Understanding cell types and mechanisms of dental growth is essential for reconstruction and engineering of teeth. Therefore, we investigated cellular composition of growing and non-growing mouse and human teeth. As a result, we report an unappreciated cellular complexity of the continuously-growing mouse incisor, which suggests a coherent model of cell dynamics enabling unarrested growth. This model relies on spatially-restricted stem, progenitor and differentiated populations in the epithelial and mesenchymal compartments underlying the coordinated expansion of two major branches of pulpal cells and diverse epithelial subtypes. Further comparisons of human and mouse teeth yield both parallelisms and differences in tissue heterogeneity and highlight the specifics behind growing and non-growing modes. Despite being similar at a coarse level, mouse and human teeth reveal molecular differences and species-specific cell subtypes suggesting possible evolutionary divergence. Overall, here we provide an atlas of human and mouse teeth with a focus on growth and differentiation.

Background: Chronic periodontitis is an inflammatory disease, which is a major cause of tooth loss. The proinflammatory cytokines interleukin‐1 (IL‐1) and interleukin‐6 (IL‐6) are key regulators of the host response to microbial infection and major modulators of extracellular matrix catabolism and bone resorption. The purpose of this study was to investigate the associations of chronic periodontitis with IL‐6 gene polymorphisms (at positions –597 [G/A], –572 [G/C], and –174 [G/C]).Methods: We analyzed allele, genotype, and haplotype distributions of the IL‐6 promoter variants in a case‐control study involving 148 patients with chronic periodontitis and 107 unrelated controls.Results: Our results showed significant differences in the distributions of alleles and genotypes of the IL‐6 (–572 G/C) polymorphism between patients and the control population (X² = 10.393, P = 0.001, P_corr <0.01). The difference was due to the underrepresentation of the –572 G/C heterozygotes in patients (6.1%) compared to controls (19.6%). Although no variant “CC” homozygotes were detected in our cases and controls, heterozygosity protected against chronic periodontitis, representing a 73% reduction of risk (odds ratio [OR] = 0.27, 95% con‐ fidence interval: 0.12‐0.61) compared to wild‐type homozygotes. However, there were no significant differences in genotype or allele frequencies between both groups for IL‐6 –597 G/A and –174 G/C polymorphisms.Conclusion: This study is the first, to our knowledge, suggesting that the –572 G/C polymorphism of the IL‐6 gene may be one of the protective factors associated with lower susceptibility to chronic periodontitis. J Periodontol 2004;75:30‐36.

Recurrent aphthous stomatitis (RAS) is the most common disease of the oral mucosa, and it has been recently associated with bacterial and fungal dysbiosis. To study this link further, we investigated microbial shifts during RAS manifestation at an ulcer site, in its surroundings, and at an unaffected site, compared with healed mucosa in RAS patients and healthy controls. We sampled microbes from five distinct sites in the oral cavity. The one site with the most pronounced differences in microbial alpha and beta diversity between RAS patients and healthy controls was the lower labial mucosa. Detailed analysis of this particular oral site revealed strict association of the genus Selenomonas with healed mucosa of RAS patients, whereas the class Clostridia and genera Lachnoanaerobaculum, Cardiobacterium, Leptotrichia, and Fusobacterium were associated with the presence of an active ulcer. Furthermore, active ulcers were dominated by Malassezia, which were negatively correlated with Streptococcus and Haemophilus and positively correlated with Porphyromonas species. In addition, RAS patients showed increased serum levels of IgG against Mogibacterium timidum compared with healthy controls. Our study demonstrates that the composition of bacteria and fungi colonizing healthy oral mucosa is changed in active RAS ulcers, and that this alteration persists to some extent even after the ulcer is healed.