Bone Infections: Osteomyelitis
Osteomyelitis is the most common pathology among infectious lesions of the skeletal system.
The inflammation involves the bone marrow and spreads to other bone structures. Staphylococci are most often the main culprits of the infection. However, the process frequently has a polymicrobial etiology: hemolytic streptococci and Escherichia coli may be found in the inflammatory focus. The typical localization of the process is the metaepiphysis of the femur and tibia, although theoretically any bone in the skeleton can be affected.
Metabolic Disorders: Osteoporosis
In addition to infectious processes, bone tissue often suffers from metabolic disorders accompanied by intensive bone resorption by osteoclasts. This leads to so-called compression fractures (especially in trabecular bone, such as vertebral bodies).
Involutional osteoporosis occurs in both sexes. Its mechanism is triggered by age-related changes: calcium is absorbed less efficiently in the intestine, leading to insufficient activation of vitamin D in the liver and kidneys. Hypocalcemia develops, which forces the parathyroid glands to produce more parathyroid hormone (PTH). The result is resorption, predominantly of tubular bones.
Secondary osteoporosis is divided into:
- General: develops against the background of hyperthyroidism, hyperparathyroidism, hypogonadism, or Cushing's syndrome.
- Local: arises due to local vascular disorders (e.g., if a limb is immobilized in a cast for a long time).
In both cases, either bone matrix substances are washed out or osteoclasts are excessively activated, which catastrophically reduces skeletal strength and leads to pathological fractures of the ribs, vertebrae, and limbs.
Rickets and Osteomalacia: Vitamin D Deficiency
This is a unified pathological process based on a lack of vitamin D, leading to a disruption of the calcium-phosphorus balance and impaired matrix mineralization. In children, this condition is called rickets (affecting the growing skeleton, growth plates, and cartilage matrix), and in adults, osteomalacia.
Normally, vitamin D is absorbed in the intestine, then converted by ultraviolet light in the liver into 25(OH)D3, and in the kidneys into its most active form (calcitriol). Active vitamin D is responsible for calcium absorption, its mobilization from stores, renal tubular reabsorption, and the regulation of osteoblast and osteoclast activity.
Pathogenetic cascade in deficiency:
- Synthesis of active vitamin forms in the liver and kidneys decreases.
- Intestinal calcium absorption drops $\rightarrow$ hypocalcemia and hypophosphatemia.
- Parathyroid glands increase PTH release, which begins to leach calcium from bones.
- Thyrocalcitonin synthesis is suppressed, and mineralization is impaired.
- Kidneys excessively excrete phosphates, and metabolic acidosis occurs, which additionally blocks bone ossification.
A characteristic triad forms in the bones: disruption of endochondral ossification, an excess of unmineralized osteoid tissue, and the development of osteomalacia. Macroscopically, this manifests as the formation of osteophytes ("rachitic rosary" on the ribs, "bracelets" on the wrists), a "square head" in early rickets, or "pigeon chest" in late rickets.
Hyperparathyroidism (Recklinghausen's Disease)
Parathyroid osteodystrophy occurs due to hyperfunction of the parathyroid glands (primary due to a tumor, or secondary against the background of renal failure and hypocalcemia). Women aged 40–50 are most frequently affected.
Excess parathyroid hormone leads to a massive release of calcium into the blood (hypercalcemia) and urinary loss of phosphorus. Bone tissue undergoes intensive remodeling: the cortical layer becomes spongy, trabeculae thin out, and the bone marrow is replaced by fibrous tissue.
"Brown tumors"—accumulations of macrophages, fibroblasts, giant osteoclast-like cells, and hemorrhages—form in the bones (especially the jaws, ribs, and tubular bones). Bones become soft enough to be cut with a knife. The disease threatens pathological fractures, metastatic calcification in organs, nephrolithiasis, and death from uremia or exhaustion.