A Gaudio1, F Muratore1, V Fiore2, R Rapisarda1, S S Signorelli2, C E Fiore3. 1. Department of Clinical and Experimental Medicine, Section of Metabolic Bone Disease, University of Catania, Clinica Medica OVE, Via Plebiscito 628, 95124, Catania, Italy. 2. Department of Clinical and Experimental Medicine, Section of Vascular Medicine, Medical Angiology Unit, University of Catania, Garibaldi Hospital, Piazza S. Maria di Gesù 5, 95123, Catania, Italy. 3. Department of Clinical and Experimental Medicine, Section of Metabolic Bone Disease, University of Catania, Clinica Medica OVE, Via Plebiscito 628, 95124, Catania, Italy. carmelo.fiore@tin.it.
Abstract
UNLABELLED: The association between peripheral arterial disease (PAD) and low bone mass is controversial. In our study, peripheral quantitative computed tomography shows a reduction of cortical but not trabecular, bone mineral density (BMD) at the forearm, in patients with subclinical PAD. INTRODUCTION: Some controversy exists regarding the association between peripheral arterial disease (PAD) and low bone mass. Previous studies have evaluated bone mineral density (BMD) in patients with subclinical PAD, with mixed results. Inconsistency of data may depend on the fact that most studies measured areal bone mineral density (aBMD) by Dual-energy-x ray absorptiometry (DXA). Because DXA cannot distinguish between cortical and trabecular compartments, we reasoned that a study aimed to establish whether these compartments were differentially affected by PAD status could give more information on the nature of this association. METHODS: In this cross-sectional study, we used peripheral quantitative computed tomography (pQCT) to examine volumetric cortical and trabecular mineral density at the radius (vBMD) in a cohort of subjects with subclinical PAD as defined by ABI ≤0.90 and compared them with healthy subjects with no evidence of PAD. RESULTS: Patients with subclinical PAD had significantly reduced cortical density (1101.0 ± 45.4 vs 1156.2 ± 51.3 mg/cm(3), p < 0.001) and cortical area (75.0 ± 20.9 vs 99.9 ± 18.2 mm(2), p < 0.001) than healthy subjects. Trabecular density (178.1 ± 47.9 vs 165.8 ± 29.6 mg/cm(3)) was not significantly different in the two groups. CONCLUSION: Subclinical PAD induces a selective bone loss at the radius compartment, not identified by standard DXA, which seems to occur primarily at the cortical level.
UNLABELLED: The association between peripheral arterial disease (PAD) and low bone mass is controversial. In our study, peripheral quantitative computed tomography shows a reduction of cortical but not trabecular, bone mineral density (BMD) at the forearm, in patients with subclinical PAD. INTRODUCTION: Some controversy exists regarding the association between peripheral arterial disease (PAD) and low bone mass. Previous studies have evaluated bone mineral density (BMD) in patients with subclinical PAD, with mixed results. Inconsistency of data may depend on the fact that most studies measured areal bone mineral density (aBMD) by Dual-energy-x ray absorptiometry (DXA). Because DXA cannot distinguish between cortical and trabecular compartments, we reasoned that a study aimed to establish whether these compartments were differentially affected by PAD status could give more information on the nature of this association. METHODS: In this cross-sectional study, we used peripheral quantitative computed tomography (pQCT) to examine volumetric cortical and trabecular mineral density at the radius (vBMD) in a cohort of subjects with subclinical PAD as defined by ABI ≤0.90 and compared them with healthy subjects with no evidence of PAD. RESULTS:Patients with subclinical PAD had significantly reduced cortical density (1101.0 ± 45.4 vs 1156.2 ± 51.3 mg/cm(3), p < 0.001) and cortical area (75.0 ± 20.9 vs 99.9 ± 18.2 mm(2), p < 0.001) than healthy subjects. Trabecular density (178.1 ± 47.9 vs 165.8 ± 29.6 mg/cm(3)) was not significantly different in the two groups. CONCLUSION: Subclinical PAD induces a selective bone loss at the radius compartment, not identified by standard DXA, which seems to occur primarily at the cortical level.
Authors: M H Criqui; R D Langer; A Fronek; H S Feigelson; M R Klauber; T J McCann; D Browner Journal: N Engl J Med Date: 1992-02-06 Impact factor: 91.245
Authors: Yumie Rhee; Eun-Young Lee; Virginia Lezcano; Ana C Ronda; Keith W Condon; Matthew R Allen; Lilian I Plotkin; Teresita Bellido Journal: J Biol Chem Date: 2013-08-20 Impact factor: 5.157