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The pathogenesis of osteoarthritis of the hip. Evidence for primary osteocyte death
Insights
Osteocyte death is common in idiopathic osteoarthritis, potentially causing the condition rather than resulting from it. This study investigated bone viability in patients with chronic hip disease.
Area of Science:
- Orthopedics
- Bone Biology
- Histopathology
Background:
- Osteocyte viability is crucial for bone health and integrity.
- Chronic hip diseases can affect bone metabolism and cell survival.
- Understanding osteocyte status may reveal disease mechanisms.
Purpose of the Study:
- To investigate osteocyte viability in femoral head bone from patients with chronic hip disease.
- To determine if patterns of osteocyte death correlate with specific hip pathologies.
- To explore the potential role of bone death in the pathogenesis of idiopathic osteoarthritis.
Main Methods:
- Histochemical staining for lactate dehydrogenase (LDH) activity to assess osteocyte viability.
- Examination of femoral head bone samples from 38 patients with various chronic hip diseases.
- Correlation of histological findings with preoperative diagnoses and radiographic evidence of bone collapse.
Main Results:
- Nonviable osteocytes were prevalent in the central regions of trabeculae in patients with idiopathic osteoarthritis and avascular necrosis.
- This pattern suggested prior bone necrosis followed by new bone formation, not seen in controls or chondrocalcinosis patients.
- Histologic bone death was observed in nine patients, with radiographic bone collapse present in these individuals.
Conclusions:
- Bone death is a frequent finding in idiopathic osteoarthritis and may be a causative factor, not merely a consequence.
- The observed pattern of osteocyte death suggests a distinct pathological process in certain hip diseases.
- Further research into the mechanisms of osteocyte death could inform osteoarthritis treatment strategies.
Abstract:
Osteocyte viability was investigated in femoral head bone removed from 38 patients with chronic hip disease, with the use of a histochemical stain to demonstrate lactate dehydrogenase (LDH) activity in osteocytes. Where the osteocyte cytoplasm did not show LDH activity, the cell was considered dead; when several adjacent osteocytes were dead, the bone in that area was regarded as nonviable. The preoperative diagnoses were idiopathic osteoarthritis in 25, chondrocalcinosis in six, rheumatoid arthritis in two, Paget's disease in two, avascular necrosis in two, and congenital dislocation of the hip in one patient. In 16 of the patients with idiopathic osteoarthritis and the two with avascular necrosis, nonviable osteocytes were present in the central regions of many trabeculae, these areas usually being separated by cement lines from viable bone. The pattern suggested previous necrosis of part of the femoral head, with later new bone formation. The pattern was not observed in either control subjects, or patients with known articular disease, such as chondrocalcinosis. Bone collapse of variable severity was apparent radiographically in nine patients with histologic bone death, but not in other patients. Bone death is commonly present in idiopathic osteoarthritis and could be a cause rather than a result of the arthritis.