Purpose: Dental implant osseointegration comprises two types of bone formation-contact and distance osteogenesis-which result in bone formation originating from the implant surface or bone edges, respectively. The physicochemical properties of the implant surface regulate initial contact osteogenesis by directly tuning the osteoprogenitor cells in the peri-implant environment. However, whether these implant surface properties can regulate osteoprogenitor cells distant from the implant remains unclear. Innate immune cells, including neutrophils and macrophages, govern bone metabolism, suggesting their involvement in osseointegration and distance osteogenesis. This narrative review discusses the role of innate immunity in osseointegration and the effects of implant surface properties on distant osteogenesis, focusing on innate immune regulation.
Study Selection: The role of innate immunity in bone formation and the effects of implant surface properties on innate immune function were reviewed based on clinical, animal, and in vitro studies.
Results: Neutrophils and macrophages are responsible for bone formation during osseointegration, via inflammatory mediators. The microroughness and hydrophilic status of titanium implants have the potential to alleviate this inflammatory response of neutrophils, and induce an anti-inflammatory response in macrophages, to tune both contact and distance osteogenesis through the activation of osteoblasts. Thus, the surface micro-roughness and hydrophilicity of implants can regulate the function of distant osteoprogenitor cells through innate immune cells.
Conclusions: Surface modification of implants aimed at regulating innate immunity may be useful in promoting further osteogenesis and overcoming the limitations encountered in severe situations, such as early loading protocol application.
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http://dx.doi.org/10.2186/jpr.JPR_D_23_00198 | DOI Listing |
Front Immunol
January 2025
Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
The innate immune system promptly detects and responds to invading pathogens, with a key role played by the recognition of bacterial-derived DNA through pattern recognition receptors. The Z-DNA binding protein 1 (ZBP1) functions as a DNA sensor inducing type I interferon (IFN) production, innate immune responses and also inflammatory cell death. ZBP1 interacts with cytosolic DNA via its DNA-binding domains, crucial for its activation.
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January 2025
Department of Biomedicine, Aarhus University, Aarhus, Denmark.
The innate immune system plays a critical role in the rapid recognition and elimination of pathogens through pattern recognition receptors (PRRs). Among these PRRs are the C-type lectins (CTLs) langerin, mannan-binding lectin (MBL), and surfactant protein D (SP-D), which recognize carbohydrate patterns on pathogens. Each represents proteins from different compartments of the body and employs separate effector mechanisms.
View Article and Find Full Text PDFAm J Blood Res
December 2024
Department of Pathology, University College of Medical Sciences and Guru Teg Bahadur Hospital Delhi, India.
Unlabelled: Iron deficiency anaemia (IDA) makes an individual prone to bacterial infections. The antimicrobial defence mechanism of neutrophils is orchestrated by Nicotinamide Adenine Dinucleotide Phosphate Hydrogen (NADPH) oxidative burst which is iron-dependent. The few previous studies documenting a decrease in neutrophil oxidative burst in iron-deficient children have been based mainly on the Nitro blue tetrazolium test (NBT).
View Article and Find Full Text PDFHeliyon
January 2025
Department of Rheumatology, Wuxi Hospital of Traditional Chinese Medicine, Wuxi, 214000, Jiangsu, China.
Rheumatoid arthritis (RA) is associated with a high rate of hepatitis B virus (HBV) infection. A large proportion of HBV reactivation may occur in RA patients after immunosuppression treatment, while fulminant hepatitis may occur in severe cases. Immunosuppressants are fundamental medications for the treatment of RA but carry the risk of inducing HBV reactivation.
View Article and Find Full Text PDFTzu Chi Med J
December 2024
Department of Obstetrics and Gynecology, College of Medicine, University of Babylon, Hilla, Iraq.
The most common STD that triggers cervical cancer is the human papillomavirus. More than 20 types of human papillomavirus (HPV) can induce uterine cervical cancer. Almost all women acquire genital HPV infection soon after their first intercourse, with most of them clearing the virus within 3 years.
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