title: Low-intensity electrical stimulation counteracts the effects of ovariectomy on bone tissue of rats: effects on bone microarchitecture, viability of osteocytes, and nitric oxide expression.
abstract: Low Intensity Electrical Stimulation (LIES) has been used for bone repair, but little is known about its effects on bone after menopause. Osteocytes probably play a role in mediating this physical stimulus and they could act as transducers through the release of biochemical signals, such as nitric oxide (NO). The aim of the present study was to investigate the effects of LIES on bone structure and remodeling, NOS expression and osteocyte viability in ovariectomized (OVX) rats. Thirty rats (200-220 g) were divided into 3 groups: SHAM, OVX, and OVX subjected to LIES (OVX + LIES) for 12 weeks. Following the protocol, rats were sacrificed and tibias were collected for histomorphometric analysis and immunohistochemical detection of endothelial NO synthase (eNOS), inducible NOS (iNOS), and osteocyte apoptosis (caspase-3 and TUNEL). OVX rats showed significant (p < 0.05 vs. SHAM) decreased bone volume (10% vs. 25%) and trabecular number (1.7 vs. 3.9), and increased eroded surfaces (4.7% vs. 3.2%) and mineralization surfaces (15.9% vs. 7.7%). In contrast, after LIES, all these parameters were significantly different from OVX but not different from SHAM. eNOS and iNOS were similarly expressed in subperiosteal regions of tibiae cortices of SHAM, not expressed in OVX, and similarly expressed in OVX + LIES when compared to SHAM. In OVX, the percentage of apoptotic osteocytes (24%) was significantly increased when compared to SHAM (11%) and OVX + LIES (8%). Our results suggest that LIES counteracts some effects of OVX on bone tissue preserving bone structure and microarchitecture, iNOS and eNOS expression, and osteocyte viability.
authors.affiliation: INSERM Unité 831, Faculté de Médecine R. T. H. Laënnec, Université de Lyon, rue G. Paradin, Lyon Cedex 08, France. analirani@fcr.epm.br
authors.forename: A P R
authors.initials: AP
authors.lastname: Lirani-Galvão
authors.forename: P
authors.initials: P
authors.lastname: Chavassieux
authors.forename: N
authors.initials: N
authors.lastname: Portero-Muzy
authors.forename: C T
authors.initials: CT
authors.lastname: Bergamaschi
authors.forename: O L
authors.initials: OL
authors.lastname: Silva
authors.forename: A B
authors.initials: AB
authors.lastname: Carvalho
authors.forename: M
authors.initials: M
authors.lastname: Lazaretti-Castro
authors.forename: P D
authors.initials: PD
authors.lastname: Delmas
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001842:Bone and Bones / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival / Q000502:physiology; D004599:Electric Stimulation Therapy; D005260:Female; D008593:Menopause; D009569:Nitric Oxide / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010011:Osteocytes / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D010052:Ovariectomy; D051381:Rats; D017208:Rats, Wistar; D013977:Tibia / Q000166:cytology / Q000502:physiology
chemical_list: D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; D053148:Caspase 3