Management of peripheral giant cell granuloma around complete-arch fixed implant-supported prosthesis: A case series.

Abnormal peri-implant tissue response in the form of benign reactive lesions, such as peripheral giant cell granuloma and pyogenic granuloma, is a less frequent biologic complication associated with dental implant therapy. However, these lesions can cause gingival pain, swelling, and discomfort, as well as peri-implant bone loss and possible implant failure. Few reports in the dental literature have described these lesions around complete-arch fixed implant-supported prostheses.

Black and Brown Oro-facial Mucocutaneous Neoplasms.

Black and brown-colored mucocutaneous lesions present a differential diagnostic challenge, with malignant melanoma being the primary clinical concern. The vast majority of pigmented lesions in the head and neck region are the result of benign, reactive factors such as post-inflammatory melanosis. However, it is not uncommon to discover a range of muco-cutaneous black and brown neoplasms in the oro-facial area.

RSK activation of translation factor eIF4B drives abnormal increases of laminin γ2 and MYC protein during neoplastic progression to squamous cell carcinoma.

Overexpression of the basement membrane protein Laminin γ2 (Lamγ2) is a feature of many epidermal and oral dysplasias and all invasive squamous cell carcinomas (SCCs). This abnormality has potential value as an immunohistochemical biomarker of premalignancy but its mechanism has remained unknown. We recently reported that Lamγ2 overexpression in culture is the result of deregulated translation controls and depends on the MAPK-RSK signaling cascade.

MAPK/ERK-dependent translation factor hyperactivation and dysregulated laminin γ2 expression in oral dysplasia and squamous cell carcinoma.

Lesions displaying a variety of dysplastic changes precede invasive oral and epidermal squamous cell carcinoma (SCC); however, there are no histopathological criteria for either confirming or staging premalignancy. SCCs and dysplasias frequently contain cells that abnormally express the γ2 subunit of laminin-332. We developed cell culture models to investigate γ2 dysregulation.

Contemporary concepts in the diagnosis of oral cancer and precancer.

This article addresses several issues in the approach to diagnosis of oral cancer. The term oral cancer is clarified. Key aspects of the biologic basis of development of oral cancer and the known risk factors associated with the disease are summarized.

Benign alveolar ridge keratosis (oral lichen simplex chronicus): A distinct clinicopathologic entity.

Benign alveolar ridge keratosis is a common benign white papule or plaque that occurs on the keratinized gingiva of the maxillary or mandibular alveolar ridge that is probably traumatic/frictional in origin, with characteristic histologic features, similar to those of lichen simplex chronicus of the skin. This is a retrospective study of 108 consecutive specimens displaying characteristic histopathologic features of benign alveolar ridge keratosis accessioned during a 36-month period. There was a male:female ratio of 3.

A keratinocyte hypermotility/growth-arrest response involving laminin 5 and p16INK4A activated in wound healing and senescence.

Keratinocytes become migratory to heal wounds, during early neoplastic invasion, and when undergoing telomere-unrelated senescence in culture. All three settings are associated with expression of the cell cycle inhibitor p16INK4A (p16) and of the basement membrane protein laminin 5 (LN5). We have investigated cause-and-effect relationships among laminin 5, p16, hypermotility, and growth arrest.

Co-expression of p16INK4A and laminin 5 by keratinocytes: a wound-healing response coupling hypermotility with growth arrest that goes awry during epithelial neoplastic progression.

The replicative lifespan of human keratinocytes in culture is restricted by a telomere-unrelated induction of p16INK4A (p16) and p14ARF. We have found that, in vivo, p16 is expressed by epidermal and oral keratinocytes at the migrating fronts of healing wounds and at the stromal interface of severely dysplastic and early invasive lesions and that such cells also invariably display increased expression of Laminin 5 (Lam5). In culture, p16 and Lam5 are coexpressed in keratinocytes at senescence, at the edges of wounds made in confluent cultures, and when cells are plated on dishes coated with the gamma2 precursor form of Lam5 (Lam5gamma2pre).

Co-expression of p16(INK4A) and laminin 5 gamma2 by microinvasive and superficial squamous cell carcinomas in vivo and by migrating wound and senescent keratinocytes in culture.

The high frequency of mutation, deletion, and promoter silencing of the gene encoding p16(INK4A) (p16) in premalignant dysplasias and squamous cell carcinomas (SCC) of epidermis and oral epithelium classifies p16 as a tumor suppressor. However, the point during neoplastic progression at which this protein is expressed and presumably impedes formation of an SCC is unknown. Induction of p16 has been found to be responsible for the senescence arrest of normal human keratinocytes in culture, suggesting the possibility that excessive or spatially abnormal cell growth in vivo triggers p16 expression.