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Alveolar Bone Loss --- diagnostic imaging.

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Periodontitis is an infection-induced inflammatory disease accounting for huge healthcare costs and socio-economic impacts. Bacteria from the indigenous oral flora colonize the interspace between the tooth and the connective tissue, which induces an inflammatory response. If the bacteria proliferate and release virulence factors, they cause an imbalance in the host inflammatory response that induces degenerative processes in the surrounding tissues. This process is often slow, and the disease affects mainly older people, but the process could be rapid and affect young individuals if certain pathogens colonize the area. The two most studied periodontal pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, express virulence factors, including proteases and exotoxins. Periodontal bacteria and their products can be translocated to the peripheral circulation and are therefore linked to the risk pattern of several systemic diseases. However, it is not known if the increased risk for systemic disease associated with periodontitis is an effect of the invading bacteria and/or their released products, the release of components from the local inflammatory response, or a common host susceptibility pattern. The most studied periodontitis-associated systemic diseases are cardiovascular diseases and rheumatoid arthritis. Here, we want to shed light on mechanisms behind the associations of periodontal infections with systemic inflammation.

Medicine --- apical periodontitis --- adaptive immunity --- saliva --- serum --- antibody --- Aggregatibacter actinomycetemcomitans --- invasiveness --- leukotoxin --- cytolethal distending toxin --- serum resistance --- outer membrane vesicles --- oral microbiome --- nitric oxide --- nitrate --- nitrite --- periodontal disease --- alveolar bone loss --- gingiva --- bacteria --- biofilm --- immunity --- inflammation --- smoking --- Rheumatoid arthritis --- Porphyromonas gingivalis --- periodontitis --- citrullination --- peptidylarginine deiminase --- ACPA --- anti-CCP --- host response --- infection --- oral microbiota --- virulence factors --- metabolites --- TREM-1 --- intervention --- LP17 --- IL-17 --- RANKL --- OPG --- cardiovascular diseases --- rheumatoid arthritis --- inflammatory response

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Periodontitis is an infection-induced inflammatory disease accounting for huge healthcare costs and socio-economic impacts. Bacteria from the indigenous oral flora colonize the interspace between the tooth and the connective tissue, which induces an inflammatory response. If the bacteria proliferate and release virulence factors, they cause an imbalance in the host inflammatory response that induces degenerative processes in the surrounding tissues. This process is often slow, and the disease affects mainly older people, but the process could be rapid and affect young individuals if certain pathogens colonize the area. The two most studied periodontal pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, express virulence factors, including proteases and exotoxins. Periodontal bacteria and their products can be translocated to the peripheral circulation and are therefore linked to the risk pattern of several systemic diseases. However, it is not known if the increased risk for systemic disease associated with periodontitis is an effect of the invading bacteria and/or their released products, the release of components from the local inflammatory response, or a common host susceptibility pattern. The most studied periodontitis-associated systemic diseases are cardiovascular diseases and rheumatoid arthritis. Here, we want to shed light on mechanisms behind the associations of periodontal infections with systemic inflammation.

Medicine --- apical periodontitis --- adaptive immunity --- saliva --- serum --- antibody --- Aggregatibacter actinomycetemcomitans --- invasiveness --- leukotoxin --- cytolethal distending toxin --- serum resistance --- outer membrane vesicles --- oral microbiome --- nitric oxide --- nitrate --- nitrite --- periodontal disease --- alveolar bone loss --- gingiva --- bacteria --- biofilm --- immunity --- inflammation --- smoking --- Rheumatoid arthritis --- Porphyromonas gingivalis --- periodontitis --- citrullination --- peptidylarginine deiminase --- ACPA --- anti-CCP --- host response --- infection --- oral microbiota --- virulence factors --- metabolites --- TREM-1 --- intervention --- LP17 --- IL-17 --- RANKL --- OPG --- cardiovascular diseases --- rheumatoid arthritis --- inflammatory response

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In the past, osseointegration was regarded to be a mode of implant anchorage that simulated a simple wound healing phenomenon. Today, we have evidence that osseointegration is, in fact, a foreign body reaction that involves an immunologically derived bony demarcation of an implant to shield it off from the tissues. Marginal bone resorption around an oral implant cannot be properly understood without realizing the foreign body nature of the implant itself. Whereas the immunological response as such is positive for implant longevity, adverse immunological reactions may cause marginal bone loss in combination with combined factors. Combined factors include the hardware, clinical handling as well as patient characteristics that, even if each one of these factors only produce subliminal trauma, when acting together they may result in loss of marginal bone. The role of bacteria in the process of marginal bone loss is smaller than previously believed due to combined defense mechanisms of inflammation and immunological reactions, but if the defense is failing we may see bacterially induced marginal bone loss as well. However, problems with loss of marginal bone threatening implant survival remains relatively uncommon; we have today 10 years of clinical documentation of five different types of implant displaying a failure rate in the range of only 1 to 4 %.

Medicine --- osseointegration --- dental implant --- peri-implantitis --- ligature-induced peri-implantitis --- aseptic loosening --- systematic review --- immune system --- biomaterials --- foreign body reaction --- in vivo study --- oral implants --- marginal bone loss --- immunomodulation --- mechanotransduction --- Crestal bone loss --- osseosufficiency --- osseoseparation --- photoacoustic ultrasound --- brain–bone axis --- overloading --- radiography --- CBCT (cone beam computerized tomography) --- osteogenesis --- osteotomy --- bone healing --- bone chips --- drilling tool design --- fused deposition modeling --- polyether ether ketone --- biocomposite --- orthopedic implant --- oral implant --- mechanical properties --- wettability --- topography --- biocompatibility --- cell adhesion --- peri-implant endosseous healing --- dental implantation --- alveolar bone loss --- alveolar bone remodeling/regeneration --- bone biology --- finite element analysis (FEA) --- biomechanics --- cell plasticity --- dental implants --- electron microscopy --- scanning transmission electron microscopy --- bone-implant interface --- bone loss --- overdenture --- implant survival --- implant surface --- soft tissue --- split-mouth design --- oral health-related quality of life --- patient-reported outcome measures --- biomaterial --- bone --- immune --- implant --- healing --- titanium --- PEEK --- Cu --- micro-RNA --- microarray --- predictive biomarker --- epigenomics --- mucositis --- diagnosis --- over-treatment --- iatrogenic damage --- abutment height --- subcrestal implants --- implant insertion depth --- vertical mucosal thickness --- biological width --- implant installation --- anchorage technique --- histology --- intraosseous temperature --- finite element model --- ligature induced peri-implantitis --- arthroplasty --- replacement --- hip --- hypersensitivity --- contact --- allergy and immunology --- cytokines --- Interleukin-8 --- surface properties --- materials testing --- implant contamination --- scanning electron microscopy --- energy-dispersive X-ray spectrometry --- convergence --- clinical study --- biofilm --- infection --- perio-prosthetic joint infection --- periimplantitis --- electrolytic cleaning --- n/a --- zirconia --- insertion --- bone–implant interface --- heat --- bone damage --- early loss --- augmentation --- air flow --- re-osseointegration --- classification of bone defects --- dog study --- brain-bone axis

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In the past, osseointegration was regarded to be a mode of implant anchorage that simulated a simple wound healing phenomenon. Today, we have evidence that osseointegration is, in fact, a foreign body reaction that involves an immunologically derived bony demarcation of an implant to shield it off from the tissues. Marginal bone resorption around an oral implant cannot be properly understood without realizing the foreign body nature of the implant itself. Whereas the immunological response as such is positive for implant longevity, adverse immunological reactions may cause marginal bone loss in combination with combined factors. Combined factors include the hardware, clinical handling as well as patient characteristics that, even if each one of these factors only produce subliminal trauma, when acting together they may result in loss of marginal bone. The role of bacteria in the process of marginal bone loss is smaller than previously believed due to combined defense mechanisms of inflammation and immunological reactions, but if the defense is failing we may see bacterially induced marginal bone loss as well. However, problems with loss of marginal bone threatening implant survival remains relatively uncommon; we have today 10 years of clinical documentation of five different types of implant displaying a failure rate in the range of only 1 to 4 %.

Medicine --- osseointegration --- dental implant --- peri-implantitis --- ligature-induced peri-implantitis --- aseptic loosening --- systematic review --- immune system --- biomaterials --- foreign body reaction --- in vivo study --- oral implants --- marginal bone loss --- immunomodulation --- mechanotransduction --- Crestal bone loss --- osseosufficiency --- osseoseparation --- photoacoustic ultrasound --- brain-bone axis --- overloading --- radiography --- CBCT (cone beam computerized tomography) --- osteogenesis --- osteotomy --- bone healing --- bone chips --- drilling tool design --- fused deposition modeling --- polyether ether ketone --- biocomposite --- orthopedic implant --- oral implant --- mechanical properties --- wettability --- topography --- biocompatibility --- cell adhesion --- peri-implant endosseous healing --- dental implantation --- alveolar bone loss --- alveolar bone remodeling/regeneration --- bone biology --- finite element analysis (FEA) --- biomechanics --- cell plasticity --- dental implants --- electron microscopy --- scanning transmission electron microscopy --- bone-implant interface --- bone loss --- overdenture --- implant survival --- implant surface --- soft tissue --- split-mouth design --- oral health-related quality of life --- patient-reported outcome measures --- biomaterial --- bone --- immune --- implant --- healing --- titanium --- PEEK --- Cu --- micro-RNA --- microarray --- predictive biomarker --- epigenomics --- mucositis --- diagnosis --- over-treatment --- iatrogenic damage --- abutment height --- subcrestal implants --- implant insertion depth --- vertical mucosal thickness --- biological width --- implant installation --- anchorage technique --- histology --- intraosseous temperature --- finite element model --- ligature induced peri-implantitis --- arthroplasty --- replacement --- hip --- hypersensitivity --- contact --- allergy and immunology --- cytokines --- Interleukin-8 --- surface properties --- materials testing --- implant contamination --- scanning electron microscopy --- energy-dispersive X-ray spectrometry --- convergence --- clinical study --- biofilm --- infection --- perio-prosthetic joint infection --- periimplantitis --- electrolytic cleaning --- zirconia --- insertion --- heat --- bone damage --- early loss --- augmentation --- air flow --- re-osseointegration --- classification of bone defects --- dog study