Author Archives: Tyler

LSJL Studies 2: Effect of holes on LSJL

Not a lot on this study relating to longitudinal bone growth.  The important takeaway is evidence that LSJL can cause bone degradation which would be an important part of the process for neo-growth plate formation.

Effects of surgical holes in mouse tibiae on bone formation induced by knee loading.

“Loads applied directly to the knee (knee loading) have induce anabolic responses in femoral and tibial cortical bone. In order to examine the potential role of intramedullary pressure in generating those knee loading responses, we investigated the effects of drilling surgical holes that penetrated into the tibial medullary cavity and thereby modulated pressure alteration. Thirty-nine C57/BL/6 female mice in total were used with and without surgical holes, and the surgical holes were monitored. The left knee was loaded for 3 days[at 5Hz at 0.5N for 3 min a day], and the contralateral limb was treated as a sham-loaded control. Mice were sacrificed 2 weeks after the last loading. Although the surgical hole induced bone formation in both loaded and non-loaded tibiae, due to regional and systemic acceleratory phenomenon the anabolic effect of knee loading was substantially diminished. Without the holes, knee loading significantly elevated cross-sectional cortical area, cortical thickness, mineralizing surface, mineral apposition rate, and bone formation rate on the periosteal surface. For example, the rate of bone formation was elevated 2.1 fold (middle diaphysis–50% site from the knee along the length of tibiae) and 2.7 fold ( distal diaphysis–75% site). With the surgical holes  knee loading did not provide significant enhancement either at the 50% or 75% site in any of the histomorphometric measurements. Alteration of intramedullary pressure is necessary for knee loading to induce bone formation in the diaphysis{it may also be necessary to induce longitudinal bone growth} .”

Now they do say however that the drilling of the epiphysis did induce a response of the bone just not the same adaptations as it did without drilling.  Note that drilling was used rather than microfracture.  Although we can’t say for sure how surgical holes would affect LSJL’s effects on longitudinal bone growth.

“On days 2 and 6 after the last loading, the mice were given an intraperitoneal injection of calcein” and the results are shown below.  Calcein is used as a Ca2+ and Mg2+ indicator which are two proteins that are strong components of bone.

Without drilling:

Note that in group D which is the loaded group there is a huge hole in the middle of bone indicating that LSJL may in fact cause bone degradation which would allow for cartilagenous growth plates.  The fluid flow degrades bone and osteomy(removal of bone) may be necessary for new chondrogenesis.  It’s possible that this degradation of bone occurs in the epiphysis as well.  In group F the hole is smaller.  Group F was farther away from the site of loading than group.  Perhaps LSJL induces bone degradation more at sites closer to loading rather than farther away from loading.
  Slides were only taken from above so it’s possible that there would be bone degradation visible if the bone was horizontally sliced.  Bone degradation from a horizontal degradation would be ideal to allow for new growth plate formation for renewed longitudinal bone growth.
With drilling:
In this group both C and D have holes but in group F versus E the hole is much bigger in F.  In D the bone degradation is much more scattered than in C.  So LSJL can increase bone degradation in the body.
Unfortunately this study was performed before Yokota and Zhang realized that Lateral Synovial Joint Loading could be used to increase bone length so they didn’t measure the things that would interest us height seekers like if the tibia and femur had increased in length.

” knee loading induces alteration of intramedullary pressure in the femoral bone cavity and this alteration is synchronous to the loading frequency in Hz”<-The higher the frequency, the greater the intramedullary pressure.  I’m not sure exactly how to alter the frequency via LSJL but I believe that clamping/release from clamping/and then clamping again.

“cyclic deformation of the epiphysis alters pressure in the medullary cavity and the pressure gradient induces fluid flow in the diaphysis “<-Although fluid flow which can increase nutrient supply to chondrocytes, the number of changes induced to the growth plate via LSJL cannot be explained by just an increase in nutrient.

“In the presence of surgical holes, it is expected that the gradient is not adequately established because of incomplete pressure sealing.”

“A pressure gradient, elevated by venous ligation, was shown to increase interstitial fluid flow and this flow-mediated bone adaptation was considered to be independent of mechanical strain ”

“During knee loading no bruising or other damage was detected at the loading site, and after loading mice did not show a weight loss or a diminished food intake.”

“Osteoblast specific factor 2 (periostin) is preferentially expressed on periosteum and considered to play a role in the recruitment and attachment of osteoblast precursors in the periosteum”

“knee loading herein induces approximately 30 μstrain at the site of bone formation and the number of loading cycles per day is 900 for 3 days”

LSJL Studies 1: Osteogenic potentials with joint loading modality

I will be going over all the LSJL studies to see if I missed anything or to find new insights.

Osteogenic potentials with joint-loading modality.

Here’s the paper: osteogenic LSJL study.
“Osteogenic potentials with a novel joint-loading modality were examined, using mouse ulnae as a model system. Load-induced deformation of rigid bone [generates] interstitial fluid flow and stimulate osteogenesis. However, in most of the previous studies, loads were applied to cortical bone. In the current study, we addressed the question of whether deformation of the epiphysis underneath the joint would enhance bone formation in the epiphysis{New bone formation in the epiphysis can increase height if the bone is added at the longitudinal ends} and the diaphysis. We applied lateral loads to a mouse elbow. Compared to the no-loading control, 0.5-N loads, applied to the elbow at 2 Hz for 3 min/day for 3 consecutive days, increased the mineralizing surface (two- to threefold), the rate of mineral apposition (three- to fivefold), and the rate of bone formation (six- to eightfold) in the ulna. Strain measurements indicated that strains of around 30 microstrain{30 microstrain is extremely low according to mechanostat theory}, induced with the joint-loading modality, were under the minimum effective strain of around 1000 microstrain, which is considered necessary to achieve strain-driven bone formation. To evaluate the induction of fluid flow with the joint-loading modality, streaming potentials were measured in separate experiments, using mouse femurs ex vivo. The streaming potentials correlated to the magnitude of the load applied to the epiphysis, as well as the flow speed in the medullary cavity.  Joint-loading [induces] osteogenesis, through a mechanism that involves the induction of fluid flow in cortical bone.”

loading versus loaded LSJLColumn 1 is unloaded.  Column 2 and 3 is LSJL loaded.   It’s hard to tell in this pictures if LSJL created any gaps in the bone where new growth plates could form.  The diagrams are not in enough to tell to notice the formation of any microgrowth plates at least in figure 2a.  Calcein staining was used in these studies which detects mostly Ca2+ and Mg+ so it cannot distinguish between potential micro-growth plates and regular bone.

Here’s what the text had to say about the above diagram:

“Cross-sections of the ulnar shafts of control (no loading) and joint-loaded mice. The zoom images on the far right show double calcein staining, where the confined area constituted bone newly formed in 4 days. A Section of the metaphysis (trabecular bone) 1 mm from the loading center. The light staining outside the periosteal surface is collagen autofluorescence in a tendon of the triceps. B Section of the diaphysis (cortical bone) 2.5 mm from the loading center. C Section of the diaphysis (cortical bone) 4.5mm from the loading center”

“Trabecular bone in the epiphysis is less stiff in the lateral direction than in the axial direction and, therefore, lateral loads to the elbow may effectively deform the epiphysis of the ulna.
Deformation of the epiphysis may then induce fluid flow in the ulnar diaphysis in cortical bone, and load-induced fluid flow may enhance bone formation in the epiphysis{and possible stimulations of the epiphysis could be such as to spur new longitudinal bone growth} and the diaphysis.”

14 week old mice were used.  “3min per day for 3 consecutive days. The loading force was sinusoidal, at 2Hz, with a peak-to-peak amplitude of 0.5N.”

“The measured intramedullary streaming potential (f1, in mV) correlated to the magnitude of the applied force, according to the equation: f1 = 7.3 ¥ F (r2 = 0.92)”

“the magnitude of the streaming potential in the medullary cavity is proportional to the lateral load applied to the joint and the speed of fluid flow.”

If you look at figure 1a you can see that the device used is a lot like a C-class clamp with the nylon screw.

“The tip of the loader had a contact area of 4 mm in diameter. In order to avoid local stress concentrations between a joint and the loader, the surface of the loader was covered with a silicon rubber sheet.”

It should be noted by analyzing Table 1 that LSJL increases the bone formation rate of bone near the periosteum than trabecular bone.   Since the periosteum is partially involved in growth plate formation this is not necessarily a bad thing and since trabecular bone is still stimulated it still means that LSJL stimulates all areas of the bone and that LSJL could target any area of the bone that could be required to be targeted for neo-growth plate formation.

“[With axial loading], the force required to elevate the rate of bone formation is reported to be 2.3 N . With the joint loading modality described here, bone formation was enhanced by loads as small as 0.5 N.”<-So LSJL requires about 21% as much load to stimulate the bone as axial loading.  Let’s say hypothetically, that 1000lbs of axial loading could stimulate neo-growth plate formation.  LSJL would only require 210lbs.  Although, the rate of bone formation is irrelevant to what we’re looking for as we’re looking for longitudinal bone formation via neo-growth plates and that may be a result of stimulus that is unique to LSJL that axial loading cannot provide.

“The cross-sectional images of the ulna, together with the data on bone strains, support the notion that enhanced formation of cortical bone was an adaptive response to mechanical stimuli rather than a response associated with wound healing. First, the histological sections clearly showed double-labeled staining on the periosteal surface, with no indication of woven bone, which would frequently be formed in the process of wound healing. Second, unlike the four-point bending modality, where woven bone is formed underneath soft connective tissues, due to bending moment or compressive stress”<-it may be better if LSJL did increase bone formation as a result of wound healing as that could indicate the formation of holes in the bone where neo-growth plates could form.  However, the lack of woven bone could mean that cartilage was formed instead of bone which would be very promising indeed.

“the speed of the intramedullary fluid flow induced by 0.5-N loads, applied to the knee, is estimated as 476micro-m/s.”

This study was published in 2005 whereas lengthening of mouse hindlimbs with joint loading was published in 2010 so they were not yet aware of the lengthening effects.  And the load was only applied for 3 days which is not a lot of time for bone lengthening to occur.

I did email the author to try get length data but I don’t know if he’ll respond.

Osteochondroma’s can grow after skeletal maturity

This can provide benefit to the theory of microgrowth plates.

CASE REPORTS: Enlargement of a Calcaneal Osteochondroma after Skeletal Maturity

“Growth or radiologic modification of an osteochondroma after the epiphyseal plate closes suggests the diagnosis of malignant transformation to a chondrosarcoma. However, extensive growth of an osteochondroma in a skeletally mature patient whose tumor proved benign has been reported. We report a similar case in an adult who had a solitary osteochondroma of the calcaneus. The lesion showed marked growth and was removed. Histologic examination showed no evidence of malignancy, and there was no recurrence during the 4-year followup.”

The man was 36 years old although it’s alluded that the osteochondroma was developed during skeletal development.

” bulky 2-cm thick cartilaginous cap, an irregular and indistinct appearance of the surface of the calcified tissues beneath the cap, scattered calcifications in the soft tissue component of the tumor, radiolucent foci in the lesion, and a large low-density soft tissue mass. However, no destruction of the adjacent bone was visible.”

The images tend to not be informative.  Just a white mass amonst the calcaneus bone.

calcaneusosteochondroma  Looking at that image it seems possible that the growth could provide a height and length increase but seems mostly lateral to the region that would increase foot height and length.

Here’s a normal calcaneus:

normal calcaneusAlthough this foot seems much larger than the normal.

“the cartilaginous cap appeared hyperplastic and had foci of increased cellularity. The chondrocytes were organized in clusters and had no significant atypia.”

“An osteochondroma develops when growth plate tissue is extruded laterally and proliferates into an exostoses. Therefore, an osteochondroma can arise in any bone that undergoes endochondral ossification, and it usually stops growing when the physes close.

Anti-epilepsy medication may increase height

P8 – 2228: The effects of anti-epileptic drugs on the growth plates of infant rats

“Epilepsy is among the most common neurologic disorders in childhood. Levetiracetam (LEV) and valproic acid (VPA) are widely used drugs in the treatment of children with epilepsy. The adverse effects of both drugs on bone metabolism and growth is defined in the literature. The present study aimed to investigate the effects of these two common anticonvulsant drugs on longitudinal bone growth in rats.

Twenty-four infant rats divided into three groups. The study groups received VPA (600 mg/kg/day) and LEV (150 mg/kg/day) for two weeks respectively. Normal saline was applied to the control group. The rats were sacrified after the appliance of the drugs and the rat femurs were removed. The thickness of the growth plates were measured by histopathologically.

All groups included four males and four females. The thickness of the growth plates were larger in VPA and LEV groups versus control group (p<0.05). In addition the measurement of the growth plate in VPA group was larger than LEV group (p<0.05).

We concluded that VPA and LEV both enlarge the growth plate on rats in this study. But this finding does not reflect all steps of endochondral bone growth. The hormonal factors and apoptotic processes also have role on longitudinal bone growth. Further investigations are needed to clarify the adverse effects of anticonvulsants on bone growth and influence on final height.”

Note though that enlargement of the growth plate does not always equal larger longitudinal bone growth.

Comparison of arthritis fingers to my finger results with LSJL

Here’s the pictures of my fingers(you can follow the link on the page to get more images).  I’ve been loading the right index finger with LSJL.

Here’s an image of osteoarthritis fingers:

osteoarthritis fingersIn contrast to heberden’s nodes my fingers are enlarged at the sides and there is no fusiform swelling of the joints.  Fusiform swelling is ” elongated and tapering at both ends; spindle-shaped  ”

“Heberden’s nodes are hard or bony swellings that can develop in the distal interphalangeal joints (DIP) (the joints closest to the end of the fingers and toes). They are a sign of osteoarthritis and are caused by formation of osteophytes (calcific spurs) of the articular (joint) cartilage in response to repeated trauma at the joint.

Heberden’s nodes typically develop in middle age, beginning either with a chronic swelling of the affected joints or the sudden painful onset of redness, numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and the patient is left with a permanent bony outgrowth that often skews the fingertip sideways. Bouchard’s nodes may also be present; these are similar bony growths in the proximal interphalangeal (PIP) joints (middle joints of the fingers), and are also associated with osteoarthritis.”

The question is, is my enlargement of the epiphysis of the fingers an osteophyte or is it a result of endochondral ossification.  Although there are lateral osteophytes.

Heberden’s and Bouchard’s nodes

Osteophyte nodes may be painless so lack of pain in my fingers is not an indication that is not an osteophyte.

“The osteophytes beneath the lateral nodes arise lateral to the extensor tendon, and although the soft tissues have been distorted by the embalming process and have to be interpreted with caution, it appears that the adjacent capsule is displaced and attenuated.”

Here’s an image of a growing osteophyte:

growing osteophyteAnd admittedly this does appear to be like enlargement of the epiphysis.

“The true osteophyte, initially a chondrophyte, is intra-articular, developing from the synovium covered surface at the cartilage margin, either from metaplasia of existing synoviocytes or differentiation of precursor cells. The chondral hyperplasia that initiates it is not intrinsically vectored to grow in any particular direction, and in practice grows in the direction of least resistance, to an extent determined by that resistance. If the adjacent cartilage surface is unloaded as a consequence of subluxation or underuse, the osteophyte will grow centripetally over the cartilage surface. More usually it grows peripherally, forming a large pedunculated osteophyte if unopposed, as in the synovial recess of the shoulder joint. Where growth is constrained by strong capsules, as in the lateral ankle, by adjacent ligaments as at the tibial spine, or by tendon insertions as in the upper humerus, growth is inhibited and the osteophyte is small. In essence it will grow until the tension induced in the stretched soft tissues matches that induced by the growing osteophyte. It follows from these known growth characteristics of osteophytes that the regular location of osteophytic nodes at specific sites in these two joints must reflect a local area of low resistance to osteophyte growth unique to these joints. ”

Here’s another image that better shows lateral nodes:

osteoarthritis nodes

Here’s what an osteophyte looks like directly on the bone:

osteophyte on the bone

Now here’s another image of my loaded finger so you can see any potential osteophyte nodes:

20140529_132338Definitely node like.  I can’t see any evidence of swelling though.  I’ve seen young people report getting finger nudes at like age 14 so arthritis may cause nodes but arthritis may not be the only source of nodes.  And most evidence suggests that nodes aren’t painful and don’t limit mobility of the finger.

I couldn’t find any evidence upon searching that these nodes increase finger length although admittedly it is incredibly hard to use a search to find anything so that does not guarantee that there are not some anecdotal reports that people got longer fingers due to nodes.

So I conclude:  LSJL caused increase in bone length and osteophytes and these two effects may be independent.  I am using as much load as I can to get more finger results this may be overload and what is causing osteophytes.  However, less load may be possible to increase finger length without causing osteophytes.  I increased arm length with no evidence of osteophytes(unfortunately I did not document this).

LSJL update-Another finger angle and wingspan

Call to action: In the comments section, post anecdotal evidence of people increasing bone length due to tensile strain(stretching).  Example exercises would be inversion(If legs are stretched), hanging, or gripping weights.  Normal stretching would not be sufficient as that would put most of the load on the muscle and not the bone.

Also, please post suggestions on how to do a before and after finger(or toe) experiment that does not require expensive x-rays.  Preferably, a suggestion that only requires easy to take pictures.

Here’s a picture that proves that my right finger is now longer:

20140521_124303You can definately see that the right index finger is longer as it is aligned at the tips and yet the knuckle sticks out higher.  Also, the left thumb seems to be bigger too which I have also been loading with LSJL.

If you haven’t already click on the last post on the finger progress here.

Here’s another image very similar to one of the images on that page:

20140519_122107

This image may look similar to the image in the other but the other image was aligned at the knuckles with the right hand being slightly higher so that I can’t be accused of knuckle manipulation.  This picture is aligned by the tip of the finger tips.  You can see in this image that the right handed knuckle is above the left handled knuckle.  Meaning that the right finger(the one I’ve been performing LSJL on) is longer.

Also, I hadn’t measured my wingspan in a while and previous wingspan measurement was 72.5″(I like a lot of people have a longer wingspan than my height).  This was about 5 years ago.

Recently, I measured my wingspan again and it was 189cm or about 74.4″.  I haven’t really been measuring the wingspan as I didn’t have faith in the methodology of LSJL on the arms.  I use the irwin quick grip to clamp the elbows but the bone structure there is clunky.  I can get a good solid clamp on my wrists though.

This has given me faith that LSJL doesn’t need the extreme force that you can generate on your fingers.  However, unlike the legs it is much easier to generate tensile strain on the bones of the arms(although you can generate tensile strain on the legs via inversion).  Although, we’ve pretty much ruled out axial loading as a method to increase height we haven’t quite ruled out tensile loading.  So it’s possible that the increase is due to hanging or holding onto dumbells or barbells which would place a bit of a stretching force on the bone.

An increase in wingspan at adult age due to farmer’s walk or hanging is less likely to be reported than an increase in height and I don’t know for sure how many people did inversion for their legs and to what extremes.  So I can’t say for certain that the gain was due to LSJL and not tensile loading.

And I don’t have before pictures aside from just me standing but this does give me faith that LSJL can generate height at less extreme forces than one can generate on the finger.  Although 1 inch per arm over five years is pretty slow.