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Thalidomide and neurotrophism.

Judith R Soper1,2, S Fiona Bonar3,4, Dudley J O'Sullivan5

  • 1Diagnostic Radiology, Royal Prince Alfred Hospital, Missenden Rd, Camperdown, Sydney, NSW, Australia. soper@bigpond.net.au.

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|October 21, 2018
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Summary

Thalidomide exposure in utero leads to limb deformities by altering mesenchymal cell proliferation, not by directly damaging bone tissue. This neurotoxic effect disrupts normal skeletal development, causing reductions or excesses in limb structures.

Keywords:
Embryonic sensorineural osteoarthropathyEmbryonic sensory neuropathyNeurotrophismQuantitative neuropathologyThalidomide

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Area of Science:

  • Developmental Biology
  • Teratology
  • Orthopedic Pathology

Background:

  • The thalidomide disaster highlighted severe limb malformations (dysmelia).
  • Previous studies by Henkel and Willert analyzed skeletal deformities in long bones and extremities.
  • This study re-examines Willert's material to understand the mechanism of thalidomide-induced skeletal reduction.

Purpose of the Study:

  • To investigate the underlying cause of skeletal reduction in thalidomide embryopathy.
  • To determine if thalidomide affects bone quality or quantity.
  • To correlate skeletal findings with neurological involvement.

Main Methods:

  • Review of original histological slides and radiographs from 30 children with thalidomide exposure.
  • Analysis of hand and foot radiographs (19 and 4 cases, respectively).
  • Histological examination of musculoskeletal tissues.

Main Results:

  • Verified original findings: radial ray reduction in hands, foot spared until later stages.
  • Hand bone reduction (aplasia/hypoplasia) correlated with C6 sensory nerve involvement.
  • Foot deformities included toe reduction (rare) and hallux polydactyly (L5 sclerotome) associated with absent tibia (L4 sclerotome).
  • Histology showed unremarkable mesenchymal components but abnormal bony architecture, indicating a discordance between microscopic and macroscopic findings.
  • No evidence of necrosis or vascular pathology was observed.

Conclusions:

  • The primary issue in thalidomide embryopathy is an abnormal quantity, not quality, of mesenchyme.
  • Neurotrophic disruption due to sensorineural injury in the embryo alters mesenchymal cell proliferation.
  • Limb malformations result from altered mesenchymal mass, with normal histological differentiation occurring later.
  • The fundamental pathology originates in the nervous system, not the skeleton itself.