What is the difference between ossification and osteoporosis

The bone is formed from connective tissue such as mesenchyme tissue rather than from cartilage. The steps in intramembranous ossification are:. These cartilage poitns are responsible for the formation of the diaphyses of long bones, short bones, and certain parts of irregular bones.

Secondary ossification occurs after birth and forms the epiphyses of long bones and the extremities of irregular and flat bones. The diaphysis and both epiphyses of a long bone are separated by a growing zone of cartilage the epiphyseal plate. When the child reaches skeletal maturity 18 to 25 years of age , all cartilage is replaced by bone, fusing the diaphysis and both epiphyses together epiphyseal closure. Osteoblasts and osteoclasts, coupled together via paracrine cell signalling, are referred to as a bone remodeling unit.

The bone remodeling period consists of the duration of the resorption, the osteoclastic reversal the phase marked by shifting of resorption processes into formative processes , and the formation periods of bone growth and development. The bone remodeling period refers to the average total duration of a single cycle of bone remodeling at any point on a bone surface.

The purpose of remodeling is to regulate calcium homeostasis and repair micro-damage from everyday stress, as well as to shape the skeleton during growth.

Osteoclasts and Osteoblasts : Bone tissue is removed by osteoclasts, and then new bone tissue is formed by osteoblasts. Bones adapt to the muscle force loads placed on them, becoming thicker and stronger under stress and use and weaker and thinner when unused.

Although we often think of the elderly as feeble and weak, regular exercise can fight osteoporosis and maintain strength and flexibility. This is demonstrated by Johanna Quaas, an year-old gymnast who can still perform an amazing routine on the parallel bars. Their bodies have reabsorbed much of the mineral that was previously in their bones. If loading on a particular bone increases, the bone will remodel itself to provide the strength needed for resistance. The internal architecture of the trabeculae undergoes adaptive changes, followed by secondary changes to the external cortical portion of the bone, perhaps becoming thicker as a result.

The opposite is true as well. If the load on a bone decreases, the bone will become weaker due to turnover. It is less metabolically costly to maintain and there is no stimulus for continued remodeling required to maintain bone mass. Muscle force is a strong determinant of bone structure, particularly during growth and development.

The gender divergence in the bone-muscle relationship becomes strongly evident during adolescence. In females, growth is characterized by increased estrogen levels and increased mass and strength of bone relative to that of muscle.

In men, increases in testosterone fuel large increases in muscle, resulting in muscle force that coincides with substantial growth in bone dimensions and strength.

In adulthood, significant age-related losses are observed for both bone and muscle tissues. In contrast, the aging of the muscle-bone axis in men is a function of age-related declines in both hormones. In addition to the well-known age-related changes in the mechanical loading of bone by muscle, newer studies appear to provide evidence of age and gender-related variations in molecular signaling between bone and muscle that are independent of purely mechanical interactions.

In summary, gender differences in acquisition and age-related loss in bone and muscle tissues may be important for developing gender-specific strategies for ways to reduce bone loss with exercise.

Tim Henman performs a backhand volley at the Wimbledon tournament in Their bodies have strengthened the bones in their racquet-holding arm since they are routinely placed under higher than normal stress. Walking is an inexpensive, practical exercise associated with low injury rates and high acceptability among the elderly.

For these reasons, walking could be an appropriate approach to prevent osteoporosis and maintain bone mass. As individuals age, bone resorption can outpace bone replacement, which can lead to osteoporosis and fractures. Although most studies examining the effects of exercise on these angiogenesis were conducted on skeletal muscles, the effects of exercise training or mechanical loading on the prevention of osteoporosis via angiogenesis partially as the interface of bone and muscle are highly possible.

However, more studies are still needed to investigate the effects of exercise on the regulation of angiogenesis and osteogenesis coupling. Exercise or physical training can prevent osteoporosis in the elderly as a non-drug preventive strategy.

The interaction of mechanical loading, hormones or cytokines, and signaling pathways induced by exercise increased bone formation and reduced bone resorption, leading to the maintenance of healthy skeleton. Dysregulation of bone angiogenesis is associated with many bone diseases including osteoporosis, and exercise improves angiogenesis in bone via the regulation of key angiogenic mediators.

Further understanding the mechanisms of angiogenesis, signaling pathways, and key regulators induced by exercise will lay the foundation for the prevention of osteoporosis in the aging population. The authors would like to thank Dr. Samuel Bennett for his critical reading. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Special Issues. Academic Editor: Toshiyuki Sawaguchi. Received 14 Dec Revised 27 Feb Accepted 08 Apr Published 18 Apr Abstract Physical activity or appropriate exercise prevents the development of osteoporosis. Introduction Osteoporosis is a skeletal disease characterized by low bone mass or bone mineral density BMD , deterioration of bone micro-architecture, and increased risk of fracture [ 1 , 2 ].

Mechanical Loadings Induced by Exercise Promote Bone Formation Studies have established that exercise and sports activities can render mechanical stimuli to the joint tissues and bone which are needed to maintain the tissue properties [ 11 ].

Hormones and Cytokines Induced by Exercise Promote Bone Formation Exercise regulates hormones in the body such as estrogen, parathyroid hormone, and glucocorticoids, which may be another key mechanism in bone metabolism and remodeling [ 18 — 21 ].

Bone Angiogenesis and Osteoporosis Bone is a highly vascularized tissue with a wide network of blood vessels and capillaries that provide oxygen and nutrients for bone formation and development, which are mediated via the regulation of different signaling pathways between endothelial cells and bone cells [ 37 , 38 ]. Bone Angiogenesis Is a Potential Target for the Prevention of Osteoporosis Bone formation occurs in two different ways: one is endochondral ossification and the other is intramembranous ossification.

The Bone Angiogenesis Induced by Exercise Previous studies have shown that exercise-mechanical loading stimulated angiogenic-osteogenic responses in bone.

HIF Hypoxia activates a variety of intracellular signaling pathways and regulates target genes by the transcriptional factor, HIF hypoxia-inducible factor. FGF Fibroblast growth factors FGFs belong to a family of eighteen different ligands and play important functions in cell survival, proliferation, and differentiation through four different tyrosine kinase receptors FGFR-1, -2, -3, and -4 [ 85 ].

MMP MMPs matrix metalloproteinases are mainly secreted by osteoclasts and vascular cells, and accumulating evidence suggests that MMPs take an active part in bone angiogenesis and bone remodeling, particularly MMP-2, -9, and Notch There is no doubt that Notch plays an important role in bone metabolism and bone angiogenesis [ 96 , 97 ].

Figure 1. The potential mechanisms of exercise in promoting osteogenesis and angiogenesis. Bliuc, D. Alarkawi, T. Nguyen, J. Eisman, and J. Wade, C. Strader, L. Fitzpatrick, M. Anthony, and C. Cheng, L. Gary, J. Curtis et al. Evans, S. Racette, R. Van Pelt, L. Peterson, and D. Wohl, S. Boyd, S. Judex, and R. Cummings, K. Ensrud, P. Delmas et al. Kennel and M. Kohrt, S. Bloomfield, K. Little, M. Nelson, and V.

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In addition, a few studies have also suggested that excessive GCs induce osteoblast and osteocyte apoptosis 43 , Impaired bone formation and increased bone resorption rates results in a disordered bone remolding process in newly formed bone callus. This is not the case in EDOP. Bone resorption exceeds bone formation, but both are elevated in the pathology of EDOP The increased bone turnover is thought to be due in part to a shortening of the lifespan of osteoblasts and a prolongation of the lifespan of osteoclasts Consist with our study, Shi et al.

Kitajima, Y. This may be the reason that the early phase of intramembranous ossification is badly impaired. Our study found that GCs and estrogen deficiency could differently affect the two repair processes. However, these processes need further extensive study in the future to fully understand their mechanism.

We are the first to report that in an endochondral ossification, using an endochondral ossification model, osteoporosis impairs endochondral ossification.

We found that the difference in endochondral ossification was much smaller than the more distinct difference between GIOP and EDOP in terms of intramembranous ossification. In the beginning of endochondral ossification, the mobilization of BMSC differentiation to chondrocytes was slightly influenced, while the chondrocyte hypertrophy was clearly delayed. The results of the in vitro study were consistent with the in vivo conclusion.

These results suggest that for different types of osteoporosis, different therapeutic strategies are needed to treat osteoporotic fractures. In conclusion, our study successfully established a bone repair model that underwent repaired via intramembranous ossification or endochondral ossification and found that bone repair was differentially influenced by GIOP versus estrogen EDOP. The mice were housed for 2 weeks to acclimate to the environment before experimentation. All methods were performed in accordance with the relevant guidelines and regulations.

After 8 weeks, 5 mice from each group were euthanatized. The right femurs were collected for Micro-CT analysis to confirm the osteoporotic condition, and the left femurs were collected for in vitro cell culture. The model of bone repair by IO was established with a drill-hole injury in the middle of anteromedial tibial.

A skin incision was made at the middle of the left anteromedial tibia. Blunt dissection of the subcutaneous tissue was performed until the periosteum was exposed. A needle that was 0. Afterward, the subcutaneous tissue was repositioned, and the skin was closed by suturing Supplemental Fig. The model of bone repair by EO was established with a scratch of the periosteum in the middle of the anteromedial tibial. After the mice were anesthetized and the periosteum was exposed, a needle tip was used to scratch the periosteum lengthwise in the middle of the left anteromedial tibia.

The length of the scratch was 0. The same conditions were used for all samples. The region of interest ROI was 0. N, Tb. Sp, trabecular thickness Tb. Th , and BMD. The operator conducting the scan analysis was blinded to the treatments associated with the specimens. The samples were then embedded in paraffin. We use BrdU to mark proliferating cells and compare the cell proliferation rate between groups.

The slides were buffered in a 0. After being washed with PBS, the slides were covered with coverslips, and examined by confocal microscopy. After staining with hematoxylin, the slides were examined with an Olympus microscope mounted with an Olympus video camera. We used Image-Pro Plus version 6. We first circled the area of interest and then measured the cumulative optical density OD of what we stained. Afterward, we determined the average OD with the cumulative OD divided by the size of the area of interest.

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