Effects of low intensity laser irradiation phototherapy on dental pulp constructs

AIM: To investigate low intensity laser irradiation phototherapy(LILIP) on the proliferation, mineralization and degradation of dental pulp constructs.METHODS: Stem cells from human exfoliated deciduous teeth(SHED) were grown to confluence and seeded on collagen scaffolds to create dental pulp constructs. LILIP was delivered to the dental pulp constructs using an 830 nm GaA IAs laser at an output power of 20 m W. The LILIP energy density was 0.4, 0.8, 1.2, and 2.4 J/cm2. After 8 d, the cell proliferation and degradation within the dental pulp constructs were measured using histologic criteria. After 28 d, the effect of LILIP on SHED mineralization was assessed by von Kossa staining.RESULTS: SHED proliferation within the dental pulp constructs varied after exposure to the 0.4, 0.8, 1.2,and 2.4 J/cm2 LILIP energy densities(P < 0.05). The maximum proliferation of SHED in nutrient deficient media was 218% after exposure to a 1.2 J/cm2 LILIP energy density. SHED grown in nutrient deficient media after exposure to a 0.4, 0.8, and 1.2 J/cm2 LILIP energy density, proliferated by 167-218% compared to the untreated(non-LILIP) control group(P < 0.05).SHED exposed to a 0.4, 0.8, and 1.2 J/cm2 LILIP energy density, and grown in optimal nutritional conditions and proliferated by 147%-164% compared to the untreated(non-LILIP) control group(P < 0.05). The exposure of SHED to the highest LILIP energy density(2.4 J/cm2) caused a reduction of the cell proliferation of up to 73% of the untreated(non-LILIP) control(P < 0.05). The amount of mineral produced by SHED increased over time up to 28 d(P < 0.05). The 0.8 and 1.2J/cm2 LILIP energy densities were the most effective at stimulating the increased the mineralization of the SHED from 150%-700% compared to untreated(nonLILIP) control over 28 d(P < 0.05). The degradation of dental pulp constructs was affected by LILIP(P <0.05). The dental pulp constructs grown in optimal nutritional conditions exposed to a 0.8 J/cm2 or 1.2 J/cm2 LILIP energy density had 13% to 16% more degradation than the untreated(non-LILIP) control groups(P < 0.05). The other LILIP energy densities caused a 1%degradation of dental pulp constructs in optimal nutritional conditions(P > 0.05).CONCLUSION: LILIP can enhance or reduce SHED proliferation, degradation and mineralization within dental pulp constructs. LILIP could promote the healing and regeneration of dental tissues.

Oral frailty and neurodegeneration in Alzheimer’s disease

Frailty is a critical intermediate status of the aging process with a multidimensional and multisystem nature and at higher risk for adverse health-related outcomes,including falls,disability,hospitalizations,institutionalization,mortality,dementia,and Alzheimer’s disease.Among different frailty phenotypes,oral frailty has been recently suggested as a novel construct defined as a decrease in oral function with a coexisting decline in cognitive and physical functions.We briefly reviewed existing evidence on operational definitions of oral frailty,assessment and screening tools,and possible relationships among oral frailty,oral microbiota,and Alzheimer’s disease neurodegeneration.Several underlying mechanism may explain the oral health-frailty links including undernutrition,sarcopenia linked to both poor nutrition and frailty,psychosocial factors,and the chronic inflammation typical of oral disease.Oral microbiota may influence Alzheimer’s disease risk through circulatory or neural access to the brain and the interplay with periodontal disease,often causing tooth loss also linked to an increased Alzheimer’s disease risk.On this bases,COR388,a bacterial protease inhibitor targeting Porphyromonas gingivalis implicated in periodontal disease,is now being tested in a double-blind,placebocontrolled Phase II/III study in mild-to-moderate Alzheimer’s disease.Therefore,oral status may be an important contributor to general health,including Alzheimer’s disease and latelife cognitive disorders,suggesting the central role of preventive strategies targeting the novel oral frailty phenotype and including maintenance and improvement of oral function and nutritional status to reduce the burden of both oral dysfunction and frailty.