Abstract

For some anophthalmic patients, the contracted socket is a severe problem that precludes the wearing of a prosthesis. A normal and cosmetically acceptable appearance is dependent on the ability of a socket to retain a prosthesis. The disfigurement and distress caused by the contracted socket and its inability to accommodate a prosthesis may have a profound detrimental effect on the patient's career, self-esteem, and psychosocial interactions. The tissue dynamics at work in the anophthalmic socket and in the contracting socket are not yet understood. There are many unanswered questions regarding the histology and anatomy of the normal, as well as the contracting, socket. The tissue responsible for clinical contraction has not been identified. This thesis, using the cynomolgus monkey socket as an experimental model, investigated healing in both the normal and contracting socket. Qualitative observations of the anatomy and histology of eight sockets were made. Two of the sockets were treated with Croton oil to induce contractions. Biopsy specimens from two human sockets, one contracted and the other merely volume deficient, were also examined. Histopathology of the normal and contracting sockets were compared. Myosin subfragment 1 staining of actin for electron microscopy and immunoperoxidase staining of actin for light microscopy were performed on selected specimens. The myofibroblast, probably a modified fibroblast, is known to be present in the early stages of open wound healing and in contracting scar tissue elsewhere in the body. The myofibroblast has been incriminated as an agent generating contractile force. Under the conditions of this experiment, cells with the characteristics of myofibroblasts were identified by both immunoperoxidase staining and electron microscopy. They were found in healing noncontracting and contracting sockets. Cytoplasmic actin was also distinguished in arterioles, venules, capillaries, myoepithelial cells, smooth muscle, and skeletal muscle.

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