Monthly Archives: May 2022

Need help evaluating x-rays

I happened to get x-rays a year ago.  I was performing bone tapping at the time and was unable to get a copy of them because I couldn’t find any computer that would play a CD.  I found something that maybe an abnormality and evidence that bone tapping can induce changes in bone morphology but since I don’t have before and after I can’t be sure.  Like I said I just happened to have had xrays ordered.

Here’s the image of what may be an abnormality(if requested I can post full versions of all three xrays I have):

Here’s another tibia x-ray:

Above is a normal tibial x-ray.  Also here the x-rays of someone who performed LSJL.  Essentially the area circled in red looks clearer(less dense) than normal.  Is that indicative of neo-bone formation?  I can’t be sure.  So if someone could find an expert that would be helpful.  I can also provide copies of all the x-rays.  Please comment or email if you can help.

Study shows proof of concept that microfractures can increase bone length

The Effect of Bone Marrow Stimulation for Cartilage Repair on the Subchondral Bone Plate
“To investigate the effect of bone-marrow stimulation (BMS) on subchondral bone plate morphology and remodeling compared to untreated subchondral bone in a validated minipig model.
Three Göttingen minipigs received BMS with drilling as treatment for two chondral defects in each knee. The animals were euthanized after six months. Follow-up consisted of a histological semiquantitative evaluation using a novel subchondral bone scoring system and micro computed tomography (µCT) of the BMS subchondral bone. The histological and microstructural properties of the BMS-treated subchondral bone were compared to that of the adjacent healthy subchondral bone.  The µCT analysis showed that subchondral bone treated with BMS had significantly higher connectivity density compared to adjacent untreated subchondral bone (26 1/mm3 vs. 21 1/mm3, P = 0.048). This was the only microstructural parameter showing a significant difference. The histological semiquantitative score differed significantly between the subchondral bone treated with BMS and the adjacent untreated subchondral (8.0 vs. 10 P = < 0.001). Surface irregularities were seen in 43% and bone overgrowth in 27% of the histological sections. Only sparse formation of bone cysts was detected (1%).BMS with drilling does not cause extensive changes to the subchondral bone microarchitecture. Furthermore, the morphology of BMS subchondral bone resembled that of untreated subchondral bone with almost no formation of bone cyst, but some surface irregularities and bone overgrowth(!).”
And the bone bone overgrowth can be seen to be length as seen in the histological slides.
“The objective of BMS is to create canals in the subchondral bone to the underlying bone marrow, either by use of a drill(subchondral drilling) or an awl (microfracture).”<- an awl is a tool for piercing holes.  It’d be hard to mimic either a drill or awl safely using non-surgical methods but I don’t believe that it’s impossible.
The study mentions that other studies also showed bone overgrowth.
“Bone overgrowth was defined as areas where the subchondral bone plate had grown into the cartilage.”<-this could be due to endochondral ossification or longitudinal appositional growth.
“Nine out of the 12 samples contained bone overgrowth corresponding to 27% of the sections.”
“Hematoxylin eosin staining, scale bars: 200 μm. Defects treated with BMS. (A) Shows irregularity of the subchondral bone plate (top arrow marks the beginning of the defect). (B) Bone cyst marked by arrows. (C) Remaining drill hole in the subchondral bone plate. (D) Overgrowth in the subchondral bone plate marked by to arrows, top arrow marks the beginning of the defect site. BMS = bone marrow stimulation.”<-so the overgrowth is very minor but if there was some way to reproduce it, it could add up to height over time.  The pigs used in the study were skeletally mature.
 Here’s the study study cited in the above that also shows bone overgrowth:
Characterization of Subchondral Bone Repair for Marrow-Stimulated Chondral Defects and Its Relationship to Articular Cartilage Resurfacing
“Trochlear cartilage defects debrided of the calcified layer were prepared bilaterally in 16 skeletally mature rabbits. Drill holes were made to a depth of 2 mm or 6 mm and microfracture holes to 2 mm. Animals were sacrificed 3 months postoperatively, and joints were scanned by micro–computed tomography before histoprocessing. Bone repair was assessed with a novel scoring system and by 3-dimentional micro–computed tomography and compared with intact controls. Correlation of subchon-dral bone features to cartilage repair outcome was performed.”
“Although surgical holes were partly repaired with mineralized tissue, atypical features such as residual holes, cysts, and bony overgrowth were frequently observed. For all treatment groups, repair led to an average bone volume density similar to that of the controls but the repair bone was more porous and branched as shown by significantly higher bone surface area density and connectivity density. Deeper versus shallower drilling induced a larger region of repairing and remodeling subchondral bone that positively correlated with improved cartilage repair.”
“Repair of subchondral bone 3 months after bone marrow stimulation does not result in complete regeneration of the normal bone structure as shown by 3-dimensional visual models (left column), 2-dimensional micro-CT images (middle column), and safranin O/fast green stain (right column). A through C, normal unoperated (control). D through F, a case of good bone repair with suboptimal lateral integration (sample from DRL2/GrpII). G through I, presence of bone overgrowth (sample from DRL6/GrpI). J through L, presence of residual holes (sample from DRL2/GrpI). M through O, presence of nonmineralized connective tissue in subchondral region—a subchondral cyst (sample from MFX2/GrpII). P through R, lack of integration to adjacent bone (sample from DRL6/GrpI). Bars = 1 mm.”
“drilling deeper to 6 mm versus 2 mm increased the volume of this repaired and remodeling subchondral bone region, resulting in greater cross-sectional area, as well as width and depth”
“Alterations of joint biomechanics and joint homeostasis caused by osteochondral defects may also contribute to the generation of bone over-growth.”<-so perhaps bone overgrowth can be generated by methods other than drilling.
The question is how can we induce something like a microfracture safely and without surgery?

Joint loading promotes stem cell migration

New study related to lateral synovial joint loading:

Knee Loading Enhances the Migration of Adipose‑Derived Stem Cells to the Osteoarthritic Sites Through the SDF‑1/CXCR4 Regulatory Axis

“Osteoarthritis (OA) is a whole joint disorder that is characterized by cartilage damage and abnormal remodeling of subchondral bone. Injecting adipose-derived stem cells (ASCs) into the knee joint cavity can assist in repairing osteoarthritic joints, but their ability to migrate to the damaged site is limited. Our previous studies have shown that knee loading can improve the symptoms of OA, but the effect and mechanism of knee loading on the migration of ASCs in OA remain unclear. We employed a mouse model of OA in the knee and applied knee loading (1 N at 5 Hz for 6 min/day for 2 weeks) after the intraarticular injection of ASCs. The cartilage and subchondral bone repair were assessed by histopathological analysis. Immunofuorescence assays were also used to analyze the migration of ASCs. Using cell cultures, we evaluated the migration of ASCs using the transwell migration and wound healing assays. In vivo experiments showed that knee loading promoted the migration of ASCs, increased the local SDF-1 level, and accelerated the repair of the OA-damaged sites. Mechanistically, the observed effects were blocked by the SDF-1/CXCR4[SDF-1/CXCR4 promotes neovascularization which is great] inhibitor. The in vitro results further revealed that knee loading promoted the migration of ASCs and the inhibition of SDF-1/CXCR4 significantly suppressed the beneficial loading effect. The results herein suggested that the migration of ASCs was enhanced by knee loading through the SDF-1/CXCR4 regulatory axis, and mechanical loading promoted the joint-protective effect of ASCs”

Now we don’t know how much more lateral knee loading stimulates neo-vascularization etc. than regular exercise.  Nor do we know if knee loading promotes subchondral bone repair independently of adipose derived stem cells.  But neovascularization and new cartilage formation are very important findings that could potentially be linked to what’s needed to grow taller.

“A variety of physical rehabilitation regimens can afect the remodeling process of articular cartilage and subchondral bone and alter the symptoms of OA, such as whole-body vibration, axial loading, and bending loading. The knee loading modality, developed by our laboratory, is a mild non-invasive physical therapy, which applies transverse loading to a synovial joint, such as the elbow, knee, and ankle. Knee loading has been shown as an effective loading option for improving OA symptoms. Previous studies showed that knee loading reduced MMP13 activity and prevented OA-induced cartilage degeneration through cross-talk of the cartilage with subchondral bone. Mechanical loading also mitigated OA symptoms by regulating the stress to the endoplasmic reticulum and autophagy. Further, knee loading facilitated repairing osteoporotic OA by relieving the abnormal remodeling of the subchondral bone via Wnt/β-catenin signaling. It contributed to promoting the diferentiation of MSCs into osteogenic and chondrogenic fates”

“Stromal cell-derived factor 1 (SDF-1), a chemokine of a CXC family, and its receptor CXC chemokine receptor 4 (CXCR4) exist widely in the body, and they regulate a variety of physiological processes, including cell proliferation, migration, adhesion, differentiation, and wound healing ”

“A total of 108 female C57BL/6 mice (14 weeks old, Animal Center of Academy of Military Medical Sciences, China) were used.”<-not quite as old as we would like.

“After the induction of OA, mice were injected with GFP-ASCs, followed by daily knee loading for 2 weeks. The injected ASCs in the knee joints of all groups were identified by immunofuorescence staining with antibodies against GFP. In vivo studies showed that GFP-positive cells were found in the OA cartilage 2 weeks after their injections”

” The number of chondrocytes and vacuolar cells was counted. The number of chondrocytes in the OA group was significantly decreased compared to the sham-treated control group, but the number was restored by knee loading or the injection of ASCs”<-it’s very promising that the chondrocyte number was restored be knee loading independently of stem cell injection but again these mice are not as old as we would like.

” IHC analysis showed that collagen II-positive cells in the OA group were significantly decreased. However, the numbers in the OAL group and OA+ASCs group were increased.”<-again very promising that collagen II positive cells were increasing independently of ASC injection

In the top images you can see that the mice still have their growth plate.  It’d be hard to distinguish between changes in the bone caused by Osteoarthritis and those caused by loading.  But if you look at the loaded groups(Loading with and without ASC) you can see in red cartilage in places that did not have cartilage in either the control or the osteoarthritis group at the longitudinal ends of the bone.  And you don’t really see that in the OA+ASC group.  I could be reading it wrong though.

Again here you see cartilage at the sides of the longtiduinal ends of the bone that you don’t really see in the non-loaded groups.