Tissue structure, and IL-1beta, IL-8, and TNF-alpha secretions after contact by engineered human oral mucosa with dentifrices.

The use of dentifrice is part of an oral prophylaxis that aims at keeping bacteria in check within the dental plaque. When introduced into the oral cavity, dentifrice also comes in close contact with the oral epithelium. Our goal was to evaluate the effects of dentifrices on tissue structure and pro-inflammatory mediator release by epithelial cells. For this purpose, tri-dimensional engineered human oral mucosa (EHOM) was produced using normal human palatal fibroblasts and epithelial cells. EHOMs were either treated with Aquafresh(R) or Crest(R) for 1, 4, 8, and 24 h, or untreated, then used for cell viability assessment and structural analyses. Cultured supernatants were used to evaluate cytokine (interleukin (IL)-1beta, IL-8 and tumor necrosis factor (TNF)-alpha) secretion, and metalloproteinase (MMP)-2 and -9 activities. The present in vitro study using engineered oral mucosa confirms that dentifrices (Aquafresh and Crest) contribute to tissue desquamation. The desquamation was substantial at 24 h of contact but was limited to the upper layers of the treated tissues. Cell death in these tissues was not increased, suggesting that the dentifrice had accelerated desquamation of the layers containing differentiated cells. Measurement of cytokines revealed that dentifrices up-regulated IL-1beta while down-regulating IL-8 and TNF-alpha secretion, thus indicating an impaired cascade of inflammatory responses. These dentifrices may also impair normal repair mechanisms as suggested by an up-regulation of gelatinase activities. In conclusion, this study suggested that, via cytokines, dentifrice contributes to the modulation of the inflammatory (pro-inflammatory/anti-inflammatory responses) process.