Can Height be Increased with Ultrasound?

Height cannot be increased(with some exceptions like stretching the type I collagen fibers) in the long bones unless you cause the differentiation of mesenchymal stems within the epiphysis into chondrocytes.  However, if Ultrasound treatment can affect stem cell proliferation + differentiation or chondrocytes proliferation or differentiation it can augment either natural growth or growth that has occurred once you cause the differentiation of mesenchymal stem cells into chondrocytes.

Comparative study of the effects of low-intensity pulsed ultrasound and low-level laser therapy on bone defects in tibias of rats. 

"[We] compare the effects of low intensity ultra-sound (LIPUS) and low-level laser therapy (LLLT) during the process of bone healing. The animals were randomly distributed into three groups of 30 animals each: the control group (bone defect without treatment); the laser-treated group: (bone defect treated with laser), and the LIPUS-treated (bone defect treated with ultrasound). Each group was further divided into three different subgroups (n = 10) and on days 7, 13, and 25 post-injury. The rats were treated with a 30-mW/cm(2) low-intensity pulsed ultrasound and a 830-nm laser at 50 J/cm(2). [There was] intense new bone formation surrounded by highly vascularized connective tissue presenting a slight osteogenic activity, with primary bone deposition being observed in the group exposed to laser in the intermediary (13 days) and late stages of repair (25 days). No remarkable differences were noticed in the specimens treated with ultrasound with regard to the amount of newly formed bone in comparison to the control group.  laser therapy improves bone repair in rats mainly at the late stages of recovery. [Laser] therapy was more effective than US to accelerate bone healing." 

This study doesn't seem to indicate a direct benefit of ultrasound on chondrogenesis.   As for the laser, maybe a laser pointer would be sufficient if it was able to to directly target the cell.  A laser might be effective at altering the biophotons stored within intracellular DNA causing up- and down-regulation of height growth genes.

"Low-intensity pulsed ultrasound (LIPUS) is a form of mechanical energy that is transmitted through and into living tissue as acoustic pressure waves."-This pressure may be able to generate sufficient hydrostatic pressure to cause height growth but in the watts typically available.  Also it's unlikely you'll be able to perform LSJL and LIPUS at the same time.  Although it may help you grow taller the perform LIPUS at some other region of the bone.  But any time you could do that then it would in turn be better to clamp that part of the bone than to perform LIPUS on it.

" LIPUS is able to increase prostaglandin E2 (PGE2) production via the induction of cyclooxygenase-2 (COX-2)[PGE2 does have inflammatory effects but it increases levels of Type II Collagen and intracellular cAMP levels which are anabolic to chondrocytes] in a mouse osteoblastic cell line to induce the transient expression of the immediate–early response gene c-Fos and to elevate gene expression for bone sialoprotein (BSP), insulin-like growth factor-1 (IGF-1), and osteocalcin (OC), to up-regulate the expression of early response genes (c-jun, c-myc, COX-2, Egr-1, TSC-22) as well as the bone differentiation marker genes osteonectin and osteopontin"<-PGE2 production in osteoblastic cells may indirectly increase height via increased type II collagen levels.

" LLLT is capable of increasing mitochondrial activity, osteoblast DNA and RNA synthesis, bone nodule formation, osteocalcin and osteopontin gene expression and ALP activity, increasing osteoblast proliferation"<-so basically Lasers make everything go faster but doesn't seem to initiate new activity on it's own although lasers also increase COX2 levels which may indirectly benefit chondrocytes.

Ultrasound-induced activation of Wnt signaling in human MG-63 osteoblastic cells. 

"The canonical Wnt signaling pathway has been recognized as one of the essential regulators of osteoblastogenesis and bone mass. Mechanical loading and fluid shear stress have been reported to activate the canonical Wnt signaling pathway in bone cells[but you still need hydrostatic pressure to induce chondrogenesis in MSCs]. activation of Wnt signaling pathway was assayed in human osteoblastic cells, and indeed, this pathway was found to be activated in MG-63 cells through the phosphoinositol 3-kinase/Akt (PI3K/Akt) and mTOR cascades following a single 10min US exposure (2W, 1.035MHz). the Wnt pathway activation was observed as nuclear localization of beta-catenin. Wnt activation showed temperature dependence at elevated temperatures, and the expression of canonical Wnt ligands was induced under the thermal exposures. existence of a specific, non-thermal US component was evident as well. Neither US nor heat exposures affected cell viability in our experiments. Wnt signaling cascade is one of the pathways activated by therapeutic US as well as by hyperthermia in human osteoblastic cells. " 

Regular stem cells are likely to be stimulated by the PI3K pathway as well which would help you grow taller once you've initiated chondrogenesis.

" the expression of transforming growth factor-β, a protein known to have a role in bone growth and repair, is regulated by US"<-TGF-Beta is also a compound very helpful for inducing chondrogenesis and chondrogenic differentiation.

"activation of Wnt pathway involves the formation of complex between the Wnt ligand, membrane receptor Frizzled, and low density lipoprotein receptor-related protein 5/6 co-receptors. This event results in stabilization, cytosolic accumulation, and nuclear import of β-catenin. In the nucleus, β-catenin forms a complex with members of the T-cell factor/Lymphoid enhancer binding factor family (TCF/LEF) and regulates the expression of Wnt-responsive genes."<-Wnt allows for the activation of Beta-Catenin and this allows for the upregulation of certain genes.  So Beta-Catenin could play a limiting factor if there is less Beta-Catenin available(due to compounds like GSK-3Beta) then there is binding factors.  So if you are in puberty and short stature is being caused by inactivation of Beta-Catenin then Ultrasound could help you grow taller.

"Wnt target genes have been reported to be up-regulated to a greater extent by mechanical loading when the canonical Wnt pathway was activated by addition of Wnt ligand Wnt3A or by inhibiting GSK3β with LiCl[Lithium Chonloride]"

"the highest US intensity P5 (407 mW/cm2) was found to be the most efficient, which is in contrast to many previous studies showing the best results with lower intensities, ranging from 30 to 50 mW/cm2"<-This is within the range of what you can get from for sale ultrasound machines.  For example, one has a maximum setting of 4.6 W which is about 4,600 mW.

"Some rounding was observed at higher temperatures[note this is osteoblastic cell line not Mesenchymal Stem cells], but stimulation of Wnt activity was evident also at lower temperature conditions where cells showed regular morphology[Elevated temperature may help induce chondrogenesis within LSJL]. Furthermore, also hydrostatic pressure has been reported to cause cell rounding[it may be this cell rounding that encourages mesenchymal stem cell chondrogenesis], but not cell death in MG-63 cells, while during recovery, these cells flattened[so the cells dedifferentiated]. In our experiments, also Hsp70 was induced at elevated temperatures, indicating a normal stress response of the cells. In addition, the Wnt induction was not related to cell detachment or lysis as observed in experiments with another, 100-times longer, pulsing sequence."<-So there are signs that Ultrasound can induce hydrostatic pressure but not enough to maintain a chondrogenic lineage.  Of course, it may be that the cell line was osteoblastic that caused the dedifferentiation not a failure of ultrasound to preserve a chondrogenic lineage.

Low-intensity pulsed ultrasound stimulation of condylar growth in rats. 

"low-intensity pulsed ultrasound (LIPUS) [was applied to] mandibular condylar cartilage. 
Thirty-five 20-day-old Sprague-Dawley rats were assigned to experimental and control groups. Experimental rats were stimulated with LIPUS in the temporomandibular joint (TMJ) region unilaterally, for 10 or 20 minutes for 20 days. After euthanasia, histological specimens were analyzed qualitatively and histomorphometrically at the anterior and posterior aspects of the mandibular condyle, including the condylar cartilage and the area and perimeter of subchondral bony trabeculae. 
LIPUS stimulation may alter the histological arrangement of the condylar bone and cartilage, showing qualitative differences on specimens treated for 10 or 20 minutes daily compared with controls. Cartilaginous layer thickness was not affected by LIPUS stimulation to a significant level, but was modified at the relative layer thickness within the cartilage at the anterior aspect of the condyle. At the subchondral bone level, 20-minute stimulation significantly increases trabecular perimeter. 
LIPUS application may affect mandibular growth pattern in rats acting at the cartilage and bone level. The effect of LIPUS on the growing condyle is expressed through a variation in trabecular shape and perimeter. A greater response is achieved when stimulated for 20 minutes instead of 10 minutes daily." 

The 10 minute ultrasound group however had a larger degree of increase in the proliferative zone than the maturation zone.  We are looking to stimulate chondrocytes not trabecular bone formation.  However, the 20 minute group had a larger maturation zone period.  So maybe, up to a certain point ultrasound can stimulate new growth but after a certain duration like 10 minutes it only encourages growth to occur faster.   

"LIPUS (30 mW/cm2, 1.5 MHz) on the temporomandibular joint (TMJ) region of growing rabbits and baboon monkeys for 20 minutes daily [showed] a significant increase in mandibular cartilaginous growth under LIPUS stimulation, especially under chronic mandibular advancement."

Mechanotransduction of Ultrasound is Frequency Dependent Below the Cavitation Threshold.

" low-intensity ultrasound directly affects nuclear processes, and the magnitude of the effect varies with frequency. In particular, we show that the transcriptional induction of first load-inducible genes, which is independent of new protein synthesis, is frequency dependent. Bovine chondrocytes were exposed to low-intensity (below the cavitational threshold) ultrasound at 2, 5 and 8 MHz. Ultrasound elevated the expression of early response genes c-Fos, c-Jun and c-Myc, maximized at 5 MHz. The phosphorylated ERK inhibitor PD98059 abrogated any increase in c-series gene expression, suggesting that signaling occurs via the MAPPK/ERK pathway. However, phosphorylated ERK levels did not change with ultrasound frequency, indicating that processes downstream of ERK phosphorylation (such as nuclear transport and chromatin reorganization) respond to ultrasound with frequency dependence. A quantitative, biphasic mathematical model based on Biot theory predicted that cytoplasmic and nuclear stress is maximized at 5.2 ± 0.8 MHz for a chondrocyte{coincidentally LSJL limb lengthening was done at a frequency of 5Hz}."

"Continuous US stimulation of chondrocytes induced phosphorylation of focal adhesion kinase, Src, p130-Crk-associated substrate (p130Cas), Crk-II and extracellular-regulated kinases (ERK)"

There are also studies that show that ultrasound makes stem cells more likely to differentiate into chondrocytes.  Ultrasounds are available for purchase if you want to experiment with it: Premium Portable Ultrasonic Ultrasound Device zza1000.  It seems like it might be an effective way to supplement height growth.