Microscopic study of chronic charcot arthropathy foot bones contributes to understanding pathogenesis - A preliminary report
- PMID: 31508805
- DOI: 10.14670/HH-18-162
Microscopic study of chronic charcot arthropathy foot bones contributes to understanding pathogenesis - A preliminary report
Abstract
Introduction: Charcot arthropathy (CA) is non-infective, chronic destructive condition affecting the pes architecture of long standing diabetic patients with neuropathy. Even though several theories have emerged to disclose its pathogenesis, inflammatory cytokine induced osteoclastogenesis stands as the chief culprit. Studies on micro-architecture of foot bones of acute stage CA patients, describes mainly destructive phase of bone remodelling. Increased osteoclast cell activity is reported in all studies communicated. No study has to the best of our knowledge detailed the microscopic structure of chronic stage CA foot bones.
Aim: To study the microscopic structure of foot bones in patients with chronic CA.
Materials and methods: Foot bones were collected from the feet of chronic CA patients (six in number) who underwent corrective foot surgery in the Department of Podiatric Surgery of a tertiary care hospital. Control samples were collected from the feet of age matched non-diabetic controls (2 in number). The samples were fixed in formalin, decalcified in 10% nitric acid, processed, sectioned and stained with haematoxylin and eosin. Histopathology and histomorphometry analysis were performed by two different pathologists.
Results: Trabeculae of chronic CA foot bones exhibited mainly a lamellar architecture, with reduced number of osteocytes and plenty of empty lacunae. Trabecular connectivity was lost and trabeculae showed considerable thinning. Trabecular osteoids lined by active osteoblast cells was a remarkable observation. Bone area was also considerably reduced in chronic CA foot bones.
Conclusion: Chronic stage CA foot bones presented features of both healing and fragile bone. The compromised bone quality may be due to thin and fragmented trabecular structure and reduced cellularity.
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