The duration of denture use, oral hygiene, smoking and male sex were identified as risk factors for oral mucosal lesions. As it is well known, all the oral mucosal lesions associated with risk factors have an important degree of malignity. Chronic mechanical irritation can be another cause of oral cancer and it is produced by the constant action of a deleterious agent from the oral cavity. Autophagy represents a complex evolutionary conserved catabolic process in which cells self-digest intracellular organelles in order to regulate their normal turnover and remove the damaged ones with compromised function to further maintain homeostasis. Autophagy is modulated by mTOR kinase and indirectly by PI3K/AKT survival pathway. Due to its dual capacity to either induce cell death or promote cell survival, important evidence pointed that autophagy has a two-faced role in response to chemotherapy in cancer. In conclusion, understanding how to overcome cytoprotective autophagy and how to take advantage of autophagic cell death is critical in order to enhance the cancer cells sensitivity to particular therapeutic agents.

In the latter part of the 20th century, remarkable developments in new dental materials and technologies were achieved. However, regarding the impact of dental resin-based materials 3D-printed on cellular responses, there have been a limited number of published studies recently. The biocompatibility of dental restorative materials is a controversial topic, especially when discussing modern manufacturing technologies. Three-dimensional printing generates the release of residual monomers due to incomplete polymerization of materials and involves the use of potentially toxic substances in post-printing processes that cannot be completely eliminated. Considering the issue of biocompatibility, this article aims to establish an overview of this aspect, summarizing the different types of biocompatibility tests performed on materials used in 3D printing in dentistry. In order to create this comprehensive review, articles dealing with the issue of 3D printing in dentistry were analysed by accessing the main specialized search engines using specific keywords. Relevant data referring to types of materials used in 3DP to manufacture various dental devices, polymerization methods, factors affecting monomer release, cytotoxicity of unreacted products or post-curing treatments, and methods for assessing biocompatibility were analysed. Although the introduction of new restorative materials used in dental treatments is subject to national and international regulations and standards, it is necessary to investigate them regarding biocompatibility in order to support or deny the manufacturers’ statements regarding this aspect.

Dental endo-osseous implants have become a widely used treatment for replacing missing teeth. Dental implants are placed into a surgically created osteotomy in alveolar bone, the healing of the soft tissue lesion and the osseointegration of the implant being key elements to long-term success. Autophagy is considered the major intracellular degradation system, playing important roles in various cellular processes involved in dental implant integration. The aim of this review is an exploration of autophagy roles in the main cell types involved in the healing and remodeling of soft tissue lesions and implant osseointegration, post-implant surgery. We have focused on the autophagy pathway in macrophages, endothelial cells; osteoclasts, osteoblasts; fibroblasts, myofibroblasts and keratinocytes. In macrophages, autophagy modulates innate and adaptive immune responses playing a key role in osteo-immunity. Autophagy induction in endothelial cells promotes apoptosis resistance, cell survival, and protection against oxidative stress damage. The autophagic machinery is also involved in transporting stromal vesicles containing mineralization-related factors to the extracellular matrix and regulating osteoblasts’ functions. Alveolar bone remodeling is achieved by immune cells differentiation into osteoclasts; autophagy plays an important and active role in this process. Autophagy downregulation in fibroblasts induces apoptosis, leading to better wound healing by improving excessive deposition of extracellular matrix and inhibiting fibrosis progression. Autophagy seems to be a dual actor on the scene of dental implant surgery, imposing further research in order to completely reveal its positive features which may be essential for clinical efficacy.

Tooth loss replacement using dental implants is becoming more frequent. Traditional dental implant materials such as commercially pure titanium and titanium aluminum vanadium alloys have well-proven mechanical and biological properties. New titanium alloying metals such as niobium provide improved mechanical properties such as lower elastic modulus while displaying comparable or even better biocompatibility. Hydroxyapatite coatings are a well-documented and widely used method for enhancing dental implants’ surface characteristics and properties and could provide a useful tool for further enhancing titanium–niobium implant properties like osteointegration. Among several coating techniques, physical deposition methods and, in particular, vapour deposition ones are the most used due to their advantages compared to wet deposition techniques for hydroxyapatite coating of metallic surfaces like that of dental implants. Considering the scarcity of data concerning the in vivo evaluation of titanium–niobium biocompatibility and osteointegration and the lack of studies investigating coating these new proposed alloys with hydroxyapatite, this review aims to further knowledge on hydroxyapatite-coated titanium niobium alloys.

Oral squamous cell carcinoma (OSCC) remains a major clinical challenge, highlighting the need for novel therapeutic strategies. Natural bioactive compounds such as curcumin (Cu) and cordycepin (Co) have shown anticancer potential; however, their effects on cancer cell morphology and behavior remain incompletely characterized. This study assessed the individual and combined effects of Cu and Co on oral squamous cell carcinoma cells (OECM-1) and normal human gingival epithelial cells (HGEpiC) over 24 and 48 h. Metabolic activity, membrane integrity, oxidative stress, apoptosis, and inflammatory responses were evaluated using MTT, LDH, ROS-H₂O₂, caspase 3/7, and NO assays. Label-free digital holographic microscopy enabled real-time monitoring of morphology, motility, and proliferation. Both compounds induced ROS-mediated cytotoxicity, but responses were notably more pronounced in OECM-1 than in HGEpiC cells. Real-time morphological profiling revealed distinct response patterns: Co primarily exerted cytostatic effects, whereas Cu induced cell shrinkage, impaired motility, and inhibited cell division. The combination treatment (CC) largely reflected Cu-driven morphological and functional changes, with Co coexisting without counteracting Cu’s effects. Taken together, these findings reveal compound-specific mechanisms of action for Cu and Co in OSCC therapy.

The aim of this study was to compare the responses of normal human gingival epithelial cells (HGEpiC) and oral squamous cell carcinoma cells (OECM-1) to apigenin, a natural flavonoid, focusing on redox balance, autophagy, and apoptosis. This study is among the first to directly compare apigenin-induced responses in normal and cancerous oral epithelial cells. Cells were exposed to apigenin for 24 or 48 h, with untreated cells as controls. Mitochondrial activity, ATP, ROS (H₂O₂), and GSH were measured. Proliferation and morphology were monitored using HoloMonitor^® M4. Autophagy was assessed by fluorescent vacuole labeling, and apoptosis-related proteins (p-AKT, p-BCL-2, p-p53, p-JNK, caspase-8/9) by Luminex assay. Late apoptosis was evaluated by caspase-3/7 activity. Apigenin elicited a differential response: in HGEpiC cells, it was non-cytotoxic and increased metabolic activity, induced a moderate ROS increase, and activated autophagy as a pro-survival mechanism; in contrast, OECM-1 cells exhibited a significant reduction in metabolic activity, a marked ATP decrease at 24 h, and a pronounced ROS increase. These alterations were associated with reduced autophagy and decreased p-JNK signaling. These findings indicate that apigenin exerted no harmful effects on HGEpiC cells, while inducing redox imbalance in OECM-1 cells, highlighting a context-dependent cellular response.