The aims of this investigation were to determine whether stabilization of maximum voluntary bite force (MVBF) occurs between 15 and 18 years of age in subjects with a normal occlusion, and to assess the influence of gender, body mass index (BMI), morphological occlusion, and jaw function measured by the number of occlusal contacts, overjet, overbite, maximal mouth opening, mandibular deflection during opening, sagittal slide between the retruded contact position and the intercuspal position, and number of dental restorations. The sample comprised 60 Caucasian subjects aged 15 (15 males and 15 females) and 18 (14 males and 16 females) years with a neutral occlusion, balanced facial profile, and absence of a previous orthodontic history. Bite force measurements were undertaken using a portable occlusal force gauge on both the left and the right sides of the jaw in the first molar region during maximal clenching. Two independent samples t-tests and multiple regression were used for statistical analysis. MVBFs were age and gender related (P < 0.05). Males showed a significant increase in bite force between 15 and 18 years of age (P = 0.002), but gender differences were significant only in the 18-year-olds (P = 0.003). In subjects with a neutral occlusion, MVBF could best be predicted using multiple regression from age and gender. The regression model accounted for 31.3 per cent of the variance in MVBF (P = 0.031), with gender contributing 17.9 per cent and age 7.9 per cent. Morphological occlusion, jaw function, and BMI explained the remaining 5.5 per cent of variance. While controlling for all other parameters, the independent contribution of gender to the prediction of MVBF was 16.2 per cent, age 6 per cent, number of occlusal contacts 3.2 per cent, and BMI 1.3 per cent.

The molecule NAD+ is a coenzyme for enzymes catalyzing cellular redox reactions in several metabolic pathways, encompassing glycolysis, TCA cycle, and oxidative phosphorylation, and is a substrate for NAD+-dependent enzymes. In addition to a hydride and electron transfer in redox reactions, NAD+ is a substrate for sirtuins and poly(adenosine diphosphate–ribose) polymerases and even moderate decreases in its cellular concentrations modify signaling of NAD+-consuming enzymes. Age-related reduction in cellular NAD+ concentrations results in metabolic and aging-associated disorders, while the consequences of increased NAD+ production or decreased degradation seem beneficial. This article reviews the NAD+ molecule in the development of aging and the prevention of chronic age-related diseases and discusses the strategies of NAD+ modulation for healthy aging and longevity.