Amyloidogenesis in healing wound. Electron microscopic studies of biopsied wounds in macular amyloidosis

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In primary skin amyloidoses, abnormal dermal fibroblasts produce amyloid precursors. This process involves initial proteinaceous substance discharge, followed by amyloid filament formation, suggesting an epidermal influence.

Area of Science:

  • Dermatology
  • Pathology
  • Biochemistry

Background:

  • Amyloidosis is a group of diseases characterized by the deposition of amyloid fibrils in various organs.
  • Primary cutaneous amyloidoses, such as macular and lichenoid amyloidosis, affect the skin.
  • The exact pathogenesis of primary cutaneous amyloidosis remains incompletely understood.

Purpose of the Study:

  • To investigate the sequential process of amyloid formation in primary cutaneous amyloidoses.
  • To identify the cellular origin and precursors of amyloid deposits in skin lesions.
  • To elucidate the relationship between fibroblasts, collagen, and amyloid deposition.

Main Methods:

  • Biopsies of clinically and histologically typical skin lesions of macular and lichenoid amyloidoses were obtained.
  • Rebiopsies were performed at intervals of 2 to 16 weeks to track amyloid development.
  • Electron microscopy was utilized to examine the ultrastructural changes during amyloidogenesis.

Main Results:

  • Initially, fibroblasts discharged a proteinaceous substance containing fine filaments, originating from the rough endoplasmic reticulum.
  • Typical amyloid filaments emerged within and around this substance, with collagen fibrils admixed in some areas.
  • Amorphous amyloid substance was observed adjacent to basal laminae, and no plasma cells were found in amyloid foci. Amyloid was absent in nonepithelialized wounds.

Conclusions:

  • Abnormal dermal fibroblasts are implicated in producing amyloid precursors in primary cutaneous amyloidoses.
  • The epidermis may influence the process of amyloid precursor production by fibroblasts.
  • The findings suggest a fibroblast-driven mechanism for amyloid deposition in the skin, potentially modulated by epidermal factors.

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