title: New insights into the effects of primary hyperparathyroidism on the cortical and trabecular compartments of bone.
abstract: In primary hyperparathyroidism (PHPT), protracted elevation of serum parathyroid hormone (PTH) is held to be associated with cortical, but not trabecular, bone loss. However, an alternative explanation for the apparent preservation of trabecular bone is fragmentation of the cortex by intracortical remodeling. The cortical fragments resemble trabeculae and so may be erroneously included in the quantification of 'trabecular' bone density. To test this hypothesis, we compared bone microarchitecture in 43 patients with untreated PHPT (mean 62.9 years, range 31-84) with 47 healthy age-matched controls and 25 patients with surgically treated PHPT (63.6 years, 30-82). Images of the distal radius and tibia were acquired using high-resolution peripheral quantitative CT and analysed using StrAx1.0, a new software program that quantifies bone morphology in-vivo. Results were expressed as the mean number of standardized deviations (SD) from the age-specific mean (Z scores, mean±SEM). In subjects with PHPT, total tibial cortical area was reduced -0.26±0.08 SD; p=0.002). Cortical volumetric bone mineral density (vBMD) was reduced (-0.29±0.06 SD; p<0.001) due to higher cortical porosity (0.32±0.06 SD; p<0.001) and lower tissue mineralization density (-0.21±0.06 SD; p=0.002). Medullary area was increased (0.26±0.08 SD; p=0.002) and trabecular vBMD was reduced (-0.14±0.04 SD; p<0.001). In subjects who underwent successful parathyroidectomy, cortical area (-0.18±0.10 SD; NS) and medullary area (0.18±0.10 SD; NS) did not differ from controls. Cortical vBMD was reduced (-0.15±0.05 SD; p=0.003) due to high porosity (0.15±0.05 SD; p=0.006), values numerically lower than in untreated PHPT. Tissue mineralization density (-0.26±0.04 SD; p<0.001) and trabecular vBMD were reduced (-0.16±0.04 SD, p<0.001). The results were similar in the distal radius. In PHPT, chronically elevated endogenous PTH does not spare trabecular bone; it causes bone loss and microarchitectural deterioration in both cortical and trabecular compartments of bone.
authors.affiliation: Department of Medicine and Endocrinology, Austin Health, University of Melbourne, Heidelberg, Australia. t.vu12@pgrad.unimelb.edu.au
authors.forename: Thuy D T
authors.initials: TD
authors.lastname: Vu
authors.forename: Xiao Fang
authors.initials: XF
authors.lastname: Wang
authors.forename: Qingju
authors.initials: Q
authors.lastname: Wang
authors.forename: Natalie E
authors.initials: NE
authors.lastname: Cusano
authors.forename: Dinaz
authors.initials: D
authors.lastname: Irani
authors.forename: Barbara C
authors.initials: BC
authors.lastname: Silva
authors.forename: Ali
authors.initials: A
authors.lastname: Ghasem-Zadeh
authors.forename: Julia
authors.initials: J
authors.lastname: Udesky
authors.forename: Megan E
authors.initials: ME
authors.lastname: Romano
authors.forename: Roger
authors.initials: R
authors.lastname: Zebaze
authors.forename: George
authors.initials: G
authors.lastname: Jerums
authors.forename: Stephanie
authors.initials: S
authors.lastname: Boutroy
authors.forename: John P
authors.initials: JP
authors.lastname: Bilezikian
authors.forename: Ego
authors.initials: E
authors.lastname: Seeman
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015519:Bone Density; D001842:Bone and Bones / Q000000981:diagnostic imaging / Q000473:pathology*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D049950:Hyperparathyroidism, Primary / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D011884:Radius / Q000000981:diagnostic imaging / Q000473:pathology; D013977:Tibia / Q000000981:diagnostic imaging / Q000473:pathology; D014057:Tomography, X-Ray Computed
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