title: CCR5 down-regulates osteoclast function in orthodontic tooth movement.
abstract: During orthodontic tooth movement, there is local production of chemokines and an influx of leukocytes into the periodontium. CCL5 plays an important role in osteoclast recruitment and activation. This study aimed to investigate whether the CCR5-receptor influences these events and, consequently, orthodontic tooth movement. An orthodontic appliance was placed in wild-type mice (WT) and CCR5-deficient mice (CCR5(-/-)). The expression of mediators involved in bone remodeling was evaluated in periodontal tissues by Real-time PCR. The number of TRAP-positive osteoclasts and the expression of cathepsin K, RANKL, and MMP13 were significantly higher in CCR5(-/-). Meanwhile, the expression of two osteoblastic differentiation markers, RUNX2 and osteocalcin, and that of bone resorption regulators, IL-10 and OPG, were lower in CCR5(-/-). Analysis of the data also showed that CCR5(-/-) exhibited a greater amount of tooth movement after 7 days of mechanical loading. The results suggested that CCR5 might be a down-regulator of alveolar bone resorption during orthodontic movement.
authors.affiliation: Department of Orthodontics, Faculty of Dentistry, Pontifícia Universidade Católica de Minas Gerais, Av. Dom José Gaspar 500, CEP 31.270-901, Belo Horizonte, Minas Gerais, Brazil. ildeu_andrade@yahoo.com.br
authors.forename: I
authors.initials: I
authors.lastname: Andrade
authors.forename: S R A
authors.initials: SR
authors.lastname: Taddei
authors.forename: G P
authors.initials: GP
authors.lastname: Garlet
authors.forename: T P
authors.initials: TP
authors.lastname: Garlet
authors.forename: A L
authors.initials: AL
authors.lastname: Teixeira
authors.forename: T A
authors.initials: TA
authors.lastname: Silva
authors.forename: M M
authors.initials: MM
authors.lastname: Teixeira
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D016723:Bone Remodeling / Q000502:physiology; D001862:Bone Resorption / Q000503:physiopathology; D056657:Cathepsin K; D002403:Cathepsins / Q000032:analysis; D002465:Cell Movement / Q000502:physiology; D018932:Chemokine CCL2 / Q000032:analysis; D054405:Chemokine CCL3 / Q000032:analysis; D018946:Chemokine CCL5 / Q000032:analysis; D050659:Core Binding Factor Alpha 1 Subunit / Q000032:analysis; D003546:Cysteine Endopeptidases / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D015536:Down-Regulation / Q000502:physiology*; D016753:Interleukin-10 / Q000032:analysis; D007527:Isoenzymes / Q000032:analysis; D053509:Matrix Metalloproteinase 13 / Q000032:analysis; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D015675:Osteocalcin / Q000032:analysis; D010010:Osteoclasts / Q000502:physiology*; D053244:Osteoprotegerin / Q000032:analysis; D053245:RANK Ligand / Q000032:analysis; D019713:Receptors, CCR5 / Q000502:physiology*; D013314:Stress, Mechanical; D000071681:Tartrate-Resistant Acid Phosphatase; D014087:Tooth Movement Techniques
chemical_list: D015415:Biomarkers; C491768:Ccl2 protein, mouse; C496534:Ccl3 protein, mouse; C503460:Ccl5 protein, mouse; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D018946:Chemokine CCL5; D050659:Core Binding Factor Alpha 1 Subunit; D016207:Cytokines; D007527:Isoenzymes; D053244:Osteoprotegerin; D053245:RANK Ligand; D019713:Receptors, CCR5; C493716:Runx2 protein, mouse; D015675:Osteocalcin; D016753:Interleukin-10; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase; D002403:Cathepsins; D003546:Cysteine Endopeptidases; D056657:Cathepsin K; C534132:Ctsk protein, mouse; D053509:Matrix Metalloproteinase 13; C507081:Mmp13 protein, mouse