Specific Bones Do Grow Bigger After Skeletal Maturity And Growth Plate Closure

I believe that even in our normal day to day life most people would be able to observe from being around a person who is going through the puberty phases in life changes to their body occurring which suggest bones are growing bigger as well.

Of course, we are not just talking about the interstitial growth of bones here. What were are saying is that there are certain bones in the human body which keep on growing in size even after all the growth plates are closed.

The evidence is from certain studies, like…

Surprising evidence of pelvic growth (widening) after skeletal maturity

It seems that while the long bones may no longer be growing vertically, they do indeed grow in width.

Of course, we already know that the long bones grows appositionally thicker over the years as the inner cambium periosteum layer deposits more and more osteoblasts onto the bones, but this is different. What we are see is an irregular bone structure, the pelvic bone becoming wider.

This makes sense due to two main things…

Factor #1: Many females have said that after going through with pregnancy and having their babies the natural way, they noticed that their hips expanded in size, and have never gotten back down to the size before they were ever pregnant. The phenomena tells us that somehow during pregnancy the pelvic bones were expanded in width.

Factor #2: The most common phenomena where the shoulders of a young teenage boy after they finish growing taller seems to grow in width and the overall torso seems to also grow wider, aka “filling out”

It would turn out after looking at the locations of cartilage in the body, the sternum/rib cage area of the body even in young teenage boys who have no more cartilage to grow taller, there is still cartilage in their front ribcage area. That is what makes the males grow wider in the shoulder area around the ages of 17-25.

Remember: When archeaologists are digging up cities from thousands back, they find skeletons with the entire ribcage being bones, which suggests that sometime after the bones that make height are bones, the ribcage which is made from fibrocartilage also slowly ossifies over time. If humans had cartilage in the front that never ossified, then the dug up skeleton from thousands of years ago would be missing the front area/sternum which is supposed to be surrounded by Costal Cartilage. Cartilage does not survive buried under ground for thousands of years. It either ossifies or gets disintegrated.

So what we are seeing is two different areas of the body that are still growing!

1. The rib cage
2. The pelvic region

In my long post about the possible reason for why some pregnant women grew taller, I had pointed at the related phenomena of pelvic girdle pain, where the little bit of cartilage (at the Symphysis Pubis) becomes stretched out, making the entire pelvic bone wider. After the findings on the ligament stretching and relaxing effects of relaxin, which is also released during pregnancy, it started to made sense. For example, the pelvic structure of females and males are already different. On average, the hips of a woman’s is proportionally larger than a mans, for childbirth and for easier passage of the baby through the birth canal.

During pregnancy, the entire area becomes widened from relaxin & the drop in calcium levels in the lumbar bones in the mother as the calcium gets transported to the developing embryo in the uterus, which means the bones become widened aka bigger. The loss in Ca means that the bones do get much weaker which means that it might be easier to stretch out the bones and remodel them.

There is now medical confirmation that certain bones in the body do keep getting bigger volumetrically. Refer to the following below…

• [Do the obstetrically relevant bony pelvic measurements change? A retrospective analysis of computed tomographic pelvic x-rays]
• Bone and body segment lengthening and widening: a 7-year follow-up study in pubertal girls.

From the 2nd source, it is written the following….

“By the age of 18 years the girls had reached their mothers’ height (101%) and humerus, radius, femur and tibia lengths (100-101%), but not their mothers’ shoulder, great pelvis and lesser pelvis widths (98%, 95% and 93%, respectively). Our data confirmed that, after bone elongation had ceased, segment width continued to increase, although at a slower speed, into early adulthood.“

If the pelvic bones are getting bigger, aka wider, how can we then use that type of knowledge to make the overall skeleton longer then?

Amateur Chinese Researchers Are Extremely Educated On Bone Interstitial Growth – Important!

Something that I have speculated on for a long time is that there are dozens, if not hundreds of individual amateur level researchers around the world like us, and I had said that most of them who are highly educated and understand the mechanics of the bone as well as any MD trained orthopedic specialist would be probably from Russia, Sweden, The Netherlands, Germany, South Korea, Japan, or China. Those are the only few countries which have the level of education, and technology sophistication to be able to play with the more advanced subjects.

I track the sources which link to this website. A link to the website has made my speculations much more concrete. It is from a Chinese based website source, and the level of knowledge expressed is above what I even understood, until I started to digg further into the technical details. Refer to the link http://bbs.wenxuecity.com/health/468959.html

The text on the page is completely in a language which I don’t understand, but fortunately for Google Chrome, it was roughly translated. I posted the translated parts below.

Some background notes on this website called Wen Xue City – After looking at its Wikipedia page, it seems that it is not some local city forum, but a very well known website that is used by the Chinese Expat community. It is supposed to be the…”largest overseas Chinese website”. From the Wiki pages, it is supposed to get around 2 Billion page views every month, and with 3 million unique visitors (is it by per day??).

First, whoever gave the reply to this person who wanted to grow taller and lengthen their bones understood the details on how Wolff’s Law is supposed to work when you put loads in certain directions on a bone. They are using words to describe which direction to apply pressure on and what would happen to the bone.

The mention of the Mechanostat Theory by Harold Frost was something I only glanced at early on in the website and forgot about. What happened is that after Wolff came out with his law, Frost came along and adjusted that law aka refined it to be much more specific and detailed on what exactly happens to the bone, while still accepting the original law laid out by Wolff.

• Source: A 2003 update of bone physiology and Wolff’s Law for clinicians.
• Source: Bone’s mechanostat: a 2003 update.

When the poster is talking about this term called “radial” I believe that they are talking about a lateral/side force/pressure used. This is similar to what Tyler proposes aka applying force laterally.

I also agree with him that if you are going to be applying a static force, the bones will not be remodeled. You need a dynamic, intermittent type of loading.

They also understand that the increase in bone thickness will always be in the area of bone which is concave in nature.

Here is the amazing point which is made, which I did not reach yet. Remodeling of bone is not possible unless the bone is curved aka concave in the area which you want to thicken/add bone to. It is not the force/pressure/load that is causing the bone to remodel, but the curved/concave nature of the surface of the bone.

Whoever wrote the post seemed to be writing it maybe for the purpose of figuring out how to grow bone density to reverse osteoporosis in the elderly, but they might also be talking about bone volumetric growth, aka making the bones bigger/longer.

What makes this link so important, and what are the implications?

If these guys were talking about how to make the bones longer for height increase, then they are much further ahead in understand the mechanics of the bone than me at least. If they are instead trying to learn Frost/s refined rule on Wolff’s Law for just increased bone density for preventing or treating osteoporosis, then they are still extremely advanced.

I think that there are probably websites and forums in the Russian, Chinese, and German internet space which are looking at the same PubMed studies like we are and have a much better grasp and understanding on what are the technical problems, and issues that are most important which we must resolve to push the effort forward.

If the person who wrote that reply (with all those pictures and diagrams on the effects of loading a femur) is any type of indication of the scientific level of bone mechanics expertise, I would then say that even these amateur level Chinese height increase researchers are much further than where we are. So did they figure out something already? I don’t think so, unless the government or military have done it and decided not to publish their top secret research and findings.

I have always believed that there are certain government groups anonymously tracking and following this website. We are not the normal type of blog talking about cooking recipes and putting Facebook pictures of their kids up. These days with the ability to get Private VPN services, and use local proxies to hide one’s IP, it is almost certain that I can not even figure out who are these people who are secretly reading the website and taking the information I leak to use for their own benefit.

I have already proved that the professional researchers in the Chinese Military Hospitals have been working to get the surgery of growth plate transplantation to work out for at least 2 decades now and that teams in a few Russian Cosmetic Clinics are also trying to get the exact same type of surgical technique to work out as well, by growing the growth plates from surgically removed fat tissue.

Non-Thermal plasma is plasma that is not in thermodynamic equilibrium.  Atmospheric pressure plasma matches the pressure of the surrounding atmosphere.

Non-Thermal Atmospheric Pressure Plasma Enhances Mouse Limb Bud Survival, Growth and Elongation.

“appendage regeneration is dependent on reactive oxygen species (ROS) production and signaling. Mesenchymal cell stimulation by non-thermal (NT)-plasma, which produces and induces ROS, would (1) promote skeletal cell differentiation and (2) limb autopod development. Stimulation with a single treatment of NT-plasma enhanced survival, growth and elongation of mouse limb autopods in an in vitro organ culture system. Noticeable changes included enhanced development of digit length and definition of digit separation. These changes were coordinate with enhanced Wnt signaling in the distal apical epidermal ridge (AER) and presumptive joint regions. Autopod development continued to advance up to 144 hr in culture, seemingly overcoming the negative culture environment normally observed in this in vitro system. Real time qPCR analysis confirmed the up-regulation of chondrogenic transcripts. Mechanistically, NT-plasma increased the number of ROS positive cells in the dorsal epithelium, mesenchyme and the distal tip of each phalange behind the AER, determined using dihydrorhodamine. The importance of ROS production/signaling during development was further demonstrated by the stunting of digital outgrowth when anti-oxidants were applied. NT-plasma initiated and amplified ROS intracellular signaling to enhance development of the autopod. Parallels between development and regeneration, suggest the potential use of NT-plasma could extend to both tissue engineering and clinical applications to enhance fracture healing, trauma repair and bone fusion.”

“Vertebrate limbs grow through the coordinated activity of numerous growth factor signaling pathways, including the Wnt, fibroblast growth factor (FGF), bone morphogenetic protein (BMP), Notch, and transforming growth factor-β pathways. ROS play a primary role in mediating the activity of these factors and/or are integrally involved in regulating downstream signaling pathways. For example, a sustained increase in ROS levels is required for Wnt β-catenin signaling and the activation of one of its main downstream targets, fgf20. In addition, naturally occurring oxidative spikes are observed in most of the transition stages throughout developmental and regenerative processes. Furthermore, there is precedence for ROS production to both direct and enhance mesenchymal cell differentiation into either chondrocyte or osteoblast lineages”

“Since the NT-plasma discharge occurs in air, it is a highly complex mix of reactive chemical species (i.e., nitric oxide [NO], ROS, oxygen singles, and ozone), free ions, visible, ultraviolet, and near-infrared light, electric fields, and electromagnetic (EM) radiation.”

“one study showed that a 2 h treatment with EM field stimulated limb growth through increased proliferation and chondrocyte differentiation”

That is an absolutely huge elongation.

“Morphological formation of the joint region and alcian blue staining of proteoglycan appeared normal in sham and NT-plasma-treated digits. Chondrocytes in the proximal segment of the sham-treated digit were entering the prehypertrophic stage, based on the larger size, greater cellular spacing, and decrease in proteoglycan (white arrowhead). This typically precedes the formation of the primary center of ossification in the diaphysis. In contrast, chondrocytes from the NT-plasma-treated digit were immature and contained large amounts of proteoglycan. Even more striking was the much larger cartilage phalangeal segments in the NT-plasma-treated digit. A white line with double arrows marks the joint between the first and second phalanges in both sections. In the sham-treated digit, the adjacent joint spaces (white arrow) can be clearly observed; whereas in the NT-plasma-treated digits, there is no evidence of the next joint space, due to the increased segment length.”<-So maybe the plasma treatment increases stem cell differentiation to chondrocytes which is what we’d be looking for.

“Histology and quantitative real time-polymerase chain reaction were used to assess chondrogenesis and molecular events associated with the accelerated development. (A) A representative, hematoxylin and eosin (H&E) and alcian blue stained sections of middle phalanges from sham and NT-plasma-treated limb autopods. A white double arrow line marks the first joint space. The white arrows mark adjacent joint spaces, and the white arrowhead marks prehypertrophic chondrocytes in the sham control. (B) At 24 h post-NT-plasma treatment, alkaline phosphate (ALKP), catalase (CAT), endothelial nitric oxide synthase (eNOS), and bone morphogenetic protein 2 (BMP2) expression increased twofold above control. BMP4 and runt-related transcription factor 2 (Runx2) increased 12-fold and 8-fold, respectively, and fibroblast growth factor (FGF)-2 showed no increase. One hundred forty-four hours later, increases for ALKP (6-fold), CAT (14-fold), and BMP2 (3.5-fold). eNOS remained increased twofold above control at 144 h. BMP4 and Runx2 showed a relatively consistent elevated expression at 24 and 144 h. The results are expressed as the mean±standard deviation (n=3 [two limbs pooled per sample], *p<0.05). ”

“NT-plasma treatment promoted both growth and differentiation of cartilaginous elements within the embryonic mouse autopod. Based on the lack of limb growth after NT-plasma treatment in an antioxidant environment, and the increase in H2O2-positive cells in and under the epithelia throughout the 6 day culture period, we propose that NT-plasma induction of intracellular ROS also plays a role in the growth and differentiation observed in the autopod. In addition, H2O2-positive cells were observed in the distal digit tips behind the AER, concurrent with enhanced Wnt signaling. These findings are consistent with the ROS dependence of signaling factors (e.g., Wnt, BMP, and FGF) required for autopod development.”

“ROS production may not be the sole mechanism driving enhanced autopod growth. A second possible reason that NT-plasma enhanced autopod growth was its inhibition of epithelial overgrowth. ”

“In limb regeneration, a thickening of the epidermis has been shown to inhibit signaling to the blastema, halting the regeneration process.”

Hard to determine causality as there are so many potential causal factors as there are so many confounding variables in plasma.

Mice growth plates do not go through the fusion stage but they do cease eventually in longitudinal bone growth due to growth plate dysfunction.  If we can reverse growth plate dysfunction in mice than perhaps we can do so in humans and get more height from the growth plate.

This study however does not discuss reversing elderly growth plate dysfunction but rather states that older mice are still capable of undergoing endochondral ossification outside the growth plate.

Fractures in Geriatric Mice Show Decreased Callus Expansion and Bone Volume.

“Using a small animal model of long-bone fracture healing based on chronologic age, we asked how aging affected (1) the amount, density, and proportion of bone formed during healing; (2) the amount of cartilage produced and the progression to bone during healing; (3) the callus structure and timing of the fracture healing; and (4) the behavior of progenitor cells relative to the observed deficiencies of geriatric fracture healing.
Transverse, traumatic tibial diaphyseal fractures were created in 5-month-old (young adult) and 25-month-old (which we defined as geriatric, and are approximately equivalent to 70-85 year-old humans) C57BL/6 mice. Fracture calluses were harvested at seven times from 0 to 40 days postfracture for micro-CT analysis (total volume, bone volume, bone volume fraction, connectivity density, structure model index, trabecular number, trabecular thickness, trabecular spacing, total mineral content, bone mineral content, tissue mineral density, bone mineral density, degree of anisotropy, and polar moment of inertia), histomorphometry (total callus area, cartilage area, percent of cartilage, hypertrophic cartilage area, percent of hypertrophic cartilage area, bone and osteoid area, percent of bone and osteoid area), and gene expression quantification (fold change).
The geriatric mice produced a less robust healing response characterized by a pronounced decrease in callus amount (mean total volume at 20 days postfracture, 30.08 ± 11.53 mm3 versus 43.19 ± 18.39 mm3; p = 0.009), density (mean bone mineral density at 20 days postfracture, 171.14 ± 64.20 mg hydroxyapatite [HA]/cm3 versus 210.79 ± 37.60 mg HA/cm3; p = 0.016), and less total cartilage (mean cartilage area at 10 days postfracture, 101,279 ± 46,755 square pixels versus 302,167 ± 137,806 square pixels; p = 0.013) and bone content (mean bone volume at 20 days postfracture, 11.68 ± 3.18 mm3 versus 22.34 ± 10.59 mm3) compared with the young adult mice. However, the amount of cartilage and bone relative to the total callus size was similar between the adult and geriatric mice (mean bone volume fraction at 25 days postfracture, 0.48 ± 0.10 versus 0.50 ± 0.13), and the relative expression of chondrogenic (mean fold change in SOX9 at 10 days postfracture, 135 + 25 versus 90 ± 52) and osteogenic genes (mean fold change in osterix at 20 days postfracture, 22.2 ± 5.3 versus 18.7 ± 5.2; p = 0.324) was similar{so the deficiencies of older mice to undergo endochondral ossification in response to fracture may be related to things other than gene expression}. Analysis of mesenchymal cell proliferation in the geriatric mice relative to adult mice showed a decrease in proliferation (mean percent of undifferentiated mesenchymal cells staining proliferating cell nuclear antigen [PCNA] positive at 10 days postfracture, 25% ± 6.8% versus 42% ± 14.5%.
the molecular program of fracture healing is intact in geriatric mice, as it is in geriatric humans, but callus expansion is reduced in magnitude.
Our study showed altered healing capacity in a relevant animal model of geriatric fracture healing. The understanding that callus expansion and bone volume are decreased with aging can help guide the development of targeted therapeutics for these difficult to heal fractures.”

So older mice are still capable of chondrogenic fracture healing which is a lot like endochondral ossification.  Therefore, this provides evidence that older humans may be capable of inducing new endochondral ossification.

“At 10 days postfracture, corresponding to peak cartilage, young adult mice produced more total cartilage than geriatric mice (302,167 ± 137,806 versus 101,279 ± 46,755 square pixels”

“No difference was found in the percent cartilage content of the callus at 10 days postfracture (41.17% ± 10.13% versus 28.94% ± 8.74%) and in the percent of total cartilage that was hypertrophic at 15 days postfracture (88.76% ± 14.56% versus 70.21 ± 16.05%; p = 0.078). Osseous tissue formation did not reach high levels until 20 days postfracture with cartilage resorption nearly complete for both groups. Geriatric mice exhibit decreased total cartilage production and delayed resorption”

If you’re deficient in Cyp26b1 then having a Vitamin A deficient diet may be a way to grow taller.

Cyp26b1 Within the Growth Plate Regulates Bone Growth in Juvenile Mice.

“Retinoic acid (RA) is an active metabolite of vitamin A and plays important roles in embryonic development. CYP26 enzymes degrade RA and have specific expression patterns that produce a RA gradient, which regulates the patterning of various structures in the embryo.  Localized RA activities in the diaphyseal portion of the growth plate cartilage were associated with the specific expression of Cyp26b1 in the epiphyseal portion in juvenile mice. To disturb the distribution of RA, we generated mice lacking Cyp26b1 specifically in chondrocytes (Cyp26b1Δchon cKO). These mice showed reduced skeletal growth in the juvenile stage. Additionally, their growth plate cartilage showed decreased proliferation rates of proliferative chondrocytes, which was associated with a reduced height in the zone of proliferative chondrocytes, and closed focally by four weeks of age, while wild-type mouse growth plates never closed. Feeding the Cyp26b1 cKO mice a vitamin A-deficient diet partially reversed these abnormalities of the growth plate cartilage. Cyp26b1 in the growth plate regulates the proliferation rates of chondrocytes and is responsible for the normal function of the growth plate and growing bones in juvenile mice, probably by limiting the RA distribution in the growth plate proliferating zone.”

“Cyp26b1 is expressed in the distal region of developing limb buds, and mice that lack Cyp26b1 show severe limb malformation due to the spreading of the RA signal toward the distal end of the developing limb, causing abnormal patterning of limb skeletal elements”

“In juveniles, focal closures of the growth plate in the distal tibia, the proximal tibia, the distal tibia, elbow, proximal femur and distal femur are caused by the treatment of acne with retinoids or the treatment of hyperkeratinosis with cis-retinoic acid. In guinea pigs, the application of RA caused closure of the growth plates in the proximal tibia”

“Excess intake of vitamin A causes growth impairment and skeletal pain in juveniles”