Inflammation-induced Bone Remodeling in Periodontal Disease and the Influence of Post-menopausal Osteoporosis

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.

2020 ◽  
Vol 11 ◽  
Author(s):  
Victor Gustavo Balera Brito ◽  
Mariana Sousa Patrocinio ◽  
Maria Carolina Linjardi de Sousa ◽  
Ayná Emanuelli Alves Barreto ◽  
Sabrina Cruz Tfaile Frasnelli ◽  
...  

Periodontal disease (PD) is a prevalent inflammatory disease with the most severe consequence being the loss of the alveolar bone and teeth. We therefore aimed to evaluate the effects of telmisartan (TELM), an angiotensin II type 1 receptor (Agtr1) antagonist, on the PD-induced alveolar bone loss, in Wistar (W) and Spontaneous Hypertensive Rats (SHRs). PD was induced by ligating the lower first molars with silk, and 10 mg/kg TELM was concomitantly administered for 15 days. The hemimandibles were subjected to microtomography, ELISA was used for detecting tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), CXCL3, and CCL2, while qRT-PCR was used for analyzing expression of components of renin-angiotensin system (RAS) (Agt, Ace, Agt1r, Agt2r, Ace2, and Masr), and bone markers (Runx2, Osx, Catnb, Alp, Col1a1, Opn, Ocn, Bsp, Bmp2, Trap, Rank, Rankl, CtsK, Mmp-2, Mmp-9, and osteoclast-associated receptor (Oscar)). The SHR + PD group showed greater alveolar bone loss than the W + PD group, what was significantly inhibited by treatment with TELM, especially in the SHR group. Additionally, TELM reduced the production of TNF-α, IL-1β, and CXCL3 in the SHR group. The expression of Agt increased in the groups with PD, while Agtr2 reduced, and TELM reduced the expression of Agtr1 and increased the expression of Agtr2, in W and SHRs. PD did not induce major changes in the expression of bone formation markers, except for the expression of Alp, which decreased in the PD groups. The bone resorption markers expression, Mmp9, Ctsk, and Vtn, was higher in the SHR + PD group, compared to the respective control and W + PD group. However, TELM attenuated these changes and increased the expression of Runx2 and Alp. Our study suggested that TELM has a protective effect on the progression of PD, especially in hypertensive animals, as evaluated by the resorption of the lower alveolar bone. This can be partly explained by the modulation in the expression of Angiotensin II receptors (AT1R and AT2R), reduced production of inflammatory mediators, the reduced expression of resorption markers, and the increased expression of the bone formation markers.


2014 ◽  
Vol 184 (4) ◽  
pp. 1142-1151 ◽  
Author(s):  
Thomas L. Andersen ◽  
Ellen M. Hauge ◽  
Lars Rolighed ◽  
Jens Bollerslev ◽  
Per Kjærsgaard-Andersen ◽  
...  

2009 ◽  
Vol 7 (44) ◽  
pp. 353-372 ◽  
Author(s):  
L. M. McNamara

Current drug treatments for post-menopausal osteoporosis cannot eliminate bone fractures, possibly because the mechanisms responsible for bone loss are not fully understood. Although research within various disciplines has significantly advanced the state of knowledge, fundamental findings are not widely understood between different disciplines. For that reason, this paper presents noteworthy experimental findings from discrete disciplines focusing on post-menopausal osteoporosis. These studies have established that, in addition to bone loss, significant changes in bone micro-architecture, tissue composition and micro-damage occur. Cellular processes and molecular signalling pathways governing pathological bone resorption have been identified to a certain extent. Ongoing studies endeavour to determine how such changes are initiated at the onset of oestrogen deficiency. It emerges that, because of the discrete nature of previous research studies, the sequence of events that lead to bone fracture is not fully understood. In this paper, two sequences of multi-scale changes are proposed and the experimental challenges that need to be overcome to fully define this sequence are outlined. Future studies must comprehensively characterize the time sequence of molecular-, cellular- and tissue-level changes to attain a coherent understanding of the events that ultimately lead to bone fracture and inform the future development of treatments for post-menopausal osteoporosis.


2021 ◽  
Vol 10 (1) ◽  
pp. e43710111975
Author(s):  
Ana Cláudia Ervolino da Silva ◽  
Fábio Roberto de Souza Batista ◽  
Juliana de Moura ◽  
Juliana Zorzi Coléte ◽  
Fernando Chiba ◽  
...  

Post-menopausal osteoporosis is detrimental to bone metabolism as well as alveolar repair. This osteometabolic disorder is an obstacle to the success of maxillofacial rehabilitations, since a large number of patients are carriers of the disease. Denosumab is widely used as a treatment for post menopausal osteoporosis. This drug exerts an antiabsorptive action by inhibiting RANKL, helping to reduce the bone loss caused by osteoporosis.  This study aimed to evaluate the repair bone formed after the extraction of the upper incisor of estrogen-deficient rats treated with anti-RANKL monoclonal antibody. The rats (Rattus novergicus albinus, Wistar) were ovariectomized or SHAM operated (n=36). Half of the ovariectomized rats were treated with osteoprotegerin with an Fc fragment (OPG-Fc; 10mg/kg, twice a week), the other half received saline solution as control. After 30 days the rats had their right upper incisor extracted. After 60 days of extraction, the alveoli were evaluated by immunohistochemical, computerized microtomography and confocal microscopy. The OPG-Fc decreased the percentage of bone volume (BV/TV), thickness (Tb.Th) and number of alveolar trabecules (Tb.N) when compared to groups that received saline solution (p<0.005). The OPG-Fc increased the separation between the trabecules (Tb.Sp) and the porosity (Po.tot) of the reparative alveolar bone (p<0.005). The OPG-Fc decreased immunolabelling for RANKL and TRAP when compared to groups that received saline solution. Treatment with OPG-Fc decreased bone neoformation but preserved preexisting bone tissue. This data is supported by the mineral apposition rate, which showed higher values for OVX/OPG-Fc when compared to the OVX group.


Author(s):  
Jun-ichi Otogoto ◽  
Hidetoshi Watanabe ◽  
Takashi Mizoguchi ◽  
Michiaki Ono ◽  
Toshi Nomura ◽  
...  

2017 ◽  
Vol 26 (3) ◽  
pp. 107-114
Author(s):  
Dan Piperea-Sianu ◽  
◽  
Adela M. Ceau ◽  
Mara Carsote ◽  
Alexandru G. Croitoru ◽  
...  

Osteoporosis and periodontal disease (PD) are two chronic diseases, characterized by bone loss, with systemic or local impact (alveolar bone). Both pathologies have a progressive evolution, leading to systemic bone loss in the case of osteoporosis and bone lysis localized in the alveolar bone in the case of periodontal disease. The present paper presents recent data from the literature on the association between periodontal disease and osteoporosis, on the role of cytokines in the bone resorption-apposition imbalance, and on how periodontal disease causes changes in serum levels of cytokines, leading to disorders in the systemic bone formation. We also found it useful, especially for rheumatologists, to outline the extent to which periodontal disease can create a systemic context favorable to the development of osteoporosis.


2017 ◽  
Vol 3 (3) ◽  
pp. S38
Author(s):  
Shah Waliullah ◽  
Vineet Sharma ◽  
R.N. Srivastava ◽  
A.A. Mahdi ◽  
Yashodhara Pradeep ◽  
...  

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

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