Trabecular bone and cortical bone have different bone remodeling levels, and the underlying mechanisms are not fully understood. In the present study, the expression of Wnt/β-catenin signaling and its downstream molecules along with bone mass in trabecular and cortical bone were compared in wild-type mice, constitutive activation of β-catenin (CA-β-catenin) mice and β-catenin deletion mice. It was found that the expression level of most of the examined genes such as Wnt3a, β-catenin, osteocalcin and RANKL/OPG ratio were significantly higher in trabecular bone than in cortical bone in wild-type mice. CA-β-catenin resulted in up-regulated expression of the above-mentioned genes except for RANKL/OPG ratio, which were down-regulated. Also, CA-β-catenin led to increased number of osteoblasts, decreased number of osteoclasts and increased bone mass in both the trabecular bone and cortical bone compared with wild-type mice; however, the extent of changes was much greater in the trabecular bone than in the cortical bone. By contrast, null β-catenin led to down-regulated expression of the above-mentioned genes except for RANKL/OPG ratio. Furthermore, β-catenin deletion led to decreased number of osteoblasts, increased number of osteoclasts and decreased bone mass when compared with wild-type mice. Again, the extent of these changes was more significant in trabecular bone than cortical bone. Taken together, we found that the expression level of Wnt/β-catenin signaling and bone remodeling-related molecules were different in cortical bone and trabecular bone, and the trabecular bone was more readily affected by changes in the Wnt/β-catenin signaling pathway. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:812-819, 2017.

Trabecular bone and cortical bone have different bone remodeling levels, and the underlying mechanisms are not fully understood. In the present study, the expression of Wnt/β-catenin signaling and its downstream molecules along with bone mass in trabecular and cortical bone were compared in wild-type mice, constitutive activation of β-catenin (CA-β-catenin) mice and β-catenin deletion mice. It was found that the expression level of most of the examined genes such as Wnt3a, β-catenin, osteocalcin and RANKL/OPG ratio were significantly higher in trabecular bone than in cortical bone in wild-type mice. CA-β-catenin resulted in up-regulated expression of the above-mentioned genes except for RANKL/OPG ratio, which were down-regulated. Also, CA-β-catenin led to increased number of osteoblasts, decreased number of osteoclasts and increased bone mass in both the trabecular bone and cortical bone compared with wild-type mice; however, the extent of changes was much greater in the trabecular bone than in the cortical bone. By contrast, null β-catenin led to down-regulated expression of the above-mentioned genes except for RANKL/OPG ratio. Furthermore, β-catenin deletion led to decreased number of osteoblasts, increased number of osteoclasts and decreased bone mass when compared with wild-type mice. Again, the extent of these changes was more significant in trabecular bone than cortical bone. Taken together, we found that the expression level of Wnt/β-catenin signaling and bone remodeling-related molecules were different in cortical bone and trabecular bone, and the trabecular bone was more readily affected by changes in the Wnt/β-catenin signaling pathway. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:812-819, 2017.

Awesome response Dr. Manivannan. There are several sudies about the function mechanotransduction regulation. And the trabecular bone and cortical bone have different bone remodeling levels like is known. In the 8th World Congress of Biomechanics (2018), Dublin, Ireland there was entire Session about 'in vivo bone remodeling mechanics'. I suggest to search and read the material of the presentations at this session. http://wcb2018.com.

These are great answers to your question, and they highlight something important, which is that osteoclasts know where they are, and what job they have to do accordingly. All remodeling takes place on surfaces. In cortical bone, the osteoclasts must create these surfaces for a variety of reasons (e.g., microcracks, increased mineralization density) which promote vascularization and the differentiation of bone lining cells to osteoblasts. The purpose is not for modulating mineral homeostasis, because this is the job of osteoclasts on trabecular bone surfaces. The trabecular bone surface area in the body is monumental, and osteoclastic activity on this surface area will rapidly respond to calcium and phosphate requirements of the bloodstream. For instance, female mammals take the enormous amount of minerals in support their fetus and milk production from vertebral trabecular bone because the surface area of this compartment is so huge. Mammal mothers, including humans, will add all of this matrix and mineral back once they stop lactating.

remodeling is the same term which can used in both cortical or spongy bones ,which many bone cells may share with this mechanism ,by the activity of the osteoblast and the asteoclast cells,but the different is in in other factors which support this mechanisms like the severity of the defect or fractures ,age, endocrinology stimulation ,calcium ions and others minerals levels ,body condition,alkaline phosphatase enzymes, and growth factors.......... .Remodeling may takes several months or even years until the bone takes its normal composition and strictures and many physical and chemical lab analysis can be used for the evaluation .and finally do not forget the bone wolf law that depend on the physical motions and the tension against the bone it self ( in others words oxygen tension and pressures ) ,so modulations and remodeling in the normal bone or in the healing processing of bone defect has the regular pathogenic s steps ,by bone formation and bone resorption with minerals depositions by the activation of the alkaline phosphatase enzymes which activated in the asteoblasts wall.and its clear that the last stages of bone growth is the lamllar bone formation and lastly compact bone in which in the center is havesian canal and surround by the active osteocytes ,which the woven bone or new trabecular bone formation in the beginning stages that convert to mature bone formation with disappears of the cavity in side the newly trabecular bone formations and filled with highly vascular connective tissues ,while in the spongy bone , the newly formed trabecular bone with the minerals depositions still not completely filled the area ,and seemed like a net work of bone .

Bonjour,

does anyone recommend a book or article on the difference in healing between cortical and cancellous bone?