title: Importance of lymph vessels in the transcapillary fluid balance in the gingiva studied in a transgenic mouse model.
abstract: The gingiva is frequently challenged by oral bacterial products leading to inflammatory responses such as increased fluid filtration and edema formation. The role of initial lymphatics for transcapillary fluid balance in the gingiva is unknown and was therefore investigated in genetically engineered K14-VEGF receptor 3-Ig (K14) lymphedema mice. The mutant mice demonstrated a total lack of lymphatics in the gingiva, whereas lymphatics were found in the submucosal parts of the alveolar mucosa, although they were almost completely absent in the mucosa. In wild-type (WT) mice, lymphatic vessels were detected in mucosal and submucosal parts of the alveolar mucosa. Interstitial fluid pressure (P(if)) measured with micropipettes was increased in the gingiva of K14 mice in the normal situation (P < 0.001) and after inflammation (P < 0.01) induced by lipopolysaccharide from the oral bacteria Porphyromonas gingivalis compared with WT littermates. Fluid volume expansion caused a >75% increase in interstitial fluid volume followed by a drop in P(if) after recovery in both strains. Continuous measurements during the expansion showed an increase in P(if) followed by a decline, suggesting that compliance is increased after the disruption of the extracellular matrix during edema formation. In the alveolar mucosa, no strain differences were observed in P(if) in the normal situation or after fluid volume expansion, suggesting that lymph vessels in the mucosa are not critical for tissue fluid regulation in any situation. Our study demonstrates an important role of gingival lymphatics in transcapillary fluid balance in the steady-state condition and during acute perturbations.
authors.affiliation: Dept. of Biomedicine, Jonas Lies vei 91, Bergen 5009, Norway.
authors.forename: Lilian Ephrem
authors.initials: LE
authors.lastname: Mkonyi
authors.forename: Athanasia
authors.initials: A
authors.lastname: Bletsa
authors.forename: Inge
authors.initials: I
authors.lastname: Fristad
authors.forename: Helge
authors.initials: H
authors.lastname: Wiig
authors.forename: Ellen
authors.initials: E
authors.lastname: Berggreen
mesh_terms: D000818:Animals; D002196:Capillaries / Q000276:immunology / Q000378:metabolism*; D002199:Capillary Permeability; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D045604:Extracellular Fluid / Q000378:metabolism; D005260:Female; D005881:Gingiva / Q000098:blood supply*; D005891:Gingivitis / Q000276:immunology / Q000378:metabolism*; D007141:Immunoglobulin Fc Fragments / Q000235:genetics; D007074:Immunoglobulin G / Q000235:genetics; D008070:Lipopolysaccharides / Q000276:immunology; D042601:Lymphatic Vessels / Q000276:immunology / Q000378:metabolism*; D008209:Lymphedema / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009061:Mouth Mucosa / Q000098:blood supply*; D016966:Porphyromonas gingivalis / Q000276:immunology; D011312:Pressure; D011401:Promoter Regions, Genetic; D013997:Time Factors; D040321:Vascular Endothelial Growth Factor Receptor-3 / Q000235:genetics
chemical_list: D007141:Immunoglobulin Fc Fragments; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D003094:Collagen; D040321:Vascular Endothelial Growth Factor Receptor-3