Please use this identifier to cite or link to this item:
- LPS Induces Greater Bone and PDL Loss in SPARC-null Mice
- Med Univ S Carolina
- Erskine Coll
- Ralph H Johnson Dept Vet Affairs Med Ctr
- Universidade Estadual Paulista (UNESP)
- National Institutes of Health
- Veteran's Administration
- NIH: T32-DE017551
- NIH: R25-HL092611
- NIH: 2P20RR017696
- NIH: HL094517
- NIH: R01-DE018290
- 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/B16 mice. A 20-mu g 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.
- Journal of Dental Research. Thousand Oaks: Sage Publications Inc, v. 90, n. 4, p. 477-482, 2011.
- Sage Publications Inc
- periodontal ligament
- extracellular matrix
- periodontal diseases
- alveolar bone resorption
- Acesso restrito
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.