Mitochondria, ubiquitous energy-producing organelles in eukaryotic cells, can have their normal functions disrupted by bacterial infections, leading to mitochondrial dysfunction. This dysfunction is closely associated with inflammatory diseases. Periodontitis, a chronic inflammatory disorder of periodontal tissues caused by pathogenic microorganisms, has been increasingly linked to mitochondrial dysfunction in its pathogenesis and progression. Compared to healthy periodontal tissues, inflammatory lesions exhibit more pronounced mitochondrial dysfunction—a pathological process that is strongly correlated with periodontal pathogen infection. Studies reveal that these pathogens disrupt mitochondrial homeostasis in host cells (e.g., gingival epithelial cells and fibroblasts) through multiple mechanisms, including disrupting mitochondrial biogenesis, altering mitochondrial dynamics (promoting excessive fission), inhibiting mitophagy, impairing mitochondrial dysfunction-associated apoptosis, and inducing endogenous oxidative stress, which upregulates pro-inflammatory cytokines. Collectively, these processes drive the establishment and persistence of an inflammatory microenvironment. This review explores how periodontal pathogens affect mitochondrial function and their mechanistic contributions to periodontitis progression, with the goal of providing novel insights for developing mitochondria-targeted therapeutic strategies.

Caries is a chronic infectious disease that occurs in the hard tissues of teeth. The interaction of oral microorganisms, host, food and time leads to the occurrence and progression of caries. Free sugar is an important food factor in the occurrence of dental caries. This paper reviews the research progress on the relationship between free sugar and caries in recent years, providing a reference for further clarifying the mechanism of the occurrence and progression of caries caused by free sugar and exploring the methods of caries prevention. The cariogenic mechanism of free sugar is multifaceted. Free sugar can not only be used by oral microorganisms in dental plaque biofilms to produce acid and synthesize intracellular and extracellular polysaccharides but also cause an imbalance in oral microecology and enhance gene expression related to the cariogenic toxicity of oral microorganisms. Based on the correlation between free sugar and caries, it is important to limit the intake amount and frequency of free sugar to prevent caries. This can be achieved mainly by formulating public health policies for reducing sugar, creating a low-sugar family environment with good eating habits, using sugar substitutes and using fluoride. There are few studies on the relationship between free sugar and oral microecology. More research is needed to better understand the effect of free sugar on oral microecology and its mechanism and to validate the caries-preventing effect of various sugar reduction measures. We believe such studies would open up new avenues for the effective prevention of caries.

Alzheimer’s disease (AD), a common neurodegenerative disease, has been linked to periodontitis, especially Porphyromonas gingivalis (P.gingivalis) infection. This review summarizes the potential mechanisms and pathways through which P.gingivalis and its virulence factors are involved in AD pathogenesis, aiming to provide the scientific basis for the development of novel prevention and treatment strategies for AD. P.gingivalis can promote AD by exacerbating neuroinflammation, facilitating amyloid beta and Tau deposition, and disrupting the blood-brain barrier. Gingipains, secreted by P.gingivalis, serve as core effector molecules by increasing the blood-brain barrier permeability. The association between P.gingivalis and its effectors and AD pathology has been validated by metagenomic analysis and sample detection, indicating that P.gingivalis may be an environmental susceptibility factor or modifiable risk factor for AD. However, the precise mechanisms by which P.gingivalis influences AD, and its interactions with other potential AD-related factors, remain unclear. Moreover, further research needs to be conducted on the therapeutic potential of P.gingvalis intervention in improving AD.

Oral health is an integral component of overall well-being, with the oral cavity serving as a channel for external communication and expression of emotions such as stress and pessimism. Oral diseases can intensify feelings of depression, whereas depression can worsen oral health conditions. As a crucial part of the human microbiome, an imbalance in oral microbiota can release oral pathogenic microbes, which, through pathways including the circulation, nervous, and immune systems, can reach the brain and significantly affect the central nervous system. This can lead to dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, further intensifying the development of depression. Similarly, an imbalance in oral microbiota in individuals with depression can intensify the occurrence of oral diseases. The relationship between depression and oral diseases is not isolated but rather a complex interplay in which they mutually influence and act as causative factors. To elucidate the causal relationship between oral diseases and depression and devise strategies for the prevention and treatment of both conditions, we explore the interaction mechanisms between oral diseases and depression from the perspective of oral microbiota. The occurrence of dental caries, periapical periodontitis, and periodontal diseases is closely associated with the excessive proliferation of specific bacteria in the oral cavity, such as Streptococcus mutans, Porphyromonas gingivalis, and Fusobacterium nucleatum. These bacteria can directly invade the brain through the compromised blood-brain barrier, activating pro-inflammatory cytokines and worsening depressive symptoms. Inflammatory conditions and ulcers in the oral mucosa are caused by various factors, including infection and immune abnormalities. Because of compromised immune function in individuals with depression, these inflammatory responses are often more severe and difficult to control. Malocclusion, trigeminal neuralgia, and temporomandibular joint disorders increase the risk of depression because of psychological stress and changes in the immune system. We also outline the diagnostic and therapeutic considerations for oral diseases in patients with depression, emphasizing the importance of early intervention for disease management. Future research will explore the therapeutic potential of oral microbiota in individuals with depression, with the aim to improve symptoms and treatment outcomes by adjusting oral microbiota, thus providing novel avenues for the prevention and treatment of depression.

Candida albicans is the most abundant fungal species in oral cavity. As a smart opportunistic pathogen, it increases the virulence by switching its forms from yeasts to hyphae and becomes the major pathogenic agent for oral candidiasis. However, the overuse of current clinical antifungals and lack of new types of drugs highlight the challenges in the antifungal treatments because of the drug resistance and side effects. Anti-virulence strategy is proved as a practical way to develop new types of anti-infective drugs. Here, seven artemisinins, including artemisinin, dihydroartemisinin, artemisinic acid, dihydroartemisinic acid, artesunate, artemether and arteether, were employed to target at the hyphal development, the most important virulence factor of C. albicans. Artemisinins failed to affect the growth, but significantly inhibited the hyphal development of C. albicans, including the clinical azole resistant isolates, and reduced their damage to oral epithelial cells, while arteether showed the strongest activities. The transcriptome suggested that arteether could affect the energy metabolism of C. albicans. Seven artemisinins were then proved to significantly inhibit the productions of ATP and cAMP, while reduced the hyphal inhibition on RAS1 overexpression strain indicating that artemisinins regulated the Ras1-cAMP-Efg1 pathway to inhibit the hyphal development. Importantly, arteether significantly inhibited the fungal burden and infections with no systemic toxicity in the murine oropharyngeal candidiasis models in vivo caused by both fluconazole sensitive and resistant strains. Our results for the first time indicated that artemisinins can be potential antifungal compounds against C. albicans infections by targeting at its hyphal development.

Articular cartilage serves as a low-friction, load-bearing tissue without the support with blood vessels, lymphatics and nerves, making its repair a big challenge. Transforming growth factor-beta 3 (TGF-β3), a vital member of the highly conserved TGF-β superfamily, plays a versatile role in cartilage physiology and pathology. TGF-β3 influences the whole life cycle of chondrocytes and mediates a series of cellular responses, including cell survival, proliferation, migration, and differentiation. Since TGF-β3 is involved in maintaining the balance between chondrogenic differentiation and chondrocyte hypertrophy, its regulatory role is especially important to cartilage development. Increased TGF-β3 plays a dual role: in healthy tissues, it can facilitate chondrocyte viability, but in osteoarthritic chondrocytes, it can accelerate the progression of disease. Recently, TGF-β3 has been recognized as a potential therapeutic target for osteoarthritis (OA) owing to its protective effect, which it confers by enhancing the recruitment of autologous mesenchymal stem cells (MSCs) to damaged cartilage. However, the biological mechanism of TGF-β3 action in cartilage development and OA is not well understood. In this review, we systematically summarize recent progress in the research on TGF-β3 in cartilage physiology and pathology, providing up-to-date strategies for cartilage repair and preventive treatment.

Early childhood caries (ECC) is a significant chronic disease of childhood and a rising public health burden worldwide. ECC may cause a higher risk of new caries lesions in both primary and permanent dentition, affecting lifelong oral health. The occurrence of ECC has been closely related to the core microbiome change in the oral cavity, which may be influenced by diet habits, oral health management, fluoride use, and dental manipulations. So, it is essential to improve parental oral health and awareness of health care, to establish a dental home at the early stage of childhood, and make an individualized caries management plan. Dental interventions according to the minimally invasive concept should be carried out to treat dental caries. This expert consensus mainly discusses the etiology of ECC, caries-risk assessment of children, prevention and treatment plan of ECC, aiming to achieve lifelong oral health.

Dental Caries is a kind of chronic oral disease that greatly threaten human being’s health. Though dentists and researchers struggled for decades to combat this oral disease, the incidence and prevalence of dental caries remain quite high. Therefore, improving the disease management is a key issue for the whole population and life cycle management of dental caries. So clinical difficulty assessment system of caries prevention and management is established based on dental caries diagnosis and classification. Dentists should perform oral examination and establish dental records at each visit. When treatment plan is made on the base of caries risk assessment and carious lesion activity, we need to work out patient-centered and personalized treatment planning to regain oral microecological balance, to control caries progression and to restore the structure and function of the carious teeth. And the follow-up visits are made based on personalized caries management. This expert consensus mainly discusses caries risk assessment, caries treatment difficulty assessment and dental caries treatment plan, which are the most important parts of caries management in the whole life cycle.

Oral bacteria directly affect the disease status of dental caries and periodontal diseases. The dynamic oral microbiota cooperates with the host to reflect the information and status of immunity and metabolism through two-way communication along the oral cavity and the systemic organs. The oral cavity is one of the most important interaction windows between the human body and the environment. The microenvironment at different sites in the oral cavity has different microbial compositions and is regulated by complex signaling, hosts, and external environmental factors. These processes may affect or reflect human health because certain health states seem to be related to the composition of oral bacteria, and the destruction of the microbial community is related to systemic diseases. In this review, we discussed emerging and exciting evidence of complex and important connections between the oral microbes and multiple human systemic diseases, and the possible contribution of the oral microorganisms to systemic diseases. This review aims to enhance the interest to oral microbes on the whole human body, and also improve clinician’s understanding of the role of oral microbes in systemic diseases. Microbial research in dentistry potentially enhances our knowledge of the pathogenic mechanisms of oral diseases, and at the same time, continuous advances in this frontier field may lead to a tangible impact on human health.