Aetiology

The aetiology of camptodactyly is an imbalance on the forces acting upon the proximal interphalangeal joint. There may be either an increase in flexion forces or a decrease in extension forces. Almost every structure around the proximal interphalangeal joint has been implicated in the pathology of camptodactyly:

• skin deficiency
• scarring within the dermis or subcutaneous tissues
• retinacular system imbalance of the transverse or retinacular ligaments
• joint changes eg:
  • contracture of the collateral ligaments
  • contracture of the volar plate
  • atypical shape of the head of the proximal phalanx or base of middle phalanx
• intrinsic muscle abnormality eg:
  • aberrant interossei
  • abnormal lumbrical:
    • relatively common cause
    • leads to an intrinsic-minus deformity with secondary flexion at PIPJ
    • pathologies include:
      • absent lumbrical
      • abnormal origin from:
        • ring finger flexor tendon
        • transverse carpal ligament
      • abnormal insertion into:
        • metacarpophalangeal joint capsule
        • flexor digitorum superficialis tendon
        • ring finger extensor apparatus
• extrinsic flexor muscle abnormality:
  • relatively common
  • flexor digitorum superficialis
    • abnormal origin eg little finger tendon from:
      • belly of ring finger FDS
      • transverse carpal ligament
      • palmar fascia
    • contracted
    • hypoplastic
    • absent
• extrinsic extensors anomalous

A deformity that is initially passively correctable i.e. flexible or reducible, can develop into a fixed or irreducible contracture with time. This is attributable to the PIPJ contracture inducing change in surrounding structures eg skin tightening volarly, fascial bands longitudinally and abnormal PIPJ remodelling.

Reference

1. Kloc J et al. Camptodactyly: From Embryological Basis to Surgical Treatment. Medicina 2023, 59(5), 966