A Boudenot1, N Presle2, R Uzbekov3, H Toumi4, S Pallu4, E Lespessailles5. 1. EA 4708 I3MTO, University of Orléans, Orléans, France. Electronic address: arnaud.boudenot@yahoo.fr. 2. UMR 7365 CNRS, Universite de Lorraine, Vandoeuvre-les-Nancy, France. 3. Department of Microscopy, University of Francois Rabelais, Tours, France. 4. EA 4708 I3MTO, University of Orléans, Orléans, France. 5. EA 4708 I3MTO, University of Orléans, Orléans, France; Service de rhumatologie, Centre hospitalier régional d'Orléans, Orléans, France.
Abstract
OBJECTIVES: The role of subchondral bone in osteoarthritis (OA) development is well admitted. Cross-talk between subchondral bone and cartilage may be disrupted in OA, leading to altered subchondral bone remodeling. Osteocytes are involved in bone remodeling control and could play a key role in OA progression. Our purpose of this study was to evaluate the preventive effect of interval-training exercise on subchondral bone and osteocyte in monosodium iodoacetate (MIA) model of experimental OA. METHODS: At baseline, 48 male Wistar rats (8 weeks old) were separated into two groups: interval-training exercise or no exercise for 10 weeks. After this training period, each group was divided into two subgroups: MIA-injected knee (1 mg/100 μl saline) and saline-injected knee. Four weeks later, rats were sacrificed and carefully dissected. Evaluated parameters were: cartilage degeneration by OA scoring, bone mineral density (BMD) by Dual energy X-ray Absorptiometry (DXA), trabecular subchondral bone microarchitecture by micro-computed tomography (μCT), cortical subchondral bone lacunar osteocyte occupancy (by Toluidine Blue staining) and cleaved caspase-3 positive apoptosis (by epifluorescence). RESULTS: Our results showed deleterious effects of MIA on cartilage. OA induced a decrease in proximal tibia (PT) BMD which was prevented by exercise. Exercise induced increase in full osteocyte lacunae surface and osteocyte occupancy (+60%) of cortical subchondral bone independently of OA. Osteocyte apoptosis (<1%) in cortical subchondral bone was not different whatever the group at sacrifice. CONCLUSION: Our results suggest that preliminary interval-training improved BMD and osteocytes lacunar occupancy in subchondral bone. Our interval-training did not prevent MIA-induced cartilage degeneration.
OBJECTIVES: The role of subchondral bone in osteoarthritis (OA) development is well admitted. Cross-talk between subchondral bone and cartilage may be disrupted in OA, leading to altered subchondral bone remodeling. Osteocytes are involved in bone remodeling control and could play a key role in OA progression. Our purpose of this study was to evaluate the preventive effect of interval-training exercise on subchondral bone and osteocyte in monosodium iodoacetate (MIA) model of experimental OA. METHODS: At baseline, 48 male Wistar rats (8 weeks old) were separated into two groups: interval-training exercise or no exercise for 10 weeks. After this training period, each group was divided into two subgroups: MIA-injected knee (1 mg/100 μl saline) and saline-injected knee. Four weeks later, rats were sacrificed and carefully dissected. Evaluated parameters were: cartilage degeneration by OA scoring, bone mineral density (BMD) by Dual energy X-ray Absorptiometry (DXA), trabecular subchondral bone microarchitecture by micro-computed tomography (μCT), cortical subchondral bone lacunar osteocyte occupancy (by Toluidine Blue staining) and cleaved caspase-3 positive apoptosis (by epifluorescence). RESULTS: Our results showed deleterious effects of MIA on cartilage. OA induced a decrease in proximal tibia (PT) BMD which was prevented by exercise. Exercise induced increase in full osteocyte lacunae surface and osteocyte occupancy (+60%) of cortical subchondral bone independently of OA. Osteocyte apoptosis (<1%) in cortical subchondral bone was not different whatever the group at sacrifice. CONCLUSION: Our results suggest that preliminary interval-training improved BMD and osteocytes lacunar occupancy in subchondral bone. Our interval-training did not prevent MIA-induced cartilage degeneration.
Authors: K E Chin; N P Karamchedu; T K Patel; G J Badger; M R Akelman; D C Moore; B L Proffen; M M Murray; B C Fleming Journal: J Biomech Date: 2016-08-24 Impact factor: 2.712
Authors: Sarah E Little-Letsinger; Janet Rubin; Brian Diekman; Clinton T Rubin; Cody McGrath; Gabriel M Pagnotti; Eric L Klett; Maya Styner Journal: Semin Cell Dev Biol Date: 2021-09-04 Impact factor: 7.727
Authors: M Horge; C Crãciun; S Tripon; D Giulei; A Jompan; A Hermenean; C Roşioru Journal: Acta Endocrinol (Buchar) Date: 2016 Oct-Dec Impact factor: 0.877