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Bone involvement in monogenic autoinflammatory syndromes.

Brigitte Bader-Meunier1,2, Erika Van Nieuwenhove3,4,5, Sylvain Breton6

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The spectrum of autoinflammatory diseases (AIDs) linked to childhood bone disease has expanded, now including newly identified conditions and recognizing bone dysplasias as AIDs. This research reviews these diverse bone manifestations and proposes new therapeutic strategies.

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Area of Science:

  • Pediatric Rheumatology
  • Genetics
  • Immunology

Background:

  • Autoinflammatory diseases (AIDs) are a group of genetic disorders characterized by} unregulated inflammation.
  • Childhood bone disease is a known manifestation of several AIDs, historically including genetically complex and monogenic forms.
  • The understanding of AIDs associated with bone disease has evolved significantly.

Purpose of the Study:

  • To provide an overview of the expanding spectrum of genetically defined autoinflammatory diseases associated with bone manifestations in childhood.
  • To discuss the potential classification of certain bone dysplasia syndromes as AIDs.
  • To explore the underlying pathophysiological mechanisms and novel therapeutic strategies for these conditions.

Main Methods:

  • Literature review and synthesis of current research on AIDs and bone disease.
  • Analysis of genetic classifications and clinical presentations of relevant disorders.
  • Discussion of emerging hypotheses on disease mechanisms.

Main Results:

  • The range of monogenic AIDs with bone involvement has broadened, encompassing type I interferonopathies and newly recognized bone dysplasias within established AIDs.
  • A proposal is made to classify specific bone dysplasia syndromes with hyperostosis and systemic inflammation as AIDs.
  • Diverse bone manifestations across genetically defined AIDs have been identified.

Conclusions:

  • The landscape of childhood autoinflammatory diseases with bone manifestations is rapidly expanding.
  • Reclassification of certain bone dysplasias as AIDs may enhance understanding and management.
  • Further research into pathophysiological mechanisms is crucial for developing targeted therapies.