The surface ultrastructure of normal and metaplastic cervical epithelia and of carcinoma in situ.

CIS of the human cervix uteri is widely accepted as a preinvasive lesion that often progresses to invasive squamous carcinoma. Similarly, CIS is believed to arise by progression from cervical dysplasia, the earliest detectable neoplastic change in cervical epithelium (16). However, there is disagree ment as to how often there is progression from dysplasia to CIS and from CIS to invasive carcinoma, and as to how often lesions remain static or perhaps even regress (6, 14, 15). In addition to occasional neoplastic change, cervical columnar epithelium may undergo physiological transformation to squamous epithelium by a process of metaplasia. This process may occur at any time, but it is most common during puberty and during the 2nd and 3rd trimesters of the 1st pregnancy (4). Neoplastic changes most frequently occur at the squamocolumnar junction or within the colposcopie transformation zone (that part of the cervix which has undergone metaplasia), and Coppleson and Reid (4) have suggested that epithelium that is undergoing metaplasia may be more susceptible to carcinogenic agents than mature columnar or squamous epithelia. The fine structure of normal metaplastic and dysplastic epithelia and of CIS and invasive carcinoma of the cervix has been studied extensively (9, 18). Increasing degrees of abnormality were noted in nuclear size and shape, chromatin distribution, number and arrangement of cytoplasmic organelles, and surface membrane features, during the change from normal to grossly neoplastic tissue. In particular, decreased numbers of desmosomes, tight junctions, and tonofilaments and increased numbers of microvilli were seen in more abnormal cells.