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.

Thus, during development it may be important to optimize your gut microbiome via possibly avoiding antibiotics, modifying diet, etc.  This also means that there is the possibility of modification of the microbiome via transfer, etc.  Although there doesn’t seem to be any clear degree of optimization as of yet.

The microbiome: A heritable contributor to bone morphology?

“Bone provides structure to the vertebrate body that allows for movement and mechanical stimuli that enable and the proper development of neighboring organs. Bone morphology and density is also highly heritable. In humans, heritability of bone mineral density has been estimated to be 50–80%. However, genome wide association studies have so far explained only 25% of the variation in bone mineral density, suggesting that a substantial portion of the heritability of bone mineral density may be due to environmental factors. Here we explore the idea that the gut microbiome is a heritable environmental factor that contributes to bone morphology and density. The vertebrae skeleton has evolved over the past ~500 million years in the presence of commensal microbial communities. The composition of the commensal microbial communities has co-evolved with the hosts resulting in species-specific microbial populations associated with vertebrate phylogeny. Furthermore, a substantial portion of the gut microbiome is acquired through familial transfer{so what the mother eats during pregenancy may affect a childs height}. Recent studies suggest that the gut microbiome also influences postnatal development. Here we review studies from the past decade in mice that have shown that the presence of the gut microbiome can influence postnatal bone growth regulating bone morphology and density. These studies indicate that the presence of the gut microbiome may increase longitudinal bone growth and appositional bone growth, resulting differences cortical bone morphology in long bones. More surprising, however are recent studies showing that transfer of the gut microbiota among inbred mouse strains with distinct bone phenotypes can alter postnatal development and adult bone morphology. Together these studies support the concept that the gut microbiome is a contributor to skeletal phenotype.”

“The majority of the mammalian microbiome is present in the gastrointestinal system. The mammalian gut microbiome consists of hundreds of distinct microbial species (bacteria, archea, viruses, single celled eukaryotes) interacting with one another and with host cells at the gut endothelial barrier. The body is first colonized by microbes soon after birth. Over the first few years of life the composition of the gut microbial community fluctuates considerably until achieving a relatively stable composition”

“The gut microbiome is also heritable: maternal transfer of the microbiome soon after birth is among the most influential contributors to the establishment of the gut microbiome; and later in life components of the gut microbiota are transferable through close contact such as that occurring within households and due to familial dietary habits. The composition of a mature gut microbiota can fluctuate on an hourly or daily basis due to variations in diet. However, the overall composition of an established gut microbiota are robust to perturbations; the vast majority of the microbial composition returns to its prior state following a mild or temporary perturbation. Hence, the composition of the gut microbiota is partially heritable and, once established, does not change substantially without a large or prolonged stimulus. That the gut microbiota is established at an early age suggests that heritable components of the gut microbiota may contribute to the patterns of bone mass accrual that determine adult bone morphology and density.”

“most bacteria associated with vertebrates reside in the gastrointestinal tract, where densities can reach ~10¹¹ cells per milliliter, yet relatively few of the constituents of this gut microbiota are known to cause disease in their hosts.”

“the composition of the gut microbiota can be influenced by environmental variation, including host diet, geography, and temperature ”

“transplantation of gut microbiota from Gairdner’s shrewmouse (Mus pahari) into germ-free house mice stunts host growth rate relative to transplantation of house-mouse gut microbiota”

“The ability of the gut microbiome to influence bone morphology has been recognized since the first animal studies of oral antibiotics in the 1920–30s which reported alterations in whole body growth as well as bone length and morphology following chronic oral antibiotic dosing”

According to Identifying Components of the Gut Microbiome that Regulate Bone Tissue Mechanical Properties, disruption in the gut microbione results in a femur length reduction.

“the absence or depletion of the gut microbiota, while potentially influencing the acquisition of trabecular bone at the growth plate, likely has little effect on the amounts of trabecular bone present at skeletal maturity.”

“Schwarzer and colleagues found that young (two month-old) germ-free mice were much smaller than conventionally raised mice in terms of whole body mass, whole body length, whole bone length and femoral cortical area”

“Yan and colleagues found that adult (10 month old) germ-free mice had smaller endosteal and periosteal diameter at the femur midshaft and shorter whole bone length in adulthood than mice that had been conventionalized at two months of age, in part leading to their conclusion that exposure to the gut microbiota leads to a net increase in bone acquisition during life. Guss and colleagues and Luna and colleagues found that disruption (but not decimation) of the gut microbiota in mice using narrow spectrum antibiotics from 1 to 4 months of age was associated with small but significant reductions in femur length “