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.