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Less of a guide more of my bone growth threads thrown together
Recent discussion in the literature has placed a great deal of emphasis on the role of human growth hormone in the development of skeletal structures and its possible implications for craniofacial development. The skeletal morphology is, however, not dominated by HGH alone. Kartogenin is one such small molecule that attracts much attention due to its stimulating effect on chondrogenesis, guiding mesenchymal stem cells toward chondrocytic lineage commitment. This does not follow the classical route of osteoblast differentiation but instead supports endochondral ossification the cartilage to bone transition. (Dont take if epiphyseal plates aren't fused)
Kartogenin acts via the filamin A-CbFβ-RUNX1 signaling pathway, a cascade implicated in extracellular matrix turnover and cartilage maturation. While not osteoanabolic like parathyroid hormone analogues or growth hormone, it is of potential value as a mediator of endochondral bone formation by virtue of its regulatory effects on matrix remodeling.
In the context of aesthetic skeletal modification, such as attempts at facial remodeling, kartogenin represents a theoretical pharmacological means of affecting local structural development. When associated with targeted mechanical loading and other osteogenic stimuli, this could lead to subtle alterations in bone architecture, improving facial symmetry and better supporting structures such as the mandible and nasal framework. However, it seems that systemic administration is inefficient based on current literature. Most studies indicate that, to reach significant biological activity within the target tissue, a localized delivery is required.
Overall, kartogenin presents a very compelling direction for future research in pharmacologically driven modulation of craniofacial structures. Its ability to modulate chondrocyte differentiation and extracellular matrix dynamics positions it as a potential component of the next generation of interventions targeted at influencing bone morphology and aesthetic outcomes.
Kartogenin acts via the filamin A-CbFβ-RUNX1 signaling pathway, a cascade implicated in extracellular matrix turnover and cartilage maturation. While not osteoanabolic like parathyroid hormone analogues or growth hormone, it is of potential value as a mediator of endochondral bone formation by virtue of its regulatory effects on matrix remodeling.
In the context of aesthetic skeletal modification, such as attempts at facial remodeling, kartogenin represents a theoretical pharmacological means of affecting local structural development. When associated with targeted mechanical loading and other osteogenic stimuli, this could lead to subtle alterations in bone architecture, improving facial symmetry and better supporting structures such as the mandible and nasal framework. However, it seems that systemic administration is inefficient based on current literature. Most studies indicate that, to reach significant biological activity within the target tissue, a localized delivery is required.
Overall, kartogenin presents a very compelling direction for future research in pharmacologically driven modulation of craniofacial structures. Its ability to modulate chondrocyte differentiation and extracellular matrix dynamics positions it as a potential component of the next generation of interventions targeted at influencing bone morphology and aesthetic outcomes.
Does bone smashing actually work? Bone smashing is the act of using a mechanical force to induce a piezoelectric microstrain response in the bone, which will theoretically respond to the load with remodelling. There are several different techniques that people use for this, including the infamous baseball trophy, as well as a lot of speculation on whether it actually works or if it will just deform you.
New evidence suggests that it is not just the act of bone smashing, it is that combined with anabolics that can provide a window of opportunity for bone remodeling. Because after all, if you hit yourself in the face and cause deformity in your bones, your bones will just try and remodel in the exact same shape they were before.
However, androgens and peptides change the way that genes express themselves in the human body, and this might give us an anabolic window that we can utilise. We can logically deduce that if we extrapolate from the concept of distraction osteogenesis, which is where bones are broken and a gap is formed and filled with bone, we might be able to get the same effect with microfractures.
However, without a consistent mechanical load and the combination of anabolics, this is likely not to work on its own.
New evidence suggests that it is not just the act of bone smashing, it is that combined with anabolics that can provide a window of opportunity for bone remodeling. Because after all, if you hit yourself in the face and cause deformity in your bones, your bones will just try and remodel in the exact same shape they were before.
However, androgens and peptides change the way that genes express themselves in the human body, and this might give us an anabolic window that we can utilise. We can logically deduce that if we extrapolate from the concept of distraction osteogenesis, which is where bones are broken and a gap is formed and filled with bone, we might be able to get the same effect with microfractures.
However, without a consistent mechanical load and the combination of anabolics, this is likely not to work on its own.
What is romosozumab, and how could it potentially induce bone growth and make you taller?
Romosozumab is a sclerostin inhibitor that activates the Wnt signalling pathway for bone formation. This is an FDA approved treatment for osteoporosis, rapidly growing bone.
Romosozumab has a short, high-gain anabolic window—mechanistically and clinically. That is why it's the front-end agent in a stack meant to form and subsequently preserve new bone after mechanical stimulus. For our purposes, we’re talking about jumping, bone-smashing, LSJL, or banded sleeping.
Transition to alendronate or denosumab after romosozumab to preserve new geometry. In a Phase 1b study, trabecular bone mass, density, and stiffness (i.e., anti-resorption) was up-regulated by 26.9% in men after three months of treatment.
This dual action of up-regulating bone formation while simultaneously decreasing resorption makes it incredibly unique when compared to other agents like PTH analogues. Heightmaxing and bone growth protocols are always experimental, but this compound might be the key puzzle piece in the stack.
Romosozumab is a sclerostin inhibitor that activates the Wnt signalling pathway for bone formation. This is an FDA approved treatment for osteoporosis, rapidly growing bone.
Romosozumab has a short, high-gain anabolic window—mechanistically and clinically. That is why it's the front-end agent in a stack meant to form and subsequently preserve new bone after mechanical stimulus. For our purposes, we’re talking about jumping, bone-smashing, LSJL, or banded sleeping.
Transition to alendronate or denosumab after romosozumab to preserve new geometry. In a Phase 1b study, trabecular bone mass, density, and stiffness (i.e., anti-resorption) was up-regulated by 26.9% in men after three months of treatment.
This dual action of up-regulating bone formation while simultaneously decreasing resorption makes it incredibly unique when compared to other agents like PTH analogues. Heightmaxing and bone growth protocols are always experimental, but this compound might be the key puzzle piece in the stack.
Most people have heard of HGH and IGF-1 for increasing bone mass and potentially influencing height, but far fewer talk about PTH analogues. These compounds are designed to mimic parathyroid hormone and are typically used to treat osteoporosis, support bone resorption, and increase bone mass. Recent animal studies suggest that PTH1R agonists can enhance mandibular growth. Both abaloparatide and teriparatide have been shown to upregulate chondrogenic markers such as Sox9 and collagen II.
The interesting aspect of PTH1R agonists is that even if the facial sutures are closed, it may still be possible to see periosteal growth in the mandibular ramus and the chin. This could contribute to a wider jaw and an improved facial profile. There is evidence indicating that the mandibular condyle cartilage contains progenitor cells and proliferative layers capable of undergoing growth after adolescence.
The interesting aspect of PTH1R agonists is that even if the facial sutures are closed, it may still be possible to see periosteal growth in the mandibular ramus and the chin. This could contribute to a wider jaw and an improved facial profile. There is evidence indicating that the mandibular condyle cartilage contains progenitor cells and proliferative layers capable of undergoing growth after adolescence.
Sclerostin neutralization has become a key strategy for amplifying osteoanabolic signaling through the release of the canonical Wnt/β-catenin pathway from its usual tonic inhibition. Under normal conditions, SOST, mainly derived from osteocytes, restricts osteoblast differentiation and matrix production. The neutralization of it removes this brake, driving sustained Wnt activation that accelerates osteoblastogenesis and indirectly suppresses osteoclastic resorption through signals such as increased osteoprotegerin. In animal models, anti-SOST therapy rapidly increases both trabecular and cortical mass, improves microarchitecture, and strengthens mechanical properties as a consequence of brief uncoupling of remodeling in favor of formation.
These mechanistic observations are reinforced by clinical studies in which monoclonal antibodies against sclerostin sharply raise bone formation markers, enhance periosteal apposition, and strengthen axial and appendicular sites. The response follows a characteristic pattern: an early modeling-based surge, followed by a steadier remodeling-driven phase. The net effect of this shift is to reshape bone toward a more youthful state, with higher mineralizing surface and reduced cortical porosity. Cumulatively, these data position SOST inhibition as a powerful means of reawakening skeletal plasticity and expanding the therapeutic toolkit for disorders of low bone mass.
These mechanistic observations are reinforced by clinical studies in which monoclonal antibodies against sclerostin sharply raise bone formation markers, enhance periosteal apposition, and strengthen axial and appendicular sites. The response follows a characteristic pattern: an early modeling-based surge, followed by a steadier remodeling-driven phase. The net effect of this shift is to reshape bone toward a more youthful state, with higher mineralizing surface and reduced cortical porosity. Cumulatively, these data position SOST inhibition as a powerful means of reawakening skeletal plasticity and expanding the therapeutic toolkit for disorders of low bone mass.
you got me haha
