Richart’s concept [1] of a step-by-step carcinogenesis from CIN1 to CIN2 to CIN3 belongs to an era in which HPV (Human Papilloma Virus) had not yet been correlated to cervical cancer and there was a static conception of preneoplastic cervical lesions (CIN) that inevitably had to progress to carcinoma. Today we know the oncogenic activity of papillomavirus [2, 3] and it is known that HPV-induced carcinogenesis is a rather slow process, characterized by a first phase of persistent HPV infection, followed by viral DNA integration and transformation of the squamous cells into CIN; the transformation of CIN3 into invasive cancer.
It is true that it is a process that takes many years, but it is also true that the process is reversible at any pre-invasive stage. The study by Oster [4] highlights the concept of CIN regression; CIN lesions are dynamic in the sense that all CINs can regress. In the literature about 60% of grade 1 cervical intraepithelial neoplasms (CIN1) regress, 30% persist, 10% progress to CIN3 and 1% progress to invasive cancer [5].
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Therefore the concept of a preneoplastic lesion becomes dynamic and related to papillomavirus, thus in March 2012 the LAST Project (Anogenital Squamous Terminology) [6], consisting of members of the college of American pathologists and the American society of colposcopy, advised the use, for the related HPV pathology of the cervix, of the term SIL (Squamous Intraepithelial Lesion) instead of CIN, already used for cytology in the Bethesda System. It calls for abandoning of the three-level classification of CIN (CIN1, CIN2, CIN3) and opens up to a two-level terminology, which better reflects the biology of viral infection, LSILCIN1, and HPV viral infection, to be used at follow-ups and HSILCIN3, the true preneoplastic lesion, worthy of excisional treatment.
In the CIN classification there is also the difficulty in the interpretation of the various histological pictures, in fact, while pathologists agree when there are findings of carcinoma and it is easy to diagnose the histological CIN3, the CIN2 category continues to be an equivocal diagnosis, because it is not easily reproducible. Since the diagnosis of CIN2 cannot be reliably differentiated only by histopathological criteria, it is recommended to test for the immunohistochemical p16 protein (IHC). Negative CIN2 p16 is considered a viral lesion (CIN1), thus it undergoes follow-up, CIN2 p16 positive is considered a preneoplastic lesion (CIN3) and is treated with excision.
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There is evidence that CIN2 has a regression rate of about 60% [7], especially in the category of young women (< 25 years old) [8, 9].
Current knowledge on CIN2 regression rates in women over the age of 25 is scarce [10].
The aim of this study was to evaluate the regression rate of CIN2 p16 positive lesions in women over 25 years of age and identify possible predictors of regression.
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