Purpose: To highlight the histopathological characteristics of the skin in congenital clubfoot and correlate the clinical findings in clubfoot with the changes in the dermal layers. Materials and methods: One hundred skin specimens, from 77 infants (6 to 12 months), were studied between 2004 and 2008. Using the Pirani scoring system, the clinical severity was recorded. The mobility of the skin and the correctability of the medial ray were assessed clinically. A skin specimen (1cm x 1mm) was taken from the medial side of the foot at surgery following failed plaster treatment. The layers were studied under light microscopy. The thickness of the dermis and the histopathological features of clubfoot skin were compared with 10 normal skin specimens. Results: The dermis of clubfoot skin showed significant fibrosis with thick bundles of collagen fibres (P = .001) on Haematoxylin and Eosin staining (H&E). The dermal thickness ranged between 1.0mm and 5.2mm in clubfoot skin, compared with controls (0.64-1.28mm). Fibrosis extended into the subcutis in a septolobular fashion in 95% of the cases. Significant atrophy of eccrine glands was seen in 98% (P = .001). Hair follicles were absent in 78%. The elastic fibres of clubfoot skin, stained with Elastic van Gieson staining (EVG), showed hypertrophy in varying degrees in all skin specimens. They were fragmented, with loss of their parallel arrangement. There was no significant inflammatory reaction in the dermis. The Pirani score was significantly increased (mean 7.8). Discussion: Fibrosis and thickening of the dermis were the most significant histopathological features of the clubfoot skin. The elastic fibres were also abnormal. There was atrophy of the skin appendages due to the fibrosis. There was a strong correlation between the Pirani score and the severity of the deformity(P 0.016). The cases with poor outcome had a higher score than those with a satisfactory outcome.Lack of a significant inflammatory reaction suggests that neither the serial manipulations of the foot, nor the repeated plaster cast changes, were responsible for the dermal fibrosis, which is probably present from birth and contributes to the deformity. / Thesis (Ph.D.)-University of KwaZulu-Natal, Durban, 2012.