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[Relapsing polychondritis and cartilage].

A Janin¹, J C Piette, P Courtin

¹Laboratoire d'Anatomie Pathologique C, Hôpital Calmette, Lille.

Revue Du Rhumatisme Et Des Maladies Osteo-Articulaires

|April 1, 1991

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Atrophic polychondritis (APC) involves damage to elastic cartilage, affecting ears, nose, eyes, and airways. Recent findings highlight significant vascular lesions and suggest a link between enzyme abnormalities and autoimmune responses.

Area of Science:

Rheumatology
Pathology
Immunology

Context:

Atrophic polychondritis (APC) is characterized by damage to elastic cartilage components.
Established clinical criteria focus on auricular, nasal, ocular, and tracheobronchial involvement.
Emerging evidence reveals frequent and severe vascular lesions, both aortic and peripheral.

Purpose:

To review the pathological mechanisms underlying atrophic polychondritis.
To integrate clinical and pathological findings regarding APC.
To explore the interplay of enzyme abnormalities and autoimmune processes in elastic cartilage destruction.

Summary:

Atrophic polychondritis (APC) involves lesions affecting elastic cartilage, with clinical manifestations including auricular, nasal, ocular, and tracheobronchial involvement.

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Pathological reviews underscore the significance of vascular lesions, encompassing both aortic and peripheral sites.

The pathogenesis likely involves multiple mechanisms, including direct enzyme abnormalities of glycosaminoglycans and elastic tissue, potentially linked to an autoimmune process involving type II anticollagen antibodies.

Impact:

Highlights the underappreciated role of vascular lesions in atrophic polychondritis.
Suggests a multifactorial etiology for elastic cartilage destruction in APC.
Provides a basis for further research into the autoimmune and enzymatic pathways involved in APC pathogenesis.