Tennis effect on growth plates

Since tennis is a method of mechanical stimulation on the bone and growth plate.  We can extrapolate its effects to other forms of mechanical stimulation.

Asymptomatic elite young tennis players show lateral and ventral growth plate alterations of proximal humerus on MRI.

“The specific aim of the study was to investigate and compare epiphyseal length and extension in the proximal humerus, closure in the growth plate and bone marrow signal intensity related to the proximal humeral physis in the dominant arm and the non-dominant arm of the asymptomatic adolescent elite tennis player.
The study sample included 35 asymptomatic elite young tennis players (15 males and 20 females, mean age 17.4 years ± 2.7). Each player contributed with two shoulders to the MRI measurement. The non-dominant arm was used as a control.
Relative reliability between the radiologists was excellent (ICC 0.78-0.96). Statistically significant differences between dominant arm and non-dominant arm in epiphyseal length (mm) laterally (DA 27.3 vs NDA 26.7) were shown. Statistically significant differences were also found in epiphyseal extension (mm) laterally (DA 36.1 vs NDA 35.1) and ventrally (DA 36.2 vs NDA 34.8). No statistically significant differences were found between dominant arm and non-dominant arm in epiphyseal extension (mm) medially (DA 31.7 vs NDA 31.7) and dorsally (DA 22.6 vs NDA 22.1).
Significant findings assessing MRI measurements of the epiphyseal plate in the asymptomatic adolescent elite tennis player might reflect a development of consecutive alterations in the epiphyseal plate in the dominant arm.”

The cartilage of the epiphyseal plate might be 2–5 times weaker than surrounding fibrous tissue; therefore, epiphyseal (growth) plates are very sensitive to their surrounding mechanical environment

“The epiphyseal plate consists of the fibrous part, providing mechanical support and the cartilaginous and bony part, acting together in transforming cartilage cells into bone. The rounded end of a long bone, the epiphysis, is divided into two types: traction epiphysis, primarily subjected to tensile forces, and pressure epiphysis, primarily subjected to compressive forces. Closure of the growth plate of the proximal humerus in the paediatric population starts around 14 years of age, and the last area to close is the posterolateral region that closes at 17 years of age”

“The shear stress arising from high torques during the arm cocking throwing phase in overhead sports is large enough to lead to deformation of the weak proximal humeral epiphyseal cartilage”

The difference in growth plate dimensions is not so much important as is the difference in overall length as higher growth plate height and width can occur in cases of stunted growth.

Playing tennis didn’t appear to have an affect on keeping the growth plate open.

“External rotation force applied to the proximal humeral physis during the overhead motion peaks just before maximal shoulder external rotation”

Knee Joint Distraction

Joint Distraction is similar to what I’m experimenting with via finger pulling.

Sustained clinical and structural benefit after joint distraction in the treatment of severe knee osteoarthritis.

Knee joint distraction (KJD) provides clinical benefit and tissue structure modification at 1-year follow-up. The present study evaluates whether this benefit is preserved during the second year of follow-up.
Patients included in this study presented with end-stage knee OA and an indication for total knee replacement (TKR); they were less than 60 years old with a VAS pain ≥60 mm (n = 20). KJD was applied for 2 months (range 54-64 days) and clinical parameters assessed using the WOMAC questionnaire and VAS pain score. Changes in cartilage structure were measured using quantitative MRI, radiography, and biochemical analyses of collagen type II turnover (ELISA).
Average follow-up was 24 (range 23-25) months. Clinical improvement compared with baseline (BL) was observed at 2-year follow-up: WOMAC improved by 74% (P < 0.001) and VAS pain decreased by 61% (P < 0.001). Cartilage thickness observed by MRI (2.35 mm (95%CI, 2.06-2.65) at BL) was significantly greater at 2-year follow-up (2.78 mm (2.50-3.09); P = 0.03). Radiographic minimum joint space width (JSW) (1.1 mm (0.5-1.7) at BL) was significantly increased at 2-year follow-up as well (1.7 mm (1.1-2.3); P = 0.03). The denuded area of subchondral bone visualized by MRI (22% (95%CI, 12.5-31.5) at BL) was significantly decreased at 2-year follow-up (8% (3.6-12.2); P = 0.004). The ratio of collagen type II synthesis over breakdown was increased at 2-year follow-up (P = 0.07).
Clinical improvement by KJD treatment is sustained for at least 2 years. Cartilage repair is still present after 2 years (MRI) and the newly formed tissue continues to be mechanically resilient as shown by an increased JSW under weight-bearing conditions.”

Below is the knee distraction method and a description:

knee distraction

“The distraction method was applied. In short, an external fixation frame consisting of two monotubes with internal coil springs was placed, bridging the knee joint. Each monotube was fixed to two bone pins on each end and, in stages, distracted for 5 mm (confirmed by X-ray). After instructions about pin site care, daily exercise, and physical therapy, the patients were discharged from the hospital. Patients were allowed and encouraged to load the distracted joint with full weight-bearing capacity, supported with crutches. In case of superficial (skin) pin tract infections, treatment with oral antibiotics for 5–7 days was provided (Flucloxacillin). Every 2 weeks the patients returned to the hospital and the monotubes were temporarily removed. The knee was bent, for 3–4 h, in a continuous passive motion device, with pain at the pin sites determining the maximum degree of flexion; on average, 25° (15–80°) flexion and full extension was reached. The monotubes were replaced and sufficient distraction was confirmed by X-ray examination and adjusted if needed.”

I think that this method of distraction is not more than can be done manually.

“newly formed cartilaginous tissue; it might be, in part, fibrocartilaginous tissue.”

This study Effects of non-surgical joint distraction in the treatment of severe knee osteoarthritis. has the analysis of non-surgical but I can’t get the full study.

The idea of joint distraction in this case is not to stimulate the articular cartilage but to stimulate longitudinal bone growth.  There is no practical evidence that this may be the case that I am aware.  It is based on the observation that developing individuals have less pronounced epiphysis’ and that therefore the epiphysis may be a constraining factor on growth.

The epiphysis may constrain growth in a number of ways for example the two epiphysis may be akin to “like” charges of a battery and repel each other inhibiting further growth.

This study here does not provide any evidence about what affect joint distraction will have on healthy adults but it does show that joint distraction does have physiological effects on bone, cartilage, and likely MSCs.  All ingredients for inducing longitudinal bone growth.

Finger pulling seems promising

So I’ve been doing finger pulling for a few weeks.  I’ve gotten a small but significant amount of results.   I’ve been doing it only on the right pinky finger.  I don’t expect you to be able to see the results but I can much more easily compare my finger length than I could do in photos.  And I’d still need x-rays before people would be convinced.  But now that I see results I am going to do more finger pulling(while still doing LSJL) to see if I can keep getting more results or if I “plateau”.

If this works then doing the arms will be easy you just pull the joints away from each other by grabbing onto your hand.  Doing spine and legs will be harder as someone would have to hold your head and pull your head and someone will have to hold your legs and pull them.

Now why would this work and not something like the rack or holding dumbells to stretch your arms?  First, your muscles are resisting the weight.  Second, one part of the joint can be stretched while the other is compressed.

This is why it’ll be hard to do it any way other than manually as you have to make sure that the joint is uniformly stretched.

So since I am starting to notice some results I’m going to increase the duration of 15 minutes to as often as possible probably 30min-1 hr while still doing LSJL.  Then we’ll see if I get more obvious results.



Formation of Synovial Joints

Understanding how Synovial Joints are formed may help us understand how to influence them to reinitiate longitudinal bone growth.

Formation of synovial joints and articular cartilage.

“Chondrocytes differentiate from mesenchymal progenitors and produce templates(anlagen) for the developing bones. Chondrocyte differentiation is controlled by Sox transcription factors. Templates for the neighbour bones are subsequently separated by conversion of differentiated chondrocytes into non-chondrogenic cells and emergence of interzone in which joints cavitation occurs. A central role in initiating synovial joint formation plays Wnt-14/beta-catenin signalling pathway.Moreover, bone morphogenetic proteins and growth and differentiation factors are expressed at the site of joint formation. Joint cavitation is associated with increased hyaluronic acid synthesis. Hyaluronic acid facilitates tissue separation and creation of a functional joint cavity{Hyaluronic acid may inhibit fusion?}. According to the traditional view articular cartilage represents part of cartilage anlage that is not replaced by bone through endochondral ossification. Recent studies indicate, however, that peri-joint mesenchymal cells take part in interzone formation and that these interzone cells subsequently differentiate into articular chondrocytes and synovial cells. Thus,anlage chondrocytes have a transient character and disappear after cessation of growth plate function while articular chondrocytes have stable and permanent phenotype and function throughout life.”

“Cartilage templates of neighbour bones are separated through development of non-cartilaginous region known as the interzone. The interzone is essential for joint formation since its removal by microdissection led to joint ablation and fusion of bones”

” During interzone formation articular progenitor cell specification prompts the downregulation of the gene for the master chondrogenic transcription factor SOX-9″

“The repressive signals that prevent chondrogenic differentiation within interzone are likely to promote differentiation along a fibrous lineage”

Since Hyaluronic Acid and Heparan Sulfate play a role in cavitation they may help create room for neo-growth plate formation(See Figure 1).

” Once formed, interzone differentiate in 3 layers: 2 chondrogenic, perichondrium-like layers that cover the cartilaginous surfaces and 1 intermediate layer of loose, avascular mesenchyme that separates them and continues peripherally in a vascular mesenchyme, the so-called synovial mesenchyme. Within interzone, along planes destined to become the articular surfaces of synovial joints cavitation occurs”

Necrosis may play a role in preventing cells in the interzone that have chondrogenic potential.  Necrosis may be a way that the body blocks neo-growth plate formation.

“HA acid may be an important factor in joint cavitation.  Activity of uridine diphosphoglucose dehydrogenase, an enzyme necessary for synthesis of UDP glucuronate, a component for HA production was increased in a narrow band of cells at the presumptive joint line prior to cavitation. These findings suggest that joint cavitation is dependent on the behaviour of fibroblastic cells and/or adjacent chondrocytes, rather than macrophages. Moreover, hyaluronan and hyaluronan synthases were present in the interzone before and at the time of cavitation”

” joint cavitation could be facilitated by a rise in local hyaluronan concentration in an area of tissue where cohesion is dependent on the interaction between cellular CD44 and extracellular hyaluronan “<-Since a kind of joint cavitation may be involved to create the region for a neo growth plate,  Hyaluronic acid may be helpful in this endeavor.

“The interaction between HA and CD44 can induce both cell adhesion and cell separation, depending on the concentration of HA surrounding a cell population via receptor saturation, with increasing HA concentrations leading to cell separation”<-However, mesenchymal consedation rather than separation is a precursor to growth plate formation.

New Experiment-Finger Pulling

toddler hands

Correlation does not imply causation.  Just because the growth plates disappear correlates with the near cessation of longitudinal bone growth does not mean that the disappearance of growth plates causes the cessation of longitudinal bone growth.  Maybe a uniform factor causes both the disappearance of growth plates and cessation of growth.  Maybe the cessation of growth causes the disappearance of growth plates.  May another factor ceases both.

I’m testing the hypothesis that maybe it’s the joints themselves that place the constraint on longitudinal bone growth.  If you look at the above image of a toddlers hands you notice the near absence of joints/knuckles.  One of the main difference between adult and childs bones is that adults have much prominent epiphysis.  LSJL attempts to stimulate that epiphysis in one way. What if the epiphysis itself constrains growth. If you look at the image below by pulling my finger that I’m sort of creating the knuckle gap that’s like the child hand.


So the test is to see if by pulling the finger that we can alleviate the potential constraints on growth.  I can’t do it 24/7 and if it does constrained growth there should only be a need for certain periods of time where growth is unconstrained by the epiphysis.  So I’m going to be pulling my right pinky finger for 15 minutes.  I need time to perform LSJL too.  All my left fingers are longer than my right and there are some images below so if my right pinky becomes longer than my left.

We can only really draw conclusions if this works.  If this works then we can see that it is the epiphysis itself that is the sole constraint on longitudinal bone growth and that by pulling the finger for enough time during the day we allow for growth to occur.  If it doesn’t work then we can’t really say anything.  Maybe I didn’t do it for enough time or maybe you need to stimulate neo-growth plate formation in addition to preventing the epiphysis’ from constraining growth.

If this works it also bodes well for growing taller via spinal height as you can stretch those as well.  However, usually when you stretch in one way you usually compress another and any activity involving the spine is more dangerous due it’s important bodily role.

This may sound crazy.  How can it possibly work?  I just saw a toddlers hands and noticed that gap where joints could be.  Then I pulled my finger and saw the gap sort of made my hand more toddler like.  The logical stretch is that how can you possibly grow without stimulating growth plates.  Well, every single field of science is understudied.  Correlation does not apply causation.  The hypothesis being tested here is:

The epiphysis puts a constraining factor on longitudinal bone growth by pulling the finger apart you allow for release from that factor temporarily allowing for possible new longitudinal bone growth to occur.

20160104_101624 20160104_101713

LSJL Update-12/10/15

I recent did some LSJL measurements and I didn’t have any significant increase in length.  I think the reason for this is that I wasn’t clamping long enough.  During the last few months I’ve been clamping hard so that I stop clamping sooner due to pain and can get it over with.  However, I don’t think that is enough time to build up hydrostatic pressure.  This is contrast to the method I post recently that had a very long clamping time.  I think that my attempt to shortcut the process by getting into more intense clamping faster denied me of results.  Slower clamping also allows for the surrounding muscles and tendons to adapt to the clamping meaning an eventual more intense clamping force before they start resisting.

Given that mesenchymal stem cells can differentiate into chondrocytes via hydrostatic pressure it’s very likely that their is an epithelial intermediary to allow for chondrogenic differentiation and epithelial cells are important to form the resting zone of the growth plate.  LSJL tries to increase hydrostatic pressure.  Although response to hydrostatic pressure may be dependent on cell matrix interactions.

I do have strong faith in LSJL given wingspan increase results and possible finger length increase.  I performed LSJL on my right finger.  My right finger appeared longer than my left.  I got X-rays and after exhaustive analysis all my left finger bones were in fact longer except for my right metacarpal.  And upon observation most of my left hand bones do appear to be longer than my right.  Thus, the difference in size between the right and left metacarpal is very likely due to LSJL.

So now I will be performing LSJL on my left index finger to try to get the left metacarpal longer than my right and I will be ramping up the clamping of other joints that I perform LSJL on more slowly and longer duration.