Crispr is an exciting technology because of the DIY possibilities facilitated by website like The ODIN.  as far as I know there have been no instances of genetic doping.  Crispr on live adult humans is in exact.  You can only edit one gene at a time and the number of cells that are actually edited may be low.  There are still a number of potential targets:

1) general anabolic target like HGH,IGF1,IGF2.  This would make it easier to see gains in slow height increase.  Some bones like the jaw do have potential to grow naturally in adulthood.  As seen in people with acromegaly.  An anabolic target would allow us to see a height increase method that may take a year to yield results get results in a much shorter time frame.  Something like HGH also increases bone turnover since cortical bone may impede height increase this would be useful for height seekers.

2)  inject specifically in the articular cartilage.  since these cells are an isolated population pretty much this is a possible target.  Even if crispr only alters one cell if it results in massive ECM production that could lead to height increase due to ECM…you could also increase chondrocyte proliferation…  this would have to be tested on animal models first as you would want to know what kind of effects this is going to have… If your knee is overproducing ECM that could result in loss of knee function. if you have open growth plates injecting there is a possibility too but again we’d want to know what happens in animal models first as you could really mess up your growth plate.

3)  target the osteoclasts.  You could weaken the bone enough to allow growth.  Cortical bone inhibits bone from growing interstitially(from within) so if you degrade it you could allow for bone to now grow interstitially.  But this could really mess up your bone and Hgh already increases bone turnover.  .  And it would be hard to inject into the bone itself.

4) weaken ligaments and periosteum which may constrain growth again would have to be tested on animals first as you would have the potential to mess up your body.

5) target the marrow cavity.  You could potentially induce differentiation of stem cells within the marrow cavity.  This could create neo-growth plates.  It would be exceptionally hard to do this as a lot depends on the microenvironment of the cell.

There’s not a lot of potential for self test for CRISPR.  At most you could target one gene in contrast to a mechanical method which can alter many genes.  The best bet is a general anabolic as making a bone length increase faster would be a huge aid in testing.  However, there are likely already people trying to do this and I haven’t seen amazing results with myostatin(which does help for bone too).

The best bet for DIY CRISPR testing is on animals.  Experiments would have to be designed carefully to not go over budget.  Ideally though a ton of genes and methods would be targeted to see what sticks.

Here’s a paper on musculoskeletal applications of CRISPR technology.

” mouse RAW264 cells deleted for Zscan10 and differentiated into osteoclasts by RANKL”

“With orthopaedic tissues, the extracellular matrix also presents a significant barrier to deliverystimulation were found to have increased osteoclast activity.”

”

This study is about preventing bony bridge formation in response to growth plate injury but could it potentially be used in healthy children to prevent growth plate fusion in them?

Adipose-derived stromal vascular fraction prevent bone bridge formation on growth plate injury in rat (in vivo studies) an experimental research

“The growth plate is cartilage tissue found at the end of long bones in children, responsible for longitudinal bone growth. Injuries to the growth plate cartilage often lead to unwanted bony repair, resulting in growth disturbances such as limb length discrepancy and angulation deformity in children. There is currently no clinical treatment that can fully repair an injured growth plate. Tissue engineering is promising for regeneration of growth plate. Adipose-derived stromal vascular fraction highlight the promising potential as tissue engineering therapy for inducing regeneration of injured growth plate and able to reduce the formation of bony repair that can lead to deformity and limb length discrepancy. Using an animal model of growth plate injury, bone bridge formation is evaluated after 28 days using Enzyme-linked Immunoassay, radiology, histopathology and Immunofloresence examination. Radiological analyses performed by evaluation of grey value using ImageJ software and diameter bone bridge measured from the end to end distance between uninjured growth plate evaluated by histopatology examination. Enzyme-linked Immunoassay and immunofloresence are used to evaluate chondrocyte and chondrogenic marker within the defect. The result shows in group with Adipose-derived stromal vascular fraction have a significant lower bone bridge formation compare to positive control group. This current study represents the first work that has utilized this animal model to investigate whether Adipose-derived stromal vascular fraction can be used to initiate regeneration at the injured growth plate.”

“gene expression for IGF-I, TGF-β1, and FGF-2 was significantly higher in SVF[Stromal Vascular Fraction] cells than in cultured ASC. Those growth factor has main role in chondrogenesis. The effects of each growth factor to mesenchymal stem cell in chondrogenesis process are TGF-β1 Increases proliferation and ECM production also downregulates collagen type 1 gene expression; IGF-I Stimulates cell proliferation, increases expression of ECM, additive effect when combined with TGF-β1; Increases Proteoglycan synthesis and increases cell proliferation”

Bony bar formation in growth plate fracture.

Intervention group.

“The AD-SVF group within the defect show regeneration occurred, demonstrated by accumulation of immature chondrocyte that characterized by poorly bordered cell, round nuclei (basophilic) and outside of lacuna (yellow arrow). Matrix of growth plate with HE stained shows grey pale colour”

It’s hard to say whether such a treatment or similar will be promising for normal teens to preserve the growth plate to potentially grow taller.  I sent an email to Panji Sananta to ask such a question.