title: Continuous parathyroid hormone induces cortical porosity in the rat: effects on bone turnover and mechanical properties.
abstract: We examined the time course effects of continuous PTH on cortical bone and mechanical properties. PTH increased cortical bone turnover and induced intracortical porosity with no deleterious effect on bone strength. Withdrawal of PTH increased maximum torque to failure and stiffness with no change in energy absorbed.
  
  
  BACKGROUND
  The skeletal response of cortical bone to parathyroid hormone (PTH) is complex and species dependent. Intermittent administration of PTH to rats increases periosteal and endocortical bone formation but has no known effects on intracortical bone turnover. The effects of continuous PTH on cortical bone are not clearly established.
  
  
  METHODS
  Eighty-four 6-month-old female Sprague-Dawley rats were divided into three control, six PTH, and two PTH withdrawal (WD) groups. They were subcutaneously implanted with osmotic pumps loaded with vehicle or 40 microg/kg BW/day human PTH(1-34) for 1, 3, 5, 7, 14, and 28 days. After 7 days, PTH was withdrawn from two groups of animals for 7 (7d-PTH/7d-WD) and 21 days (7d-PTH/21d-WD). Histomorphometry was performed on periosteal and endocortical surfaces of the tibial diaphysis in all groups. microCT of tibias and mechanical testing by torsion of femora were performed on 28d-PTH and 7d-PTH/21d-WD animals.
  
  
  CONCLUSIONS
  Continuous PTH increased periosteal and endocortical bone formation, endocortical osteoclast perimeter, and cortical porosity in a time-dependent manner, but did not change the mechanical properties of the femur, possibly because of addition of new bone onto periosteal and endocortical surfaces. Additionally, withdrawal of PTH restored normal cortical porosity and increased maximum torque to failure and stiffness. We conclude that continuous administration of PTH increased cortical porosity in rats without having a detrimental effect on bone mechanical properties.
authors.affiliation: Department of Orthopedics, Mayo Clinic, Rochester, Minnesota 55905, USA. lotinun.sutada@mayo.edu
authors.forename: Sutada
authors.initials: S
authors.lastname: Lotinun
authors.forename: Glenda L
authors.initials: GL
authors.lastname: Evans
authors.forename: James T
authors.initials: JT
authors.lastname: Bronk
authors.forename: Mark E
authors.initials: ME
authors.lastname: Bolander
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Wronski
authors.forename: Erik L
authors.initials: EL
authors.lastname: Ritman
authors.forename: Russell T
authors.initials: RT
authors.lastname: Turner
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D016723:Bone Remodeling / Q000187:drug effects*; D001842:Bone and Bones / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000648:ultrastructure; D005260:Female; D010052:Ovariectomy; D010281:Parathyroid Hormone / Q000008:administration & dosage / Q000494:pharmacology* / Q000633:toxicity; D016062:Porosity; D011859:Radiography; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D010281:Parathyroid Hormone