Human saliva exposure modulates bone cell performance in vitro.
Various situations encountered by a clinician during the daily routine including surgical periodontitis therapy, dental implant insertion, or tooth extraction involve the contact of saliva with the jaw bone. However, there are only sparse data concerning the influence of saliva on bone cells. Saliva specimens were incorporated within culture medium and administered to murine MC3T3 osteoblasts, of which the morphology (REM), proliferation (EZ4U), and differentiation (qRT-PCR, alkaline phosphatase activity, extracellular matrix calcification) were assessed. Simultaneously, the composition of saliva media was analyzed with respect to the content of lactoferrin, activities of classical salivary enzymes, and the ability to provoke inflammatory cytokine production (enzyme-linked immunosorbent assay) in MC3T3 osteoblasts. The morphology, proliferation, and expression of differentiation-associated genes were seriously handicapped by saliva contact. Saliva-touched cells exhibited less alkaline phosphatase but normal levels of extracellular matrix mineralization. Saliva-containing culture media featured physiological activities of salivary enzymes and considerable amounts of lactoferrin but almost completely lacked salivary alkaline phosphatase and unspecific proteases. Upon saliva incubation, MC3T3 osteoblasts did not release noteworthy levels of interleukin-1 beta or tumor necrosis factor alpha. Although saliva is generally considered to vitalize oral tissues, this study reveals that it harms osteoblast-like cells more due to the presence of salivary enzymes than by triggering of inflammation. This issue is clinically relevant because it broadens the understanding of the bone cell fate within the rather complex cosmos of the oral cavity thereby providing a basis for clinical decision making and treatment guidelines. It seems to be reasonable to restrict the contact period between saliva and bone.
Department of Operative Dentistry and Periodontology, Dental School and Hospital, University Medical Center Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany. susanne.proksch@uniklinik-freiburg.de
Susanne
S
Proksch
Thorsten
T
Steinberg
Constantin
C
Keller
Martin
M
Wolkewitz
Margit
M
Wiedmann-Al-Ahmad
Guenter
G
Finkenzeller
Christian
C
Hannig
Elmar
E
Hellwig
Ali
A
Al-Ahmad
D016475:3T3 Cells; D000469:Alkaline Phosphatase / Q000032:analysis; D000818:Animals; D002113:Calcification, Physiologic / Q000502:physiology; D002118:Calcium / Q000032:analysis; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D048430:Cell Shape; D003124:Colorimetry; D003470:Culture Media; D016207:Cytokines / Q000032:analysis; D005109:Extracellular Matrix / Q000502:physiology; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D007781:Lactoferrin / Q000032:analysis; D008297:Male; D051379:Mice; D008855:Microscopy, Electron, Scanning; D010006:Osteoblasts / Q000502:physiology*; D010447:Peptide Hydrolases / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012463:Saliva / Q000737:chemistry / Q000201:enzymology / Q000502:physiology*; D012471:Salivary Proteins and Peptides / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D003470:Culture Media; D016207:Cytokines; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D012471:Salivary Proteins and Peptides; D014409:Tumor Necrosis Factor-alpha; D000469:Alkaline Phosphatase; D010447:Peptide Hydrolases; D007781:Lactoferrin; D002118:Calcium
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