aetiology
Last reviewed 01/2018
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
- abnormal origin eg little finger tendon from:
- 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.