The most common periodontal biotype in the Chinese population is thin, which obviously limits orthodontic tooth movement. Periodontally accelerated osteogenic orthodontics (PAOO) can not only accelerate tooth movement through corticotomy but also expand the range of orthodontic tooth movement by alveolar bone augmentation, which could reduce the periodontal complications of orthodontic therapy. The development of PAOO has gone through a long and tortuous historical process over more than 100 years: from osteotomy based on "bony block movement" at the beginning to cortical osteotomy based on "the regional acceleratory phenomenon" and then to PAOO based on "bone tissue engineering". Throughout its development history, the understanding of the biological basis determines the development of the clinical technology. Therefore, PAOO should be based on basic research. Both the present clinical practice and future surgical improvements should be based on the fundamentals of bone repair and regeneration. According to the current evidence, it is suggested that piezocision and laser-assisted flapless corticotomy should be chosen only for simple cortical osteotomy, and surgical navigation technology or 3D-printed surgical guides are recommended. When a large amount of bone augmentation is needed, PAOO with an intact flap is still the first choice. A stable and infection-free healing environment is the key to wound healing; therefore, in addition to infection control, the surgical area should also be protected from external forces. At present, there are few high-quality clinical studies on PAOO. Multicenter, large-sample, randomized controlled clinical trials are needed to evaluate the clinical efficacy of different PAOO techniques in the future. The present article introduces the development history, fundamentals and operation precautions of PAOO, and a new perspective is also proposed, which may provide a reference for clinical practice.

Periodontal disease is highly prevalent, exerting detrimental effects on oral health and posing serious threats to systemic health. Over the past three decades, research exploring the impact of periodontal disease on systemic diseases has rapidly advanced. Nevertheless, numerous challenges and unanswered questions remain, necessitating further investigation. Therefore, this article first elucidates the association between periodontal disease and systemic diseas-es. Then, the key evidence supporting their relationship is graded according to the Oxford Centre for Evidence-Based Medicine levels of evidence criteria. Specifically, periodontal disease emerges as an independent risk factor for diabetes mellitus (level A evidence) and cardiovascular diseases (level B evidence). As such, it represents a potential risk factor for rheumatoid arthritis (level B evidence), chronic obstructive pulmonary disease (level B evidence), and inflammatory bowel disease (level B evidence). Furthermore, periodontal disease is closely linked to adverse pregnancy outcomes. Second, this article delineates the plausible mechanisms through which periodontal disease influences systemic diseases, explicitly showing that the foundational elements underlying their connection are bacteria and inflammation. The circulation pathway and saliva pathway specifically mediate this connection. Finally, in light of the current ambiguities surrounding the relationships between periodontal disease and certain systemic diseases, as well as the insufficient depth of mechanism research, this article outlines several considerations for future clinical research and animal experiment designs. Implementing large-sample, multi-center, high-quality clinical studies, utilizing multi-omics analyses for more indepth exploration of mechanisms, and actively promoting clinical translational research are recommended. This article aims to advance the field of periodontal medicine, while simultaneously offering evidence-based insights to inform the implementation of public health policies.

The aim of this study was to identify whether periodontitis induces gut microbiota dysbiosis via invasion by salivary microbes. First, faecal and salivary samples were collected from periodontally healthy participants (PH group, n = 16) and patients with severe periodontitis (SP group, n = 21) and analysed by 16S ribosomal RNA sequencing. Significant differences were observed in both the faecal and salivary microbiota between the PH and SP groups. Notably, more saliva-sourced microbes were observed in the faecal samples of the SP group. Then, the remaining salivary microbes were transplanted into C57BL6/J mice (the C-PH group and the C-SP group), and it was found that the composition of the gut microbiota of the C-SP group was significantly different from that of the C-PH group, with Porphyromonadaceae and Fusobacterium being significantly enriched in the C-SP group. In the colon, the C-SP group showed significantly reduced crypt depth and zonula occludens-1 expression. The mRNA expression levels of pro-inflammatory cytokines, chemokines and tight junction proteins were significantly higher in the C-SP group. To further investigate whether salivary bacteria could persist in the intestine, the salivary microbiota was stained with carboxyfluorescein diacetate succinimidyl ester and transplanted into mice. We found that salivary microbes from both the PH group and the SP group could persist in the gut for at least 24 h. Thus, our data demonstrate that periodontitis may induce gut microbiota dysbiosis through the influx of salivary microbes.