Amorphous Calcium Phosphate (ACP) is an essential mineral phase formed in mineralized tissues and the first commercial product as artificial hydroxyapatite. ACP is unique among all forms of calcium phosphates in that it lacks long-range, periodic atomic scale order of crystalline calcium phosphates. The X-ray diffraction pattern is broad and diffuse with a maximum at 25 degree 2 theta, and no other different features compared with well-crystallized hydroxyapatite. Under electron microscopy, its morphological form is shown as small spheroidal particles in the scale of tenths nanometer. In aqueous media, ACP is easily transformed into crystalline phases such as octacalcium phosphate and apatite due to the growing of microcrystalline. It has been demonstrated that ACP has better osteoconductivity and biodegradability than tricalcium phosphate and hydroxyapatite in vivo. Moreover, it can increase alkaline phosphatase activities of mesoblasts, enhance cell proliferation and promote cell adhesion. The unique role of ACP during the formation of mineralized tissues makes it a promising candidate material for tissue repair and regeneration. ACP may also be a potential remineralizing agent in dental applications. Recently developed ACP-filled bioactive composites are believed to be effective anti-demineralizing/remineralizing agents for the preservation and repair of tooth structures. This review provides an overview of the development, structure, chemical composition, morphological characterization, phase transformation and biomedical application of ACP in dentistry.

The most potent virulence factors of the periodontal pathogen Porphyromonas gingivalis are gingipains, three cysteine proteases (RgpA, RgpB, and Kgp) that bind and cleave a wide range of host proteins. Considerable proof indicates that RgpA contributes to the entire virulence of the organism and increases the risk of periodontal disease by disrupting the host immune defense and destroying the host tissue. However, the functional significance of this proteinase is incompletely understood. It is important to analyze the effect of arginine-specific gingipain A gene (rgpA) on selected virulence and physiological properties of P. gingivalis. Electroporation and homologous recombination were used to construct an rgpA mutant of P. gingivalis ATCC33277. The mutant was verified by polymerase chain reaction and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Cell structures of the mutant were examined by transmission electron microscopy and homotypic biofilm formation was examined by confocal laser scanning microscopy. Gene analysis revealed that the rgpA gene was deleted and replaced by a drug resistance gene marker. The defect of the gene resulted in a complete loss of RgpA proteinase, a reduction of out membrane vesicles and hemagglutination, and an increase in homotypic biofilm formation. Our data indicate that an rgpA gene deficient strain of P. gingivalis is successfully isolated. RgpA may have a variety of physiological and pathological roles in P. gingivalis.

Periodontitis is a hypoxic infectious disease. When periodontal tissues are affected by disease and the microenvironment becomes inflamed, the release of local inflammatory factors and increased tissue metabolism lead to an imbalance between oxygen supply and demand. This inflammatory environment disrupts blood microcirculation, causing the local periodontal tissue to enter a relatively ischemic and hypoxic state. Deep periodontal pockets and periodontal pathogenic bacteria further reduce the oxygen tension in periodontal tissues, exacerbating the progression of periodontitis. Current treatment strategies for improving the inflammatory microenvironment include mechanical therapy and systemic or localized antibiotic administration. However, these existing methods fail to effectively restore the microbiota balance, ensure sustained drug release, or maintain drug presence at the lesion site. Hydrogels, due to their low cytotoxicity, excellent water retention properties, and ability to control drug release, serve as an effective drug delivery pathway that supplies oxygen to inflammatory sites. This article reviews the mechanisms and recent advancements in using hydrogel-based therapies to improve the hypoxic microenvironment of periodontal tissues, thereby promoting periodontal regeneration, and provides clinical insights for future applications in periodontal regeneration.

Periodontitis is a chronic inflammatory disorder characterized by a sustained inflammatory stimulus that creates an oxidative stress microenvironment within periodontal tissues. Under such conditions, elevated levels of reactive oxygen species (ROS) disrupt the structural and functional integrity of periodontal ligament stem cells (PDLSCs), inhibit osteogenic differentiation, and impair the regeneration of periodontal bone defects. Herein, a ROS-responsive degradable hydrogel loaded with growth differentiation factor 5 (GDF5) was developed to target this pathological microenvironment. By incorporating a thioketal (TK) linker that can be cleaved by ROS, the hydrogel reacts with high concentrations of ROS, improving the oxidative stress environment. As the reaction occurs, the hydrogel is degraded, and during this process, GDF5 is successfully released into the microenvironment, then exerts a sustained osteogenic-promoting effect. This study does not simply expose GDF5 to a harmful environment. Instead, our hydrogel first rapidly scavenges high levels of ROS upon sensing them, creating a redox-balanced microenvironment for the cells; subsequently, it releases GDF5 through an ROS-triggered mechanism. This sequential logic of “clearing the environment first, then treating” is designed to ensure that the released GDF5 can function in an optimized and functional microenvironment, thereby maximizing its protective effects and promoting its osteogenic activity.