Correlation between Absence of Bone Remodeling Compartment Canopies, Reversal Phase Arrest, and Deficient Bone Formation in Post-Menopausal Osteoporosis

2014 ◽  
Vol 184 (4) ◽  
pp. 1142-1151 ◽  
Author(s):  
Thomas L. Andersen ◽  
Ellen M. Hauge ◽  
Lars Rolighed ◽  
Jens Bollerslev ◽  
Per Kjærsgaard-Andersen ◽  
...  
2006 ◽  
Vol 85 (7) ◽  
pp. 584-595 ◽  
Author(s):  
U.H. Lerner

Bone mass in the skeleton is dependent on the coordinated activities of bone-forming osteoblasts and bone-resorbing osteoclasts in discrete bone multi-cellular units. Remodeling of bone in these units is important not only for maintaining bone mass, but also to repair microdamage, to prevent accumulation of too much old bone, and for mineral homeostasis. The activities of osteoblasts and osteoclasts are controlled by a variety of hormones and cytokines, as well as by mechanical loading. Most importantly, sex hormones are very crucial for keeping bone mass in balance, and the lack of either estrogen or testosterone leads to decreased bone mass and increased risk for osteoporosis. The prevalence of osteoporotic fractures is increasing dramatically in the Western part of the world and is a major health problem in many countries. In the present review, the cellular and molecular mechanisms controlling bone remodeling and the influence of sex hormones on these processes are summarized. In a separate paper in this issue, the pathogenesis of post-menopausal osteoporosis will be compared with that of inflammation-induced bone remodeling, including the evidence for and against the hypothesis that concomitant post-menopausal osteoporotic disease influences the progression of periodontal disease.


2006 ◽  
Vol 85 (7) ◽  
pp. 596-607 ◽  
Author(s):  
U.H. Lerner

During physiological conditions, the skeleton is remodeled in so-called bone multi-cellular units. Such units have been estimated to exist at 1–2 x 106 sites in the adult skeleton. The number and activities of these units are regulated by a variety of hormones and cytokines. In post-menopausal osteoporosis, lack of estrogen leads to increased numbers of bone multi-cellular units and to uncoupling of bone formation and bone resorption, resulting in too little bone laid down by osteoblasts compared with the amount of bone resorbed by osteoclasts. Inflammatory processes in the vicinity of the skeleton, e.g., marginal and apical periodontitis, will affect the remodeling of the nearby bone tissue in such a way that, in most patients, the amount of bone resorbed exceeds that being formed, resulting in net bone loss (inflammation-induced osteolysis). In some patients, however, inflammation-induced bone formation exceeds resorption, and a sclerotic lesion will develop. The cellular and molecular pathogenetic mechanisms in inflammation-induced osteolysis and sclerosis are discussed in the present review. The cytokines believed to be involved in inflammation-induced remodeling are very similar to those suggested to play crucial roles in post-menopausal osteoporosis. In patients with periodontal disease and concomitant post-menopausal osteoporosis, the possibility exists that the lack of estrogen influences the activities of bone cells and immune cells in such a way that the progression of alveolar bone loss will be enhanced. In the present paper, the evidence for and against this hypothesis is presented.


2014 ◽  
Author(s):  
Renato Pastore ◽  
Patrizio Pasqualetti ◽  
Laura Chioma ◽  
Giuseppe Vancieri ◽  
Simona Frontoni

2010 ◽  
Vol 2 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Annie Shirwaikar ◽  
Saleemulla Khan ◽  
Yogesh H. Kamariya ◽  
Bharatkumar D. Patel ◽  
Falguni P. Gajera

Bone ◽  
2010 ◽  
Vol 46 ◽  
pp. S67-S68
Author(s):  
Thomas Andersen ◽  
Ellen Hauge ◽  
Jens Bollerslev ◽  
Jean-Marie Delaisse

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