title: Adverse mandibular bone effects associated with kidney disease are only partially corrected with bisphosphonate and/or calcium treatment.
abstract: OBJECTIVE
  Patients with chronic kidney disease (CKD) have a high prevalence of periodontal disease that may predispose to tooth loss and inflammation. The goal of this study was to test the hypotheses that a genetic rat model of progressive CKD would exhibit altered oral bone properties and that treatment with either bisphosphonates or calcium could attenuate these adverse changes.
  
  
  METHODS
  At 25 weeks of age, rats were treated with zoledronate (ZOL), calcium gluconate, or their combination for 5 or 10 weeks. Mandible bone properties were assessed using micro-computed tomography to determine bone volume (BV/TV) and cementum-enamel junction to alveolar crest distance (CEJ-AC).
  
  
  RESULTS
  Untreated CKD animals had significantly lower BV/TV at both 30 (-5%) and 35 (-14%) weeks of age and higher CEJ-AC (+27 and 29%) compared to normal animals. CKD animals had a significantly higher parathyroid hormone (PTH) compared to normal animals, yet similar levels of C-reactive protein (CRP). ZOL treatment normalized BV/TV over the first 5 weeks but this benefit was lost by 10 weeks. Calcium treatment, alone or in combination with ZOL, was effective in normalizing BV/TV at both time points. Neither ZOL nor calcium was able to correct the higher CEJ-AC caused by CKD. Calcium, but not ZOL, significantly reduced serum PTH, while neither treatment affected CRP.
  
  
  CONCLUSIONS
  (i) This progressive animal model of CKD shows a clear mandibular skeletal phenotype consistent with periodontitis, (ii) the periodontitis is not associated with systemic inflammation as measured by CRP, and (iii) reducing PTH has positive effects on the mandible phenotype.
authors.affiliation: Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Ind., USA.
authors.forename: Matthew R
authors.initials: MR
authors.lastname: Allen
authors.forename: Neal X
authors.initials: NX
authors.lastname: Chen
authors.forename: Vincent H
authors.initials: VH
authors.lastname: Gattone
authors.forename: Sharon M
authors.initials: SM
authors.lastname: Moe
mesh_terms: D000818:Animals; D001847:Bone Diseases / Q000150:complications* / Q000000981:diagnostic imaging / Q000188:drug therapy*; D002097:C-Reactive Protein / Q000737:chemistry; D002118:Calcium / Q000627:therapeutic use*; D003739:Dental Cementum / Q000737:chemistry; D003743:Dental Enamel / Q000737:chemistry; D004164:Diphosphonates / Q000627:therapeutic use*; D004195:Disease Models, Animal; D006579:Heterozygote; D007093:Imidazoles / Q000627:therapeutic use*; D007249:Inflammation; D007674:Kidney Diseases / Q000150:complications* / Q000000981:diagnostic imaging; D008297:Male; D008334:Mandible / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000473:pathology; D010281:Parathyroid Hormone / Q000378:metabolism; D010518:Periodontitis / Q000188:drug therapy; D010641:Phenotype; D051381:Rats; D014057:Tomography, X-Ray Computed; D055114:X-Ray Microtomography; D000077211:Zoledronic Acid
chemical_list: D004164:Diphosphonates; D007093:Imidazoles; D010281:Parathyroid Hormone; D000077211:Zoledronic Acid; D002097:C-Reactive Protein; D002118:Calcium