Squamous cell carcinoma of the vulva accounts for about 4% of all gynecological malignancies. Clinically, it is a very important disease because of its marked detrimental effect on quality of life. Two major forms of vulvar squamous cell carcinoma are recognized: a more common, HPV-related malignancy occurring mostly among younger women and a less common, idiopathic malignancy occurring in elderly women. Historically, it has been well recognized that the latter, non-HPV related, idiopathic form of squamous cell carcinoma arises either de novo or in association with certain other vulvar precursor lesions. The precise identification of these associated lesions and the determination of the frequency with which malignancy arises in them, has been hampered by problems of terminology. Originally, the white color that was often present suggested that the process was analogous oral leukoplakia. All of these lesions, then, were believed to be premalignant and, as such, they required early and extensive surgical removal. This erroneous belief began to change some 40 years ago when it became apparent that only a small percentage of these lesions progressed to malignancy. At that point, the more neutral, identifying term "dystrophy" was introduced and it was recommended that these lesions be followed by sequential biopsy rather than by total excision. Now, due to better clinical and histological expertise, we can reliably identify these precursor lesions as the specific diseases, lichen sclerosus or lichen planus. The term "dystrophy" can be discontinued as inaccurate and superfluous. Recent studies suggest that the risk of squamous cell carcinoma developing in lichen sclerosus or lichen planus is less than 4%. This risk may be decreased even further when patients are treated with appropriate medical therapy. The multi-step process by which malignancy arises in lichen sclerosus and lichen planus appears to involve both DNA damage, occurring as a result of chronic inflammation, and squamous cell proliferation that is driven by retarded, or even failed, attempts at epithelial wound repair. Somewhat similar epithelial thickening also develops as a result of chronic rubbing and scratching (such as occurs in lichen simplex chronicus) but this type of epithelial cell proliferation is rarely, if ever, associated with the development of squamous cell carcinoma.
Premalignant aspect of the vulvar nonneoplastic epithelial disorders (formerly the vulvar dystrophies)
MICHELETTI, Leonardo;
2005-01-01
Abstract
Squamous cell carcinoma of the vulva accounts for about 4% of all gynecological malignancies. Clinically, it is a very important disease because of its marked detrimental effect on quality of life. Two major forms of vulvar squamous cell carcinoma are recognized: a more common, HPV-related malignancy occurring mostly among younger women and a less common, idiopathic malignancy occurring in elderly women. Historically, it has been well recognized that the latter, non-HPV related, idiopathic form of squamous cell carcinoma arises either de novo or in association with certain other vulvar precursor lesions. The precise identification of these associated lesions and the determination of the frequency with which malignancy arises in them, has been hampered by problems of terminology. Originally, the white color that was often present suggested that the process was analogous oral leukoplakia. All of these lesions, then, were believed to be premalignant and, as such, they required early and extensive surgical removal. This erroneous belief began to change some 40 years ago when it became apparent that only a small percentage of these lesions progressed to malignancy. At that point, the more neutral, identifying term "dystrophy" was introduced and it was recommended that these lesions be followed by sequential biopsy rather than by total excision. Now, due to better clinical and histological expertise, we can reliably identify these precursor lesions as the specific diseases, lichen sclerosus or lichen planus. The term "dystrophy" can be discontinued as inaccurate and superfluous. Recent studies suggest that the risk of squamous cell carcinoma developing in lichen sclerosus or lichen planus is less than 4%. This risk may be decreased even further when patients are treated with appropriate medical therapy. The multi-step process by which malignancy arises in lichen sclerosus and lichen planus appears to involve both DNA damage, occurring as a result of chronic inflammation, and squamous cell proliferation that is driven by retarded, or even failed, attempts at epithelial wound repair. Somewhat similar epithelial thickening also develops as a result of chronic rubbing and scratching (such as occurs in lichen simplex chronicus) but this type of epithelial cell proliferation is rarely, if ever, associated with the development of squamous cell carcinoma.
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