I am still working on finding a method to grow taller. A lot of it is self testing as not a lot of the published papers published lately show promise of non surgical longitudinal bone growth that I could see.
Mechanisms of synovial joint and articular cartilage development
“Articular cartilage is formed at the end of epiphyses in the synovial joint cavity and permanently contributes to the smooth movement of synovial joints. Most skeletal elements develop from transient cartilage by a biological process known as endochondral ossification. Accumulating evidence indicates that articular and growth plate cartilage are derived from different cell sources and that different molecules and signaling pathways regulate these two kinds of cartilage{Could we inject these cell sources into the articular cartilage? Could we mimic the molecules and signaling pathways with various stimuli?}. As the first sign of joint development, the interzone emerges at the presumptive joint site within a pre-cartilage tissue. After that, joint cavitation occurs in the center of the interzone, and the cells in the interzone and its surroundings gradually form articular cartilage and the synovial joint. During joint development, the interzone cells continuously migrate out to the epiphyseal cartilage and the surrounding cells influx into the joint region. These complicated phenomena are regulated by various molecules and signaling pathways, including GDF5, Wnt, IHH, PTHrP, BMP, TGF-β, and FGF. .”
“Matured articular cartilage is also referred to as hyaline cartilage because of its translucent appearance that reflects its unique constituents, such as type II collagen, glycosaminoglycans (GAGs), and low cellularity. In addition, articular cartilage does not have blood vessels, lymphatic vessels, or nerves. Articular chondrocytes produce extracellular matrices and maintain their environment with very little or no cell turnover{we want cell turnover, HGH increases cell turnover and HGH can make you very tall in certain circumstances}”
” most parts of articular cartilage derive from different lineages from the growth plate cartilage. The first signs of joint development are presented by the appearance of condensed flattened cells at the presumptive joint site within a pre-cartilage tissue known as the interzone, the origin of the joint. Removal of the interzone from a chick embryo leads to an uninterrupted long bone lacking joints, indicating that the interzone provides segmentation of skeletal elements in limbs. The interzone arises from mesenchymal/pre-cartilaginous tissue in which the cells initially express chondrocyte marker genes such as type II collagen, aggrecan, and matrillin-1 ”
“Instead of the decreased expression of these chondrogenic markers, the interzone cells acquire the expression of growth differentiation factor 5 (Gdf5), formerly known as bone morphogenetic protein 14 (BMP14), or cartilage derived morphogenetic protein 1 (CDMP1). Gdf5 is a representative marker for the interzone during early joint development. In addition to Gdf5, Wnt4, Wnt9a (formerly known as Wnt14), Wnt16, Erg, doublecortin, and Gli are also expressed in the interzone”
“Gdf5-expressing cell lineage gives rise to all mature joint structures including articular cartilage, meniscus, ligaments, and synovium ”
” joint components are formed by the integration of peripheral cells in joint development. Epiphyseal chondrocytes migrate into the interzone at early stages, and the external regions of joints such as the synovium/joint capsule and outer parts of the meniscus are mainly composed of lately integrated cells. Thus, the fate of embryonic interzone cells, the surrounding cells, and their progeny cells may be determined by their spatiotemporally environment. “<-so growth plate cells become integrated into the articular cartilage interzone cells but these cells are affected by the articular cartilage cells and microenvironment so that the articular cartilage overall environment is unaltered. Maybe we can do the reverse and make the articular cartilage more growth plate like…
“IHH is produced from pre-hypertrophic chondrocytes and up-regulates PTHrP expression in peri-articular chondrocytes. PTHrP inhibits the differentiation of proliferating chondrocytes into pre-hypertrophic chondrocytes. This feedback loop determines the length of long bones. Before the feedback loop, pre-hypertrophic chondrocytes around the center of anlagen are associated with interzone generation through the secretion of IHH. The loss of IHH causes not only dwarfism but also joint fusion in distal limb joints ”
“excessive IHH signaling activity in the interzone progeny induces ectopic cartilage formation in the knee ”
“Unlike in endochondral ossification, IHH and PTHrP seem to be independent in interzone generation and joint development. The genetic alteration of PTHrP causes the impairment of endochondral ossification, but no severe changes in joints. Even after IHH signaling becomes silent, PTHrP-expressing cells exist in articular cartilage over a lifetime. Recombinant human PTH (1–34) suppresses osteoarthritis development, and PTH/PTHrP signaling induces lubricin”<-Can we use this fact to become taller?
