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Experimental Alternative-LSJL Routine Part 2


Here’s the new LSJL routine I’m trying.  It’s not quite the same as LSJL as it’s not based on loading the synovial joints really, it’s more about loading groups of bones that are connected close to another bone by it’s growth plates.  It’s based on the observation that my arms gained in length relatively consistently but not the rest of my body.  The manner in which I clamp my elbow is relatively unchanged versus how I clamped it into LSJL.

For example, in LSJL you clamp the synovial joint on it’s side.

If you clamp the knee on it’s side you are pressing ligaments against the growth plate.

However by pressing the patella against the growth plate line you are not just pressing the ligament near the growth plate line(growth plate remnant), you are pressing the bone against the ligament which would generate a new stimulus.

The philosophy behind LSJL was to induce lateral compression of the bones to induce fluid flow in the bone to generate hydrostatic pressure to induce mesenchymal condensation to form neo-growth plates to grow taller.

Ligaments and other connective tissue have stem cells and coincedentally some run directly into the growth plate region.  Osteoclasts could theoretically eat away at bone and ligament stem cells could migrate and form neo growth plates within this growth plate line.  I’ll be posting some things to explore this theory.

Here’s where and how I’m clamping.  I know the pictures are bad but even if the pictures were better you’d still have to feel and experiment with the optimal clamping position.  But the idea is to clamp one bone against another bone.  So you clamp the fibula against the tibia or the patella against the femur.  Since bones often are connected to each other near the growth plate region this allows for the possibility of stimulating growth plate regeneration.

Now I haven’t tested this routine that long and ligaments and soft tissue are more fragile then bone.  So do this routine at your own risk especially something like the patella clamp.  I also have pretty minimal evidence so far as the only clamp that’s proved to be decently effective is the elbow clamp.  Most I’ve done for these clamps is a count of 120 but I get results for elbow clamping with about that much.  I’m going for several sessions a day though.

I might have to do a video as well for each to explain how I find the right clamping spots.

Patella clamp:



Fibula clamp:



Ankle(Tibia and Fibula) Clamp:


Cuneiforms and Metatarsals Clamp:


Elbow(humerus clamp):


Radius and Ulna(Wrist) Clamp:


Metacarpal bones(clamp):



Featured post

New Experimental LSJL routine

Here’s the old routine and I am still doing that but I’m adding something else.

I was looking through some old LSJL studies and I noticed an interesting image.


knee loading image

This image is from the study Mechanical Intervention for the Maintenance of Cartilage Bone which is not a bone lengthening study but still pertinent.  You’ll note that the loading does not appear to be strictly on the lateral side of the knee but on the diagonal so the top and bottom of the knee is getting loaded a bit as well.

Here’s a mouse and rat knee:
mouse and rat knee

Here’s the explanatory text: “MRI images of a rat (Wistar) and mouse (C57BL/6) knee joint. (A) 3D spin echo MR image (117 × 114 × 144 μm) of a rat knee ex vivo displaying the anatomical landmarks of the articular joint: a = femur condyle, b = tibia, c = patella, d = patellar ligament, e = meniscus, f = articular cartilage and g = intrapatellar fat pad. (B) Histological image of the knee joint. The MR images provided an excellent visualisation of the rat knee anatomy, with detailed observations on the subchondral bone and in the articular synovial space. (a, b, c, d) Sequential fast spin echo multi-slices images (axial views from proximal to palmar) from the proximal region of the mouse knee (512 × 512 μm). The MR images displayed the bones of the area of knee joint (1 = patella; 2 = femur; 3, 3′ = femur condyles), providing good views of the subpatellar region and the synovial cavity (see arrows). Images acquired in a 9.4-T Varian scanner (Varian, Inc., Oxford, UK) with 100 G/cm gradient coils and a Rapid bird-cage RF coil. ”  You can also see that the patella has a position relatively close to the growth plate.

Mice and rats do have patellas.

Here’s the image of the loading under Lengthening of Mouse Hindlimbs with Joint Loading which is a lengthening study:
lengthening of mousehindlimbs
On the right diagram you can see that the patella is loaded as well.  What is on either side of the growth plate?  Bone and bone.  What is on the other side of the knee joint?  Bone and bone.  Loading bone directly against bone may have a unique response.

I gained in height initially but not so much lately but I have been gaining in wingspan.  On that post I reported a wingspan of 74.5″ but lately I’ve been getting closer to 75″.

Notice something about the elbow joint:
elbow xray

Lots of potential for bone on bone contact.

Now notice the knee joint from a lateral view:

lateral knee xray

Not much potential for bone on bone contact unless you load the fibula or patella.

I found evidence that my right metacarpal grew longer than my left but so much the other parts of the bone.  My left side was longer than my right before so growth may even be more than as noted.  Growth was about 0.8% of Right metacarpal versus left.  An 0.8% increase in height would be about half an inch.

What do you notice about the palm of hand bones(which includes the metacarpal) versus the finger bones?
hand xray

Much more bone on bone action.    I clamped the palm of my hand close to the index finger metacarpal.  I’ll have to post an image of how I did it next post.  But according to my theory the index finger grew from the thumb bone pressing down on it then my middle finger bone should’ve grown from the index finger pushing down.

Also, if you look at my first method for performing LSJL when I did initially gain length:


initial LSJL

I generated force like this and this would press the fibula against the tibia.  The reason gains begin to cease is that my ability to increase force was limited with this whereas clamping can generate much more force.

Interestingly I did not any results on ankle loading producing lengthening which gives me theory credence and Hiroki Yokota stated that he did not study it.

So expect some images of how I’m going to explore this theory and some studies on bone against bone(with tissue in between) especially loading against a growth plate region like patella against the femur.

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Glucosamine and Chondroitin may contribute to height by slowing down growth plate senescence

This study attempts to accelerate growth plate senescence by removing rat ovaries.  Chondroitin and Glucosamine appear to counteract the effects of senesence on growth plate fusion.  So even if say hypothetically GS+Chondroitin may do nothing normally, when growth plate is close to senesence or cessation of growth GS+Chondroitin may extend this period to be longer allowing height to grow further.  Unfortunately, they do not measure longitudinal bone growth directly.

But Glucosamine+Chondroitin is available for sale and the potential toxicity for the supplement seems to be extremely low so I consider it worth trying if growth plates appear close to fusion.

Glucosamine and chondroitin sulfate association increases tibial epiphyseal growth plate proliferation and bone formation in ovariectomized rats

“The growth plate consists of organized hyaline cartilage and serves as a scaffold for endochondral ossification, a process that mediates longitudinal bone growth. Based on evidence showing that the oral administration of glucosamine sulfate (GS) and/or chondroitin sulfate (CS) is clinically valuable for the treatment of compromised articular cartilage, the current study evaluated the effects of these molecules on the tibial epiphyseal growth plate in female rats.

The animals were divided into two control groups, including vehicle treatment for 45 days (GC45) and 60 days (GC60) and six ovariectomized (OVX) groups, including vehicle treatment for 45 days (GV45), GS for 45 days (GE45GS), GS+CS for 45 days (GE45GS+CS), vehicle for 60 days (GV60), GS for 60 days (GE60GS) and GS+CS for 60 days (GE60GS+CS). At the end of treatment, the tibias were dissected, decalcified and processed for paraffin embedding.

Notably, after 60 days of treatment, the number of proliferative chondrocytes increased two-fold, the percentage of remaining cartilage increased four-fold and the percentage of trabecular bone increased three-fold in comparison to the control animals.

GS and CS treatment drugs led to marked cellular proliferation of the growth plate and bone formation, showing that drug targeting of the tibial epiphyseal growth plate promoted longitudinal bone growth.”

An OVX female mice is a mice that has had their ovaries removed and this is used to simulate osteoperosis.  So there’s guarantee that this will be applicable to a healthy individual.  The rats in this study were 16-weeks old.

The control OVX groups in this study had disorganized growth plates and reduced growth plate size.

OVX growth plates +- CS

“Growth plate photomicrographs of the following: A – non-OVX rats treated for 45 days with vehicle (GC45); B – OVX rats treated for 45 days with vehicle (GV45); C – non-OVX rats treated for 60 days with vehicle (GC60); D – OVX rats treated for 60 days with vehicle (GV60), E – OVX rats treated for 45 days with GS (GE45GS); F – OVX rats treated for 45 days with GS+CS (GE45GS+CS); G – OVX rats treated for 60 days with GS (GE60GS); and H – OVX rats treated for 60 days with GS+CS (GE60GS+CS). Sirius red-hematoxylin staining. (r: resting cartilage; p: proliferative cartilage; h: hypertrophic cartilage, c: remaining cartilage, o: trabecular bone, m: bone marrow). Scale bar = 75 µm.”

Here’s an LSJL growth plate for reference from this LSJL study:

The mice in this study were not OVX and were 8 weeks old.  The growth plates do not appear to be more disorganized.

“Compared to GV45 and GV60, the GE45GS, GE45GS+CS, GE60GS and GE60GS+CS groups presented an organized cellular arrangement and increases in the number of resting and proliferative chondrocytes, PZ thickness, remaining cartilage and the trabecular bone area. In addition, these groups showed a decrease in the number of hypertrophic chondrocytes in the bone marrow area, as well as a decrease in RZ and HZ thickness.”

The GC45 and GC60 are the control groups were looking at since those are the control groups that are not OVX.  They will help answer the question if Chondroitin and Glucosamine stimulated growth beyond just eliminating the deficit caused by OVX.  Compared to control, Chondroitin and Glucosamine treated OVX rats had more resting and proliferative chondrocytes and less hypertrophic chondrocyes.  So CS+GS may inhibit chondrocyte hypertrophy.

Cartilage thickness was about equal total but the CS+GS OVX group had more thickness in the proliferative zone.  CS+GS OVX group had more hyaluronan in the hypertrophic zone and after 60 days had more remaining cartilage but less bone marrow than the control group.

“In older rats, the growth plate structure and thickness is maintained but is not functional and longitudinal growth ceases at a certain point”

“To accelerate the senescence process in adult animals, OVX was performed in our study.”




Knowledge about the attachment of ligaments and tendons to bone is important to the new method of LSJL loading.

According to Physical Therapies in Sport and Exercise there is no communication between tendons and bone however.  It describes the tendon enthesis as as an unmineralized bundle of rounded cell fibrocartilage wrapped in bundles of type II collagen.  It states though that these cells do not have connective arms to other cells so tendons and bones would have no communication.

Enthesis fibrocartilage cells originate from a population of Hedgehog-responsive cells modulated by the loading environment.

“Tendon attaches to bone across a specialized tissue called the enthesis. This tissue modulates the transfer of muscle forces between two materials, i.e. tendon and bone, with vastly different mechanical properties. The enthesis for many tendons consists of a mineralized graded fibrocartilage that develops postnatally, concurrent with epiphyseal mineralization.  By genetically demarcating cells expressing Gli1 in response to Hedgehog (Hh) signaling, we discovered a unique population of Hh-responsive cells in the developing murine enthesis that were distinct from tendon fibroblasts and epiphyseal chondrocytes. Lineage-tracing experiments revealed that the Gli1 lineage cells that originate in utero eventually populate the entire mature enthesis. Muscle paralysis increased the number of Hh-responsive cells in the enthesis, demonstrating that responsiveness to Hh is modulated in part by muscle loading{surprisingly lower muscle loading seems to increase responsiveness}. Ablation of the Hh-responsive cells during the first week of postnatal development resulted in a loss of mineralized fibrocartilage, with very little tissue remodeling 5 weeks after cell ablation. Conditional deletion of smoothened, a molecule necessary for responsiveness to Ihh, from the developing tendon and enthesis altered the differentiation of enthesis progenitor cells, resulting in significantly reduced fibrocartilage mineralization and decreased biomechanical function. Hh signaling within developing enthesis fibrocartilage cells is required for enthesis formation.”

“Fibrous entheses include a periosteal component and typically insert into the metaphyses or diaphyses of long bones. By contrast, fibrocartilagenous attachments typically insert into epiphyses or bone ridges. These attachments are characterized by a partially mineralized region of fibrocartilage at the tendon-bone interface, with a round cell morphology and increased proteoglycan content relative to tendon. Due to these characteristics, mature entheses have been likened to arrested growth plates

Since tendons at first glance do not have much communication between themselves and bones how about ligaments?

Establishing a Coculture System for Ligament-Bone Interface Tissue Engineering

“Ligament-bone interface (enthesis) is a complex structure which comprises of ligament, fibrocartilage and bone. The fibrocartilage transformation adds significant insertional strength to the interface and makes it highly resistant to avulsion forces. Many ACL grafts cannot generate native interfacial region, leading to their failure. Co-culture has proved to be an effective way to generate new tissues in tissue engineering. Studies have found important signaling molecules in transduction pathway of chondrogenesis to be transmitted via gap junctions. We hypothesized that stem cells cocultured between ligament and bone cells would enable transmission of chondrogenic factors from bone/ligament cells to bone marrow stem cells (BMSCs) via gap junctions, resulting in their differentiation into fibrocartilage. To test this hypothesis, we studied to establish effective co-culture system. In this study, two set of co-culture (BMSCs and ligament cells; BMSCs and bone cells) were established. Confocal microscopy showed efficient dye transfer from bone/ligament cells into BMSCs. This was further confirmed and quantified by FACS, which showed a gradual temporal increase in the percentage of BMSCs acquiring Calcein.”

This study also states that there is ligament and bone communication:

In vitro study of stem cell communication via gap junctions for fibrocartilage regeneration at entheses.

Entheses are fibrocartilaginous organs that bridge ligament with bone at their interface and add significant insertional strength. To replace a severely damaged ligament, a tissue-engineered graft preinstalled with interfacial fibrocartilage, which is being regenerated from stem cells, appears to be more promising than ligament-alone graft. Such a concept can be realized by a biomimetic approach of establishing a dynamic communication of stem cells with bone cells and/or ligament fibroblasts in vitro.

The current study has two objectives. The first objective is to demonstrate functional coculture of bone marrow-derived stem cells (BMSCs) with mature bone cells/ligament fibroblasts as evidenced by gap-junctional communication in vitro. The second objective is to investigate the role of BMSCs in the regeneration of fibrocartilage within the coculture.

Rabbit bone/ligament fibroblasts were dual-stained with DiI-Red and calcein (gap-junction permeable dye), and cocultured with unlabeled BMSCs at fixed ratio (1:10). The functional gap junction was demonstrated by the transfer of calcein from donor to recipient cells that was confirmed and quantified by flow cytometry. Type 2 collagen (cartilage extracellular matrix-specific protein) expressed by the mixed cell lines in the cocultures were estimated by real-time reverse transcription PCR and compared with that of the ligament-bone coculture (control).

Significant transfer of calcein into BMSCs was observed and flow cytometry analyses showed a gradual increase in the percentage of BMSCs acquiring calcein with time. Cocultures that included BMSCs expressed significantly more type 2 collagen compared with the control.

The current study, for the first time, reported the expression of gap-junctional communication of BMSCs with two adherent cell lines of musculoskeletal system in vitro and also confirmed that incorporation of stem cells augments fibrocartilage regeneration. The results open up a path to envisage a composite graft preinstalled with enthesial fibrocartilage using a stem cell-based coculture system.”

” Inside the embryo, tendons and ligaments appear as fibrous cellular outgrowths from the perichondrium of cartilaginous precursor to later bone. In the neonates, as the cartilaginous anlage ossifies, fibrocartilaginous elements of the ligament are cemented into the initial calcified cartilage, which is later replaced by mature bone. Only a thin layer of proliferative epiphyseal cartilage remains at the interface{this is a very promising fact}. The resulting mature tendon or ligament insertion comprises four zones: collagenous ligament or tendon, nonmineralized fibrocartilage, mineralized fibrocartilage and cancellous bone”

The role of muscle loading on bone (Re)modeling at the developing enthesis.

“Muscle forces are necessary for the development and maintenance of a mineralized skeleton. Removal of loads leads to malformed bones and impaired musculoskeletal function due to changes in bone (re)modeling. In the current study, the development of a mineralized junction at the interface between muscle and bone was examined under normal and impaired loading conditions. Unilateral mouse rotator cuff muscles were paralyzed using botulinum toxin A at birth. Control groups consisted of contralateral shoulders injected with saline and a separate group of normal mice. It was hypothesized that muscle unloading would suppress bone formation and enhance bone resorption at the enthesis, and that the unloading-induced bony defects could be rescued by suppressing osteoclast activity. In order to modulate osteoclast activity, mice were injected with the bisphosphonate alendronate. Bone formation was measured at the tendon enthesis using alizarin and calcein fluorescent labeling of bone surfaces followed by quantitative histomorphometry of histologic sections. Bone volume and architecture was measured using micro computed tomography. Osteoclast surface was determined via quantitative histomorphometry of tartrate resistant acid phosphatase stained histologic sections. Muscle unloading resulted in delayed initiation of endochondral ossification at the enthesis, but did not impair bone formation rate. Unloading led to severe defects in bone volume and trabecular bone architecture. These defects were partially rescued by suppression of osteoclast activity through alendronate treatment, and the effect of alendronate was dose dependent. Similarly, bone formation rate was increased with increasing alendronate dose across loading groups. The bony defects caused by unloading were therefore likely due to maintained high osteoclast activity, which normally decreases from neonatal through mature timepoints. These results have important implications for the treatment of muscle unloading conditions such as neonatal brachial plexus palsy, which results in shoulder paralysis at birth and subsequent defects in the rotator cuff enthesis and humeral head. ”

This study only studied tendon and not ligament entheses though.

This site has a lot of into about entheses:

“The normal enthesis has a tendency to develop new bone formation with ageing. This manifests as incidental “bony spurs” that are visible on X-rays”

“Joint tissues under tension favours bone development and the outermost part of the enthesis is subject to predominant tension (pulling force).”

Here’s an entheses with neo-bone formation:
enthesesFc stands for fibrocartilage and the arrows are pointing at abnormal bone formation.  Not how the fibrocartilage is shaped into the bone like a zone of ranvier.
zone of ranvier

Evidence that loading Ligaments near the epiphysis can encourage growth

Loading bones against each other also loads the ligaments against the growth plate.  One method of LSJL involves pushing bones against each other at the points of the epiphysis.

Mesenchymal stem cell characteristics of human anterior cruciate ligament outgrowth cells.

“When ruptured, the anterior cruciate ligament (ACL) of the human knee has limited regenerative potential. However, the goal of this report was to show that the cells that migrate out of the human ACL constitute a rich population of progenitor cells and we hypothesize that they display mesenchymal stem cell (MSC) characteristics when compared with adherent cells derived from bone marrow or collagenase digests from ACL. We show that ACL outgrowth cells are adherent, fibroblastic cells with a surface immunophenotype strongly positive for cluster of differentiation (CD)29, CD44, CD49c, CD73, CD90, CD97, CD105, CD146, and CD166, weakly positive for CD106 and CD14, but negative for CD11c, CD31, CD34, CD40, CD45, CD53, CD74, CD133, CD144, and CD163. Staining for STRO-1 was seen by immunohistochemistry but not flow cytometry. Under suitable culture conditions, the ACL outgrowth-derived MSCs differentiated into chondrocytes, osteoblasts, and adipocytes and showed capacity to self-renew in an in vitro assay of ligamentogenesis. MSCs derived from collagenase digests of ACL tissue and human bone marrow were analyzed in parallel and displayed similar, but not identical, properties. In situ staining of the ACL suggests that the MSCs reside both aligned with the collagenous matrix of the ligament and adjacent to small blood vessels. We conclude that the cells that emigrate from damaged ACLs are MSCs and that they have the potential to provide the basis for a superior, biological repair of this ligament.”

“mobile population of MSCs within the ACL”

“cells derived from both ACL sources and bone marrow underwent chondrogenic differentiation in the presence, but not absence, of TGF-β1″

“MSCs migrate to sites of injury”

So ligaments near the epiphysis can differentiate into chondrocytes.

Chondrocyte phenotype and ectopic ossification in collagenase-induced tendon degeneration.

“We report chondrocyte phenotype and ectopic ossification in a collagenase-induced patellar tendon{in the new LSJL model the patella is a targetfor loading} injury model. Collagenase or saline was injected intratendinously in one limb. The patella tendon was harvested for assessment at different times. There was an increase in cellularity, vascularity, and loss of matrix organization with time after collagenase injection. The tendon did not heal histologically until week 32. Ectopic mineralization as indicated by von Kossa staining started from week 8. Tendon calcification was mediated by endochondral ossification, as shown by expression of type X collagen. viva CT imaging and polarization microscopy showed characteristic bony porous structures and collagen fiber arrangement, respectively, in the calcific regions. Marrow-like cells and blood vessels were observed inside calcific deposits. Chondrocyte-like cells as indicated by morphology, expression of type II collagen, and sox 9 were seen around and embedded inside the calcific deposits. Fibroblast-like cells expressed type II collagen and sox 9 at earlier times, suggesting that erroneous differentiation of healing tendon fibroblasts may account for failed healing and ossification in collagenase-induced tendon degeneration.”

“Chondrocyte markers were expressed in the clinical samples of calcific insertional Achilles tendinopathy”

“Chondrocyte-like cells as indicated by cellular morphology and expression of sox 9 and type II collagen were observed around the calcific deposits in collagenase-induced degenerative tendon injury”

“The differentiation of tendon progenitor cells into chondrocytes and bone cells was reported to be modulated by the expression of small leucine-rich repeat proteoglycans such as biglycan and fibromodulin, which control the differentiation process associated with BMP-2 activities ”

Tendons can differentiate into cells that undergo endochondral ossification.

knee tendonsThe tendons are relatively close to the epiphysis as well.

The origin points of the knee collateral ligaments: an MRI study on paediatric patients during growth

“Different femoral origins for both the medial collateral ligament (MCL) and the lateral collateral ligament (LCL) have been reported in the growing skeleton (epiphyseal and metaphyseal). This study assesses the femoral origins of the knee collateral ligaments in skeletally immature individuals.
MRIs of 336 knee joints (median age 15 years (range 2–18 years), m = 209 and f = 127) were retrospectively analysed to assess the distances between the femoral origins of the MCL and LCL to the distal femoral growth plate.
Both MCL and LCL ligament origins were invariably located on the epiphysis. Mean MCL origin–growth plate distance was 9.6 mm (SD 2.1 mm; range 2.2–13.6 mm) in boys and 8.6 mm (SD 1.5 mm; range 3.4–12.0 mm) in girls{The MCL ligament is very close to the growth plate}. Mean LCL origin–growth plate distance was 9.3 mm (SD 1.8 mm; range 4.3–13.0 mm) in boys and 8.2 mm (SD 1.5 mm; range 3.4–11.8 mm) in girls{The LCL ligament is very close to the growth plate}. The distance between the growth plate and both collateral ligaments as well as the length of the LCL correlated positively with patients’ age and body size (MCL R 2 = 0.673 and 0.556, LCL R 2 = 0.734 and 0.645, LCL length R 2 = 0.589 and 0.741).
During growth, the femoral origins of the MCL and the LCL are constantly located on the distal femoral epiphysis. There is a linear increase in the distances from the ligaments’ origins to the growth plate according to age and body size.”

“The LCL attaches slightly closer to the growth plate than the MCL. The distances between the origins of the ligaments and the distal femoral growth plate increase in a nearly linear pattern until closure of the growth plate.”

Where tendons and ligaments meet bone: attachment sites (‘entheses’) in relation to exercise and/or mechanical load.

“Entheses (insertion sites, osteotendinous junctions, osteoligamentous junctions) are sites of stress concentration at the region where tendons and ligaments attach to bone.”

“Tendons and ligaments can be regarded as machines with multiple moving parts (fibrils, fibres and fascicles) that perform the basic function of force transfer to and from the skeleton. They distribute the loads applied to them dynamically in order to execute movement patterns. Their complex response to loading allows for multi-axis bending, and this adds to the stress concentration in the region where they attach to bone. This attachment site will be referred to in this review as an ‘enthesis’, but it is also known as an ‘insertion site’, or an ‘osteotendinous’ or ‘osteoligamentous’ junction.”

The tissue at the enthesis insertion site is either fibrous or fibrocartilagenous.

“chondral–apophyseal entheses are found at the ends of the long bones and periosteal–diaphyseal attachments occur on the shafts.”

“At fibrous entheses, the tendon or ligament attaches either directly to the bone or indirectly to it via the periosteum. In both cases, dense fibrous connective tissue connects the tendon/ligament to the periosteum and there is no evidence of (fibro)cartilage differentiation”

” fibrocartilaginous entheses are sites where chondrogenesis has occurred and thus four zones of tissue are commonly present: pure dense fibrous connective tissue, uncalcified fibrocartilage, calcified fibrocartilage and bone”

“The inclusion of a zone of ‘pure dense fibrous connective tissue’ and a zone of ‘bone’ at a fibrocartilaginous enthesis highlight the difficulty of defining with any degree of precision where such an enthesis begins and ends.”<-Thus the ligament that attatches to the epiphysis near the growth plate line may extend partially into the bone itself.

“the proportion of the enthesis subchondral bone plate which consists of calcified fibrocartilage increases with age, because of a thinning of the cortical bone”

“Although tendons and ligaments are often viewed as non-distensible, they do have the ability to stretch and recoil by approximately 6% of their original length without any obvious signs of damage.”

“entheses can act as growth plates for apophyses at tendon and ligament attachment sites.”

“cartilage at the enthesis is initially derived from that of the embryonic bone rudiment.”

“this hyaline cartilage is eroded during endochondral ossification and replaced by enthesis fibrocartilage that develops within the adjacent ligament by fibroblast metaplasia.”

“Bony spurs (enthesophytes) are well documented at numerous entheses as bony outgrowths that extend from the skeleton into the soft tissue of a tendon or ligament at its enthesis”<-our goal is a cartilage ingrowth into the bone from the tendon/ligament.

Magnetic resonance imaging of entheses. Part 1.
enthesis attachment

“Achilles tendon, sagittal, histological section stained with Toluidine blue. Enthesis (EF) sesamoid (SF) and periosteal (PF) fibrocartilages are seen. The retrocalcaneal bursa (B) lies between the tendon and the bone and contains the tip of Kager’s retromalleolar fat pad (KP).”

One of the interesting features of fibrocartilaginous entheses is the paucity[scarcity] of compact bone (often referred to as the cortical shell) immediately beneath the attachment site. The subchondral plate (i.e. the associated calcified fibrocartilage and cortical shell) is often very thin and in many fibrocartilaginous entheses, there are local areas where subchondral bone and calcified fibrocartilage are absent.“<-Thus, it would be easier for cells to migrate there.

“Fibrocartilage forms in tendons that are translocated around bony pulleys and regresses in tendons that are re-routed so that they are no longer subject to compression in the same region.”

New Home Page from LSJL Scientists

HIroki Yokota and Ping Zhang are two of the scientists responsible for studying mechanical load driven bone lengthening.

What can their latest website (you must visit this site to understand the rest of the post)tell us about their plans to study this further?

On their research page, both knee loading(LSJL) and spinal loading(perhaps developing a way to lengthening the spinal column) are mentioned but only as a means of strengthening bone.

They mention that they are studying the regeneration of cartilage tissue which means that it’s a possibility that they are studying growth plate regeneration but more likely they are focused on the regeneration of articular cartilage. Their method for cartilage regeneration mentioned does not involve stimulation of mesenchymal stem cells to differentiate into chondrocytes but rather stimulation of aggreccan and type II collagen expression.

Unfortunately it says that Ping Zhang is a collaborating past lab member and Ping Zhang was the driving force behind studying lengthening effects.  It mentions that PIng Zhang is studying mechanical loading, osteoperosis, and fracture healing but nothing on bone lengthening specifically.

Interesting Review Paper on Bone Growth

Factors affecting bone growth

“Longitudinal bone growth depends on the growth plate{although some other regions may contribute in a minor way}. The growth plate has 5 different zones—each with a different functional role—and is the final target organ for longitudinal growth. Bone length is affected by several systemic, local, and mechanical factors. All these regulation systems control the final length of bones in a complicated way. ”

“Bone growth in width is also controlled by genetic factors, but mechanical loading regulates periosteal apposition”<-periosteal stem cells have the potential to differentiate into chondrocytes so it would be possible to use the mechanical loading to induce new longitudinal bone growth.

“Differences in bone size are established early in life, before puberty and perhaps even in utero. Bone begins to form when mesenchymal cells form condensations—clusters of cells that adhere through expression of adhesion molecules”

“Two models for control of bone growth in width have been suggested—the mechanostat theory (mechanical requirements regulate periosteal apposition) and the sizostat hypothesis (a master gene or set of genes regulates bone growth in width so bone reaches a preprogrammed size, independent of mechanical requirements)”

“The growth plate consists mainly of collagen fibrils, proteoglycans, and water, arranged to form a sort of sponge with very small pores. The growth plate is located between epiphyseal and metaphyseal bone at the distal end of long bones and is strain-rate–dependent, which means it is hard when squeezed rapidly but soft when deformed slowly{the means that the frequency to which stimuli is applied to the growth plate can result in a large variation in response}. The growth plate becomes ossified after puberty and epiphyseal fusion.”

“Histologically, the growth plate consists of horizontal zones of chondrocytes at different stages of differentiation. The germinal zone, at the epiphyseal end of the growth plate, contains resting chondrocytes, which seem crucial in orienting the underlying columns of chondrocytes and, therefore, in unidirectional bone growth, probably by secretion of a growth plate–orienting factor. Next is the proliferative zone, a matrix-rich zone in which flattened chondrocytes undergo longitudinal cell division and orient themselves in typical column-wise fashion. At some point, proliferating chondrocytes lose their capacity to divide; they start to differentiate and become prehypertrophic, coinciding with a size increase. Proliferating chondrocytes are located in the transition (maturation or prehypertrophic) zone. In the hypertrophic zone, round chondrocytes secrete matrix proteins in large amounts. This stage is characterized by an increase in intracellular calcium concentration, which is essential in the production of matrix vesicles. These vesicles, small membrane-enclosed particles, are released from chondrocytes and secrete calcium phosphates, hydroxyapatite, and matrix metalloproteinases, resulting in mineralization of the vesicles and their surrounding matrix. The chondrocytes in this mineralized zone eventually undergo programmed cell death (apoptosis), leaving a scaffold for new bone formation. ”

“Generally, bones increase in length as long as new material is being squeezed between the reserve zone of the growth plate and the zone of provisional calcification.”<-Can we still do this post epiphyseal fusion?

“Intracellular calcium concentration increases in the hypertrophic chondrocytes in the hypertrophic zone of growth plate cartilage; at some point, these chondrocytes begin to mineralize the longitudinal septa in the surrounding matri. At the growth cartilage junction, mononuclear cells of undetermined origin resorb the unmineralized horizontal septa of the growth cartilage. These cells are called septoclasts or chondroclasts. Blood vessels invade the area and pave the way for bone cell precursors. Eighty percent of the longitudinal septa of the growth cartilage is rapidly resorbed in the metaphyseal zone immediately behind the invading blood vessels, paving the way for bone cell precursors. About 40% of mineralized septa serves as scaffold for the formation of primary bone trabeculae; the other 60% is absorbed by chondroclasts (osteoclasts) near the vascular invasion front. ”

The scientists list factors that positively influence bone growth:

I think to or after a certain level should be applied to almost all of these like Estrogen.  This list shouldn’t be taken as gospel as there is a lot more detail in how these hormone influence longitudinal bone growth.  Innervation is to supply a body part with nerves and I think too has a more complex relationship to longitudinal bone growth than is alluded too.

“GH acts on resting zone chondrocytes and is responsible for local IGF-1 production, which stimulates clonal expansion of proliferating chondrocytes in an autocrine/paracrine manner. Infusion of GH or IGF-1 shortens stem- and proliferating-cell cycle times in the growth plate of hypophysectomized rats and decreases the duration of the hypertrophic differentiation phase, with GH being more effective. According to [an] experimental study, GH or IGF-1 treatment restores mean cell volume and height, but the growth rate is not normalized by either hormone. ”

“hyperthyroidism increases the growth rate in children but also leads to premature growth plate fusion and short stature. T3 seems to stimulate recruitment of cells from the germinal zone to the proliferating zone and facilitates differentiation of growth plate chondrocytes. Its precursor, T4, increases the number of [3H]methylthymidine-labeled chondrocyte nuclei and [35S]incorporation in Snell dwarf mice growth plates, suggesting a stimulatory role in chondrocyte proliferation and differentiation”

However, I think this view overemphasizes the importance of hormones.  You can read more on hormones in the full study which I provided a link too in the top.

“If compression always inhibited bone growth, as it was believed, growth plates would be extremely unstable, as any slight deviation from the straight alignment of the long bones of the lower extremities would induce a vicious circle of positive feedback and result in catastrophic deformities. Mild compression leads to increased, not decreased, growth. Nevertheless, when compression on one side of the growth plate exceeds a certain level, growth is indeed suppressed, and the lesion begins to worsen.”

Hypothesized theory of input of compression and tension on growth rate.

“bone cells accommodate to a customary mechanical loading environment, making them less responsive to routine loading signals”

“muscle pull affects periosteal tension and, consequently, bone form and growth in length”

“wider bones must have higher midshaft periosteal apposition rates, as this is how they
become wider.”