Rogaine can make you taller?

Minoxidil is most commonly known as Rogaine(Minoxidil-5% Extra Strength Hair Regrowth for Men, 6 Month Supply-Not sure how effectively this could be absorbed by our target cells like this within the bone).  A recent post over at the grow tall forum stated that rogaine can be involved in a type of acromegaly called psuedoacromegaly. 

Pseudoacromegaly induced by the long-term use of minoxidil. 

"Acromegaly is an endocrine disorder caused by chronic excessive growth hormone secretion from the anterior pituitary gland. Significant disfiguring changes occur as a result of bone, cartilage, and soft tissue hypertrophy, including the thickening of the skin, coarsening of facial features, and cutis verticis gyrata{thickening of the scalp, the scalp contains a flat bone, it's like a long bone that's sideways so it's easier to increase height there}. Pseudoacromegaly, on the other hand, is the presence of similar acromegaloid features in the absence of elevated growth hormone or insulin-like growth factor levels. A patient with pseudoacromegaly resulted from the long-term use of minoxidil at an unusually high dose." 

"Bone and cartilage changes pri-marily affect the face and skull. The calvaria thickens, and the frontal sinuses enlarge, which leads toprominent supraorbital ridges. Anterior and inferior growth of the mandible results in prognathism and widely spaced teeth."

Minoxidil may increase growth by increasing the deposition of GAG molecules.

"IGF-1 and GH levels along with radiographs of the chest and long bones (femora andhumeri) were all normal"

First, Acromegaly is not necessarily caused by excessive growth hormone as the effectiveness of growth hormone is based on the number of growth hormone receptors. Also, it's only one patient so it could just be a coincidence.  Also, the patient didn't really have any effects on bones only skin but that could be because only the skin cells could absorb the rogaine.  It could help us grow taller though if minoxidil had anabolic affects on chondrocytes, osteoblasts, or stem cells.  There doesn't seem to be a whole lot of new studies on minoxidil and bone but there are relevant studies that could be key in relating minoxidil(Rogaine) and height growth. 

Use of minoxidil to demonstrate that prostacyclin is not the mediator of bone resorption stimulated by growth factors in mouse calvariae. 

"Growth factors, such as human transforming growth factor-alpha (hTGF alpha) and epidermal growth factor, as well as human tumor necrosis factor (hTNF) stimulate the resorption of bone in neonatal mouse calvariae in organ culture via a prostaglandin (PG)-mediated pathway. In response to such factors mouse calvariae produce substantial quantities of prostaglandin E2 (PGE2) and prostacyclin (PGI2). We have selectively inhibited the production of PGI2, but not PGE2, using the drug minoxidil and have measured the effects on stimulated bone resportion and arachidonic acid metabolism. The increased production of 6-keto-PGF1 alpha (6k-PGF1 alpha), the hydrolytic product of PGI2, stimulated by recombinant hTGF alpha and hTNF as well as murine epidermal growth factor was inhibited by minoxidil. There was no inhibition by minoxidil of PGE2 production. Despite essentially complete inhibition of stimulated 6k-PGF1 alpha formation, there was no inhibition of bone resorption. The possibility was investigated that growth factors and TNF enhanced enzymatic conversion of PGI2 to 6k-PGE1, which stimulates bone resorption in mouse calvariae with a potency about one fourth that of PGE2. Enzymatic conversion of PGI2 to 6k-PGE1 is inhibited by rutin. Rutin did not inhibit bone resorption stimulated by hTGF alpha or hTNF.  The cyclooxygenase product that acts as the mediator of bone resorption enhanced by growth factors and TNF in mouse calvariae is probably PGE2." 

"Even concentrations of minoxidil as high as 500 micromillimeters had no inhibitory effect on PGE2 production by mouse bone, although there was complete inhibition of 6k- PGF1a production enhanced by hTGFa"

So Minodixil inhibits PGI2.  Can inhibiting PGI2 affect height growth?  

Immunohistochemical detection of prostaglandin I2 synthase in various calcified tissue-forming cells in rat. 

"Localization of prostaglandin (PG) I2 synthase immunoreactivity was examined in demineralized sections of rat pulpal, periodontal and skeletal tissues using isn-1, a monoclonal antibody raised against the enzyme. chondrocytes were immunoreactive for PGI2 synthase suggesting that they are capable of producing PGI2. In odontoblasts and chondrocytes, the reactivity increased gradually with maturation{PGI2 could play a role is ossification}.  PGI2 [may regulate] the metabolism of various calcified tissues." 

"PGE, and PGI2, are the major metabolites produced by cultured chondrocytes"

Since chondrocytes become more sensitive to PGI2 as they mature(undergo endochondral ossification) it is logical to think that maybe PGI2 plays a role in terminal differentiation. 

Prostacyclin IP receptor up-regulates the early expression of C/EBPbeta and C/EBPdelta in preadipose cells. 

"Prostacyclin (PGI(2)) and its stable analogue carbacyclin (cPGI(2)) are known to trigger the protein kinase A pathway after binding to the cell surface IP receptor and to promote or enhance terminal differentiation of adipose precursor cells to adipose cells[PGI2 is involved in terminal differentiation albeit for adipose cells]. The early expression of C/EBPbeta and C/EBPdelta is known to be critical for adipocyte differentiation in vitro as well as in vivo. We report herein that in Ob1771 and 3T3-F442A preadipose cells, activation of the IP receptor by specific agonists (PGI(2), cPGI(2) and BMY 45778) is sufficient to up-regulate rapidly the expression of C/EBPbeta and C/EBPdelta. Cyclic AMP-elevating agents are able to substitute for IP receptor agonists, in agreement with the coupling of IP receptor to adenylate cyclase. Consistent with the fact that PGI(2) is released from preadipose cells and behaves as a paracrine/autocrine effector of adipose cell differentiation, the present results favor a key role of prostacyclin by means of the IP receptor and its intracellular signaling pathway in eliciting the critical early expression of both transcription factors." 

PGI2 is involved in the early expression of transcription factors that may promote terminal differentiation.  Again this is for adiposal cells(there are no studies linking PGI2 and chondrocytes) but it is logical to think that there may be a similar link between PGI2 and terminal differentiation in chondrocytes.   But here's a study about bone and PGI2(prostacyclin). 

Increased bone mass in adult prostacyclin-deficient mice. 

"Prostaglandins (PGs) are key regulatory factors that affect bone metabolism. Prostaglandin E(2) (PGE(2)) regulates bone resorption and bone formation. Prostacyclin (PGI(2)) is one of the major products derived from arachidonic acid by the action of cyclooxygenase and PGI(2) synthase (PGIS). Unlike PGE(2), there are few reports about the role of PGI(2) in bone regulation. We used PGIS knockout (PGIS(-/-)), PGIS heterozygous (PGIS(+)(/-)), and wild-type mice to investigate the role of PGI(2). PGIS(-/-) mice gradually displayed an increase in trabecular bone mass in adolescence. Adult PGIS(-/-) mice showed an increase in trabecular bone volume/tissue volume. PGIS(-/-) mice displayed increases in both bone formation and bone resorption parameters. Levels of serum osteocalcin and C-telopeptides were increased in adult PGIS(-/-) mice. The increased bone mass patterns were rescued in PGIS(-)/(tg) mice. Adult PGIS(-/-) mice displayed an overall increase in the levels of both bone formation and bone resorption parameters, which suggests that PGI(2) deficiency accelerates high bone turnover activity with a greater increase in bone mass in aging. PGI(2) may contribute to the maintenance of normal bone mass and micro-architecture in mice in age-dependent manner." 

Inhibiting PGI2 via Minoxidil definitely increases bone density.  It also increases serum osteocalcin(which increases bone formation) and C-telopeptides(basically collagen).  This alone doesn't seem like it would increase height but it shows that inhibiting PGI2 is anabolic. 

"Prostacyclin (PGI2), a product converted by COXs and PGI2 synthase (PGIS), up-regulates cAMP levels through the activation of a PGI2 receptor"

"Resident bone cells; osteoblasts and osteocytes, can produce both PGE2 and PGI2 under mechanical loading"

Interestingly, younger PGIS null mice had lower bone mass than controls but eventually had high higher bone mass.

The increase in bone turnover alone explains the psuedoacromegaly case.  However, it is possible that minoxidil mediated inhibition of PGI2 may help to increase height by slowing down terminal differentiation of chondrocytes.