Infectious Bone Diseases: Osteomyelitis
Osteomyelitis represents the most common pathology among infectious lesions of the skeletal system.
The inflammation encompasses the bone marrow and spreads to other bone structures. Staphylococci most frequently act as the main culprit of the infection. However, the process is often of polymicrobial etiology: hemolytic streptococci and Escherichia coli may be detected in the inflammatory focus. The typical localization of the process is the metaepiphyses of the femur and tibia, although theoretically any bone of the skeleton can be subject to the lesion.
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 spongy bones, e.g., vertebral bodies).
Involutional osteoporosis is encountered in both sexes. Its mechanism is triggered by age-related changes: calcium is absorbed less effectively in the intestine, due to which vitamin D is insufficiently activated in the liver and kidneys. Hypocalcemia occurs, which forces the parathyroid glands to produce more parathyroid hormone. The outcome is resorption predominantly of tubular bones.
Secondary osteoporosis is subdivided into:
- General: develops against the background of hyperthyroidism, hyperparathyroidism, hypogonadism, or Cushingoid syndrome.
- Local: arises due to local vascular disorders (for example, if a limb is immobilized in a cast for a long time).
In both cases, either bone matrix substances are leached 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 single pathological process based on a lack of vitamin D, leading to a disruption of the phosphorus-calcium balance and impaired matrix mineralization. In children, this condition is called rickets (damaging the growing skeleton, growth plates, and cartilaginous matrix), and in adults, osteomalacia.
Normally, vitamin D is absorbed in the intestine, then under the influence of ultraviolet light, it is converted 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 depots, reabsorption in the kidneys, and regulates the function of osteoblasts and osteoclasts.
Pathogenetic cascade in deficiency:
- Synthesis of active forms of the vitamin in the liver and kidneys drops.
- Intestinal calcium absorption decreases $\rightarrow$ hypocalcemia and hypophosphatemia.
- Parathyroid glands increase the release of parathyroid hormone, which begins to leach calcium from the bones.
- Synthesis of thyrocalcitonin is suppressed, mineralization is impaired.
- Kidneys intensively excrete phosphates, metabolic acidosis arises, which additionally blocks bone ossification.
A characteristic triad is formed in the bones: disruption of enchondral ossification, 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), "square head" in early rickets, or "pigeon chest" in late rickets.
Hyperparathyroidism (Recklinghausen's Disease)
Parathyroid osteodystrophy arises 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 more frequently affected.
Excess parathyroid hormone leads to massive release of calcium into the blood (hypercalcemia) and loss of phosphorus in the urine. Bone tissue is intensively remodeled: the cortical layer becomes spongy, trabeculae thin out, and the bone marrow is replaced by fibrous tissue.
In the bones (especially in the jaws, ribs, and tubular bones), "brown tumors" are formed — accumulations of macrophages, fibroblasts, giant osteoclast-like cells, and hemorrhages. Bones soften to such an extent that they can be cut with a knife. The disease threatens with pathological fractures, metastatic calcification in organs, nephrolithiasis, and a fatal outcome from uremia or exhaustion.
Briefly: answers to topical questions
What are the pathways of infection penetration into bone tissue in osteomyelitis?
Hematogenic and non-hematogenic pathways of infection penetration into bone tissue are distinguished. Non-hematogenic pathways include:
- Traumatic — in open injuries (fractures) and their infection, including gunshot wounds.
- Contact (per continuitatem) — spread of purulent inflammation to the bone from surrounding soft tissues.
- Spread from neighboring organs — spread of the purulent-destructive process to the bone from affected tissues.
- Odontogenic — spread of the process from tooth or periodontal tissues.
- Surgical — infection during a surgical intervention.
What stages are distinguished in the morphogenesis of acute hematogenous osteomyelitis?
A sequential cascade of changes is distinguished in the morphogenesis of acute hematogenous osteomyelitis. The process includes the following stages:
- Serous inflammation — appearance of a focus in the bone marrow.
- Stasis in capillaries — arises due to slowing of the blood flow.
- Increased pressure — occurs in the closed space of the bone marrow and Haversian canals due to the accumulation of serous exudate.
- Focal bone necrosis — develops as a result of venule and arteriole thrombosis and cessation of blood flow.
- Phlegmon — transformation of the exudate into purulent.
- Subperiosteal abscess and fistula — form with the progression of bone marrow and compact bone necrosis.
What local complications develop when osteomyelitis transitions into a chronic form?
When osteomyelitis transitions into a chronic form, the following may develop:
- Pathological fractures of the affected bone.
- False joints (pseudoarthrosis).
- Hemorrhages from formed fistulas.
- Tumors in the lesion zone.
What microscopic changes in bone tissue are characteristic of osteoporosis?
Microscopic changes in osteoporosis are characterized by a decrease in bone tissue mass per unit volume of bone. At the microscopic level, the bone tissue itself appears normal, but its quantity is impaired. There is a thinning of the bone volume and an increase in pores. These changes are caused by osteoclast activity exceeding osteoblast function, which leads to the predominance of resorption over bone formation.
Rickets triad: HOM — Cartilage (impaired conversion to bone), Osteoid (excessive accumulation), Mineralization (impaired ossification).
Class and exam questions
Which bones are most commonly affected in osteomyelitis?
The process can affect any bone, but the metaepiphyseal regions of the femur and tibia are the most vulnerable.
What is the difference between rickets and osteomalacia?
This is the same disease associated with vitamin D deficiency. Rickets develops in children and affects the growing skeleton, while osteomalacia develops in adults.
What is the «brown tumor» of hyperparathyroidism?
This is not a true neoplasm, but a macroscopic bone change caused by the accumulation of fibroblasts, macrophages, osteoclast-like cells, and hemorrhages.
What else to study on this topic
- Vitamin D metabolism in the liver and kidneys
- Hereditary forms of rickets (D-dependent and D-resistant)
- Morphological differences between early and late rickets
- Complications of rickets (metastatic calcification, pathological fractures)
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