title: LPS induces greater bone and PDL loss in SPARC-null mice.
abstract: Individuals with periodontal disease have increased risk of tooth loss, particularly in cases with associated loss of alveolar bone and periodontal ligament (PDL). Current treatments do not predictably regenerate damaged PDL. Collagen I is the primary component of bone and PDL extracellular matrix. SPARC/Osteonectin (SP/ON) is implicated in the regulation of collagen content in healthy PDL. In this study, periodontal disease was induced by injections of lipopolysaccharide (LPS) from Aggregatibacter actinomycetemcomitans in wild-type (WT) and SP/ON-null C57/Bl6 mice. A 20-µg quantity of LPS was injected between the first and second molars 3 times a week for 4 weeks, whereas PBS control was injected into the contralateral maxilla. LPS injection resulted in a significant decrease in bone volume fraction in both genotypes; however, significantly greater bone loss was detected in SP/ON-null maxilla. SP/ON-null PDL exhibited more extensive degradation of connective tissue in the gingival tissues. Although total cell numbers in the PDL of SP/ON-null were not different from those in WT, the inflammatory infiltrate was reduced in SP/ON-null PDL. Histology of collagen fibers revealed marked reductions in collagen volume fraction and in thick collagen volume fraction in the PDL of SP/ON-null mice. SP/ON protects collagen content in PDL and in alveolar bone in experimental periodontal disease.
authors.affiliation: Department of Craniofacial Biology and Center for Oral Health Research, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: J
authors.initials: J
authors.lastname: Trombetta-Esilva
authors.forename: H
authors.initials: H
authors.lastname: Yu
authors.forename: D N
authors.initials: DN
authors.lastname: Arias
authors.forename: C
authors.initials: C
authors.lastname: Rossa
authors.forename: K L
authors.initials: KL
authors.lastname: Kirkwood
authors.forename: A D
authors.initials: AD
authors.lastname: Bradshaw
mesh_terms: D016976:Aggregatibacter actinomycetemcomitans; D016301:Alveolar Bone Loss / Q000145:classification* / Q000209:etiology / Q000473:pathology; D000818:Animals; D002452:Cell Count; D024042:Collagen Type I / Q000187:drug effects; D003238:Connective Tissue / Q000187:drug effects / Q000473:pathology; D016326:Extracellular Matrix Proteins / Q000187:drug effects; D005838:Genotype; D005882:Gingival Diseases / Q000145:classification / Q000209:etiology / Q000473:pathology; D007091:Image Processing, Computer-Assisted; D008070:Lipopolysaccharides / Q000009:adverse effects*; D008437:Maxilla / Q000187:drug effects / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D015676:Osteonectin / Q000235:genetics / Q000502:physiology*; D010513:Periodontal Ligament / Q000187:drug effects* / Q000473:pathology; D010518:Periodontitis / Q000145:classification* / Q000209:etiology / Q000473:pathology; D055114:X-Ray Microtomography
chemical_list: D024042:Collagen Type I; D016326:Extracellular Matrix Proteins; D008070:Lipopolysaccharides; D015676:Osteonectin