• Primary healing. The ideal option. Lasts about 5 weeks, is not accompanied by the formation of a massive osteocartilaginous callus, and concludes with complete restoration (restitution).
• Secondary healing. Occurs with fragment mobility and their loose apposition. Inevitably includes the fibrocartilaginous callus stage.
• Pseudoarthrosis (false joint). An unfavorable outcome. Coarse connective tissue proliferates between the ends of the broken bone. Due to metaplasia, it becomes fibrous cartilage containing foci of fibrinoid necrosis. Consequently, a cavity lined with synovial cells is formed.

Hereditary muscular dystrophies (myopathies)

Myopathies are primary hereditary diseases of striated muscles characterized by selective involvement of certain muscle groups and progressive weakness.

Duchenne myopathy is caused by an X-linked mutation in the dystrophin gene (a protein maintaining the shape and contractility of muscle fibers). Affects boys (manifestation at 3–5 years). Pelvic and leg muscles weaken first. Microscopically, fiber polymorphism, necrosis, macrophage phagocytosis, and compensatory proliferation of myosatellite cells are visible. Ultimately, muscles are replaced by adipose and fibrous tissue; myocardial fibrosis leads to heart failure (fatal outcome around 20 years of age).

Becker myopathy has a similar etiopathogenesis, but proceeds significantly more mildly. Affects older boys, the heart is involved less frequently, so patients live longer.

Myotonic dystrophies (specifically the congenital form) are inherited in an autosomal dominant manner. The main symptom is myotonia (involuntary contractions and difficulty with relaxation). The disease starts in adolescence with foot weakness, later joined by ptosis, facial muscle atrophy, and cataract.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Histological differences between pigmented villonodular synovitis and giant cell tumor.
• Mechanisms of endochondral ossification in poor blood supply of the bone callus.
• The role of osteoclasts and Haversian systems in bone remodeling.
• Classification and pathogenesis of acquired (toxic, autoimmune) myopathies.

Other topics in the section "Chapter 22. Diseases of the Musculoskeletal System"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.