Gingival recession (GR) is characterized by exposure of the root surface into oral environment due to apical migration of the marginal gingiva to the cementoenamel junction (CEJ). A high prevalence of GR has been reported in several representative population samples. GR may result in a certain degree of functional and aesthetic alterations if left untreated for long periods. In severe cases, root-dentin hypersensitivity, abrasion, abfraction and root caries may also be involved in GR, which increases the challenge of plaque control. The etiology of GR is multifactorial, including periodontal disease, local anatomical variation, tooth malposition, improper tooth brushing, mechanical trauma and iatrogenic factors, of which periodontal disease is the most common cause. The treatments of GR consist of nonsurgical and surgical therapy, and the latter generally involves mucogingival surgery to restore the aesthetics and function of the local gingival recession. However, over the past 50 years, the periodontal plastic surgical technique has evolved from the traditional free gingival graft method into a more advanced, minimally invasive tunnel technique. For this technique, sulcular incisions instead of vertical relieving incisions are provided through each recession area, and full thickness mucoperiosteal flaps are created and extended beyond the mucogingival junction to facilitate coronal displacement. Each pedicle adjacent to the recession is gently undermined to create a tunnel at recipient site, where either autograft or allograft can be used. A minimally invasive tunnel technique is a better method for root coverage and reduced postoperative patient discomfort. This technique is characterized by both practical and aesthetic features.

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.

Periodontitis and rheumatoid arthritis (RA) are chronic inflammatory diseases that share similar inflammatory mechanisms and characteristics. Programmed cell death (PCD) has recently garnered attention for its crucial role in regulating inflammation and maintaining tissue homeostasis, as well as for its potential to link these two diseases. The various forms of PCD --including apoptosis, pyroptosis, and necroptosis--are closely controlled by signaling pathways such as Toll-like receptor 4 (TLR4)/NF-κB and MAPK. These pathways determine cell fate and influence inflammatory responses, tissue destruction, and repair, and they both play important roles in the pathogenesis of RA and periodontitis. In periodontitis, periodontal pathogens such as Porphyromonas gingivalis (P. gingivalis) and its virulence factors, including lipopolysaccharide (LPS), induce pyroptosis and necroptosis in immune cells such as macrophages via the TLR4/NF-κB pathway, which leads to an excessive release of pro-inflammatory cytokines such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α. Concurrently, these pathogens inhibit the normal apoptotic process of immune cells, such as neutrophils, prolonging their survival, exacerbating immune imbalance, and aggravating periodontal tissue destruction. Similarly, in RA synovial tissue, fibroblast-like synoviocytes (FLS) acquire apoptosis resistance through signaling pathways such as the Bcl-2 family, JAK/STAT, and NF-κB, allowing for the consistent proliferation and secretion of matrix metalloproteinases and pro-inflammatory cytokines. Meanwhile, the continuous activation of pyroptotic pathways in neutrophils and macrophages results in the sustained release of IL-1β, further exacerbating synovial inflammation and bone destruction. Notably, dysregulated PCD fosters inter-organ crosstalk through shared inflammatory mediators and metabolic networks. Damage-associated molecular patterns (DAMPs) and cytokines that originate from periodontal lesions can spread systemically, influencing cell death processes in synovial and immune cells, thereby aggravating joint inflammation and bone erosion. By contrast, systemic inflammation in RA can upregulate osteoclastic activity or interfere with the normal apoptosis of periodontal cells via TNF-α and IL-6, ultimately intensifying periodontal immune imbalance. This review highlights the pivotal bridging role of PCD in the pathogenesis of both periodontitis and RA, providing a reference for therapeutic strategies that target cell death pathways to manage and potentially mitigate these diseases.

Periodontitis is a chronic inflammatory disease of the periodontal supporting tissues caused by plaque microorganisms, whereas inflammatory bowel disease (IBD) is a chronic inflammatory disease characterized by gastrointestinal tract damage. Studies have revealed a close association between periodontitis and IBD, and gut microbiota has been shown to play an important role in the development of IBD. When the gut microbiota is disturbed, it leads to intestinal barrier disruption, triggers immune-inflammatory responses, and influences IBD progression. There are significant differences between the salivary microbiota of periodontitis patients and healthy individuals, and periodontal pathogens can enter the intestinal tract with saliva and participate in the development of IBD by influencing the interactions between gut microbiota composition, immune responses, metabolite production, and intestinal barrier function. Current gut microbiota-targeted intervention strategies, such as fecal microbiota transplantation (FMT) and probiotic supplementation, have shown potential therapeutic value in the treatment of periodontitis. These approaches may exert synergistic effects on both periodontitis and IBD through microbiota modulation. This review summarizes research progress on the relationship between periodontitis and IBD to provide a foundation for the prevention and treatment of these two diseases.

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.

With the increasing demand for beauty, the treatment of gingival recession has become a common request among patients. Clinically, gingival recession is mainly treated by surgery. The common surgical methods include free gingival grafting, pedicled flap technology and double flap technology (subepithelial connective tissue transplantation combined with coronally advanced flaps). If patients with indications are selected, satisfactory surgical results will be obtained. However, there are still some shortcomings in the above mentioned methods, such as the root coverage effect not being satisfactory. In recent years, researchers have put forward some improved schemes to minimize the shortcomings of the above methods to treat different degrees of gingival recession. A gingival unit graft containing gingival papilla and free gingiva can improve the blood supply of the recipient area and improve the effect of root coverage. It can obtain better root coverage for slight retraction, widening of the angular gingiva and deepening of the vestibular sulcus, but there may be issues with inconsistent color and shape of the gingiva after surgery, as well as poor aesthetic effects. Modified coronally advanced flaps, flaps prepared by the technique of half-thickness, full-thickness and half-thickness, and modified coronally advanced envelope flap technology are designed with the most serious retraction teeth as the center in the case of multiple gingival retractions, both of which can improve the effect of root covering. Tunnel technology and modified tunnel technology, without severing the gingival papilla and tunneling the gingival flap to accommodate the graft, can effectively reduce tissue damage and promote wound healing. This paper reviews the literature and summarizes the outcome of the modified surgery techniques in the treatment of gingival recession. These treatment options for gingival recession are proposed with the aim of improving clinical work, and some suggestions for the treatment of gingival recession to achieve a stable root coverage effect are put forward. In the future, the development direction of mucogingival surgery is to reduce trauma and have a stable curative effect.

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.