Peri-implant keratinized mucosa (PIKM) augmentation refers to surgical procedures aimed at increasing the width of PIKM. Consensus reports emphasize the necessity of maintaining a minimum width of PIKM to ensure long-term peri-implant health. Currently, several surgical techniques have been validated for their effectiveness in increasing PIKM. However, the selection and application of PIKM augmentation methods may present challenges for dental practitioners due to heterogeneity in surgical techniques, variations in clinical scenarios, and anatomical differences. Therefore, clear guidelines and considerations for PIKM augmentation are needed. This expert consensus focuses on the commonly employed surgical techniques for PIKM augmentation and the factors influencing their selection at second-stage surgery. It aims to establish a standardized framework for assessing, planning, and executing PIKM augmentation procedures, with the goal of offering evidence-based guidance to enhance the predictability and success of PIKM augmentation.
Humans ; Consensus ; Dental Implants ; Mouth Mucosa/surgery* ; Keratins

Objective To investigate the therapeutic effects and mechanisms of Aurantii Fructus Immaturus(AFI)on slow-transit constipation(STC)in mice.Methods A STC model was established via intragastric administration of Loperamide Hydrochloride.Successfully modeled mice were randomized into a model group,low-and high-dose AFI groups,a high-dose AFI+Masitinib[tyrosine kinase(c-Kit)inhibitor]group,additionally,a normal group was set up.After intervention,intestinal transit rate,6-hour fecal pellet number,fecal water content,and colonic histomorphology(hematoxylin-eosin staining)were assessed.Enzyme-linked immunosorbent assay(ELISA)was used to measure levels of 5-hydroxytryptamine(5-HT),vasoactive intestinal polypeptide(VIP),substance P(SP),nitric oxide(NO),and nitric oxide synthase(NOS)activity in colon tissue.Quantitative real-time PCR(qRT-PCR)was used to evaluate mRNA expression of stem cell factor(SCF)and c-Kit in colon tissue,Western Blot was used to analyze relative protein expression of aquaporin 3(AQP3),aquaporin 8(AQP8),SCF,and c-Kit in colon tissue.Results Compared with the normal group,there was devere colonic damage observed in the colon tissue of the mice in the model group,the fecal pellet number,fecal water content,intestinal transit rate,colon tissue SP content,c-Kit and SCF gene and protein expression levels were reduced.The contents of 5-HT,VIP and NO,NOS activity and the protein expression levels of AQP3 and AQP8 in colon tissue were increased,and the differences were statistically significant(P＜0.05).Compared with the model group,the colonic injury of mice in the low-and high-does AFI groups showed obvious improvement,the fecal pellet number,fecal water content,intestinal transit rate,colon tissue SP content,c-Kit and SCF gene and protein expression levels were increased,the contents of 5-HT,VIP and NO,NOS activity and the protein expression levels of AQP3 and AQP8 in colon tissue were decreased(P＜0.05).Masitinib partially reversed the laxative effects of AFI(P＜0.05).Conclusion AFI enhances intestinal motility,alleviates colonic injury,and improves defecation in STC mice,potentially via activation of the SCF/c-Kit pathway.

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues. Magnesium has been proved to promote bone healing under normal conditions. Here, we elucidate the mechanism by which Mg²⁺ promotes angiogenesis and osseointegration in diabetic status. We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised, with significantly decreased angiogenesis. We then developed Mg-coating implants with hydrothermal synthesis. These implants successfully improved the vascularization and osseointegration in diabetic status. Mechanically, Mg²⁺ promoted the degradation of Kelch-like ECH-associated protein 1 (Keap1) and the nucleation of nuclear factor erythroid 2-related factor 2 (Nrf2) by up-regulating the expression of sestrin 2 (SESN2) in endothelial cells, thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia. Altogether, our data suggested that Mg²⁺ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.
Mice ; Animals ; Kelch-Like ECH-Associated Protein 1/metabolism* ; Magnesium/metabolism* ; Osseointegration ; Diabetes Mellitus, Experimental/metabolism* ; Endothelial Cells/metabolism* ; NF-E2-Related Factor 2/metabolism*

Inflammation is involved in the development of various acute and chronic diseases in the body. Sustained inflammatory responses are key driving factors for diseases such as cancer， neurodegenerative diseases， cardiovascular diseases， metabolic syndrome， inflammatory bowel disease， and arthritis. Therefore， finding anti-inflammatory drugs is crucial for the prevention and treatment of various diseases. In recent years， there has been increasing attention to finding natural drugs with minimal toxic side effects. Lonicerae Japonicae Flos and Lonicerae Flos， as traditional Chinese medicines potent in clearing heat and removing toxins， have strong biological activity and multiple pharmacological effects. They are widely distributed in the plant world and have significant medicinal value. With the continuous advancement of the research on Lonicerae Japonicae Flos and Lonicerae Flos， they have been widely used in the medical field and possess great development potential. Currently， research mainly focuses on the anti-inflammatory mechanisms of Lonicerae Japonicae Flos and Lonicerae Flos， while systematic summaries of their anti-inflammatory active ingredients are rare. Therefore， this paper focuses on the differential analysis of the anti-inflammatory active components of Lonicerae Japonicae Flos and Lonicerae Flos. In addition， it reviewed the possible mechanisms by which extracts and active ingredients of Lonicerae Japonicae Flos and Lonicerae Flos may exert anti-inflammatory effects through various pathways， such as influencing the release of cellular inflammatory factors， regulating inflammatory signaling pathways such as nuclear factor-κB （NF-κB）， mitogen-activated protein kinase （MAPK）， signal transducer and activator of transcription 3 （STAT3）， MAPK/extracellular signal-regulated kinase （ERK）/c-Jun N-terminal kinase （JNK）， phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/NF-κB， and Janus kinase （JAK）/signal transducer and activator of transcription （STAT） signaling pathways， increasing antioxidant stress capacity， enhancing immune defense capabilities， and improving intestinal microbiota， aiming to provide a theoretical basis for the rational clinical application of Lonicerae Japonicae Flos and Lonicerae Flos.

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues.Magnesium has been proved to promote bone healing under normal conditions.Here,we elucidate the mechanism by which Mg2+ promotes angiogenesis and osseointegration in diabetic status.We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised,with significantly decreased angiogenesis.We then developed Mg-coating implants with hydrothermal synthesis.These implants successfully improved the vascularization and osseointegration in diabetic status.Mechanically,Mg2+ promoted the degradation of Kelch-like ECH-associated protein 1(Keap1)and the nucleation of nuclear factor erythroid 2-related factor 2(Nrf2)by up-regulating the expression of sestrin 2(SESN2)in endothelial cells,thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia.Altogether,our data suggested that Mg2+ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues.Magnesium has been proved to promote bone healing under normal conditions.Here,we elucidate the mechanism by which Mg2+ promotes angiogenesis and osseointegration in diabetic status.We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised,with significantly decreased angiogenesis.We then developed Mg-coating implants with hydrothermal synthesis.These implants successfully improved the vascularization and osseointegration in diabetic status.Mechanically,Mg2+ promoted the degradation of Kelch-like ECH-associated protein 1(Keap1)and the nucleation of nuclear factor erythroid 2-related factor 2(Nrf2)by up-regulating the expression of sestrin 2(SESN2)in endothelial cells,thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia.Altogether,our data suggested that Mg2+ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues.Magnesium has been proved to promote bone healing under normal conditions.Here,we elucidate the mechanism by which Mg2+ promotes angiogenesis and osseointegration in diabetic status.We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised,with significantly decreased angiogenesis.We then developed Mg-coating implants with hydrothermal synthesis.These implants successfully improved the vascularization and osseointegration in diabetic status.Mechanically,Mg2+ promoted the degradation of Kelch-like ECH-associated protein 1(Keap1)and the nucleation of nuclear factor erythroid 2-related factor 2(Nrf2)by up-regulating the expression of sestrin 2(SESN2)in endothelial cells,thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia.Altogether,our data suggested that Mg2+ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues.Magnesium has been proved to promote bone healing under normal conditions.Here,we elucidate the mechanism by which Mg2+ promotes angiogenesis and osseointegration in diabetic status.We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised,with significantly decreased angiogenesis.We then developed Mg-coating implants with hydrothermal synthesis.These implants successfully improved the vascularization and osseointegration in diabetic status.Mechanically,Mg2+ promoted the degradation of Kelch-like ECH-associated protein 1(Keap1)and the nucleation of nuclear factor erythroid 2-related factor 2(Nrf2)by up-regulating the expression of sestrin 2(SESN2)in endothelial cells,thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia.Altogether,our data suggested that Mg2+ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues.Magnesium has been proved to promote bone healing under normal conditions.Here,we elucidate the mechanism by which Mg2+ promotes angiogenesis and osseointegration in diabetic status.We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised,with significantly decreased angiogenesis.We then developed Mg-coating implants with hydrothermal synthesis.These implants successfully improved the vascularization and osseointegration in diabetic status.Mechanically,Mg2+ promoted the degradation of Kelch-like ECH-associated protein 1(Keap1)and the nucleation of nuclear factor erythroid 2-related factor 2(Nrf2)by up-regulating the expression of sestrin 2(SESN2)in endothelial cells,thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia.Altogether,our data suggested that Mg2+ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues.Magnesium has been proved to promote bone healing under normal conditions.Here,we elucidate the mechanism by which Mg2+ promotes angiogenesis and osseointegration in diabetic status.We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised,with significantly decreased angiogenesis.We then developed Mg-coating implants with hydrothermal synthesis.These implants successfully improved the vascularization and osseointegration in diabetic status.Mechanically,Mg2+ promoted the degradation of Kelch-like ECH-associated protein 1(Keap1)and the nucleation of nuclear factor erythroid 2-related factor 2(Nrf2)by up-regulating the expression of sestrin 2(SESN2)in endothelial cells,thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia.Altogether,our data suggested that Mg2+ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.