Me: This study is one of those studies which make me believe that the LSJL method may actually indeed work in causing some form of long bone lengthening. Sure, there are some obvious clear differences between the two ideas. The biggest one is that while this study involved axial compression on the long bone, the LSJL loading method involved loading and compression in a lateral direction. Right off the bat the researchers admit that with again, the skeleton lose its ability to respond to mechanical stimuli, so at least they get that quick rebuttal in theory arguement taken care of. They are hypothesizing that the loading would be less responsive but we already know that (so why are they doing this experiment??). From both the aged and young mice, if we load on the mid diaphysis area of the long bones, there is an analbolic response from the periosteal side (outside layer) and the endocortical side (inside layer). They say that with increase peak force, the bone formation was higher. Apparently aged mice had a far bigger response to the loading than young mice at least for the endocortical (inside) layer which surprised the researchers. The results…”Responses at the periosteal surface did not differ between age groups (p > .05). The loading-induced increase in bone formation resulted in increased cortical area in both age groups (loaded versus control, p < .05).” They conclude with..”In summary, 1 week of daily tibial compression stimulated a robust endocortical and periosteal bone-formation response at the mid-diaphysis in both young-adult and aged male BALB/c mice. We conclude that aging does not limit the short-term anabolic response of cortical bone to mechanical stimulation in our animal model.
Implications: This does make me wonder whether LSJL might really do work since we can use a thought experiment (like how einstein used to do). Let’s imagine that the long bone is surrounding by some thicker layer of cortical bone even in the epiphysis. If the compression at a axial direction on the middle diaphysis area results in the same rate of periosteal growth in both aged and young mice, then the compression of the epiphysis may actually in crease bone lengthening because the periosteum wraps around the entire long bone and even underneath the articular cartilage of the. The loading of the epiphysis would lead the bones to react by causing the peristeal layer to grow appositionally on the epiphysis which means that the axial ends do indeed get thicker and thicker which means the bones really do get longer so height is increased. Age seems to have no effect in decreased bone sensitivity, at least for the initial beginning loading. It might be that what you do from the beginning of LSJL program is what can result in the most bone/ periosteal growth lengthening, or at least until you might stop doing it for a while and go back to it a few weeks later allowing for the bone sensitivity to come back, if it ever truly do.
From PubMed study link HERE…
J Bone Miner Res. 2010 Sep;25(9):2006-15.
Aged mice have enhanced endocortical response and normal periosteal response compared with young-adult mice following 1 week of axial tibial compression.
Department of Orthopaedic Surgery, Washington University, School of Medicine, St Louis, MO 63110, USA.
With aging, the skeleton may lose its ability to respond to positive mechanical stimuli. We hypothesized that aged mice are less responsive to loading than young-adult mice. We subjected aged (22 months) and young-adult (7 months) BALB/c male mice to daily bouts of axial tibial compression for 1 week and evaluated cortical and trabecular responses using micro-computed tomography (µCT) and dynamic histomorphometry. The right legs of 95 mice were loaded for 60 rest-inserted cycles per day to 8, 10, or 12 N peak force (generating mid-diaphyseal strains of 900 to 1900 µε endocortically and 1400 to 3100 µε periosteally). At the mid-diaphysis, mice from both age groups showed a strong anabolic response on the endocortex (Ec) and periosteum (Ps) [Ec.MS/BS and Ps.MS/BS: loaded (right) versus control (left), p < .05]. Generally, bone formation increased with increasing peak force. At the endocortical surface, contrary to our hypothesis, aged mice had a significantly greater response to loading than young-adult mice (Ec.MS/BS and Ec.BFR/BS: 22 months versus 7 months, p < .001). Responses at the periosteal surface did not differ between age groups (p > .05). The loading-induced increase in bone formation resulted in increased cortical area in both age groups (loaded versus control, p < .05). In contrast to the strong cortical response, loading only weakly stimulated trabecular bone formation. Serial (in vivo) µCT examinations at the proximal metaphysis revealed that loading caused a loss of trabecular bone in 7-month-old mice, whereas it appeared to prevent bone loss in 22-month-old mice. In summary, 1 week of daily tibial compression stimulated a robust endocortical and periosteal bone-formation response at the mid-diaphysis in both young-adult and aged male BALB/c mice. We conclude that aging does not limit the short-term anabolic response of cortical bone to mechanical stimulation in our animal model.
© 2010 American Society for Bone and Mineral Research.
- PMID: 20499381 [PubMed – indexed for MEDLINE]
- PMCID: PMC3153404