I’m not sure how this can be applied in practice but since periosteum is on the surface of the bone and it is easier to stimulate the surface of the bone than the interior of the bone this could have some practical implications. For example, a foam roller could be used to stimulate the periosteum.
Periosteal stem cells control growth plate stem cells during postnatal skeletal growth
“The ontogeny and fate of stem cells have been extensively investigated by lineage-tracing approaches. At distinct anatomical sites, bone tissue harbors multiple types of skeletal stem cells, which may independently supply osteogenic cells in a site-specific manner. Periosteal stem cells (PSCs) and growth plate resting zone stem cells (RZSCs) critically contribute to intramembranous and endochondral bone formation, respectively. However, it remains unclear whether there is functional crosstalk between these two types of skeletal stem cells. Here we show PSCs are not only required for intramembranous bone formation, but also for the growth plate maintenance and prolonged longitudinal bone growth. Mice deficient in PSCs display progressive defects in intramembranous and endochondral bone formation, the latter of which is caused by a deficiency in PSC-derived Indian hedgehog (Ihh). PSC-specific deletion of Ihh impairs the maintenance of the RZSCs, leading to a severe defect in endochondral bone formation in postnatal life. Thus, crosstalk between periosteal and growth plate stem cells is essential for post-developmental skeletal growth.”
“After four weeks of the PSC deletion, the mice exhibited an impaired periosteal bone formation with a compensatory increase in endosteal bone formation”<-this is interesting as it means that the bone compensates in growth in a mechanism in which it is not impaired.
“Ihh was among the genes highly specific to PSCs and is known to be involved in the regulation of endochondral bone formation”<-so then an interesting study would be to compensated for PSC deletion via increasing IHH levels and see how much that rescues the impaired bone formation of the PSC deletion phenotype. According to the study osteoclasts were not impacted so we know that inability to remodel is not one of the factors.
“During development, growth plate-derived Ihh acts on cells in the periosteum/perichondrium, leading to the activation of PTHrP expression in the periarticular chondrocytes through a poorly understood mechanism. PTHrP then maintains chondrocytes in a proliferative, less differentiated state and inhibits the production of Ihh from the growth plate. This Ihh/PTHrP loop coordinates the synchronized chondrocyte differentiation in the growth plate during early life stages”<-manipulation of IHH-PTHrP production may be able to manipulate height but it is unlikely to totally be able to do it due to other factors like for example of other nutrients required for the growth plate to grow and eventually the cells will no longer be able to divide due to things like methylation and telomeres etc.