Cigarette Smoke Exposure Inhibits Osteoclast Apoptosis via the mtROS Pathway

Qin, Yi; Jiang, Yiyang; Mei, Shenghui; Feng, Jiaxuan; Guo, Lijia; Du, Juan; Graves, Dana T.; Liu, Y.

doi:10.1177/00220345211009471

Cited by 13 publications

(16 citation statements)

References 42 publications

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“…Cigarette smoke increases bone resorption, which may be due to a number of factors One involves the direct effect of smoke components on osteoclasts. Cigarette smoke exposure increases alveolar bone remodeling and osteoclastogenesis ( 173 ). The increase in osteoclasts can be explained mechanistically due to smoke-induced down-regulation of the caspase 3 pathway in these cells.…”

Section: Periodontal Diseasementioning

confidence: 99%

“…The increase in osteoclasts can be explained mechanistically due to smoke-induced down-regulation of the caspase 3 pathway in these cells. In addition, cigarette smoke affects osteoclast-precursors so that they are predisposed to form osteoclasts ( 173 ). Long term smokers have increased oxidative stress that enhances osteoclast formation and survival.…”

Section: Periodontal Diseasementioning

confidence: 99%

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Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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Periodontitis involves the loss of connective tissue attachment and alveolar bone. Single cell RNA-seq experiments have provided new insight into how resident cells and infiltrating immune cells function in response to bacterial challenge in periodontal tissues. Periodontal disease is induced by a combined innate and adaptive immune response to bacterial dysbiosis that is initiated by resident cells including epithelial cells and fibroblasts, which recruit immune cells. Chemokines and cytokines stimulate recruitment of osteoclast precursors and osteoclastogenesis in response to TNF, IL-1β, IL-6, IL-17, RANKL and other factors. Inflammation also suppresses coupled bone formation to limit repair of osteolytic lesions. Bone lining cells, osteocytes and periodontal ligament cells play a key role in both processes. The periodontal ligament contains cells that exhibit similarities to tendon cells, osteoblast-lineage cells and mesenchymal stem cells. Bone lining cells consisting of mesenchymal stem cells, osteoprogenitors and osteoblasts are influenced by osteocytes and stimulate formation of osteoclast precursors through MCSF and RANKL, which directly induce osteoclastogenesis. Following bone resorption, factors are released from resorbed bone matrix and by osteoclasts and osteal macrophages that recruit osteoblast precursors to the resorbed bone surface. Osteoblast differentiation and coupled bone formation are regulated by multiple signaling pathways including Wnt, Notch, FGF, IGF-1, BMP, and Hedgehog pathways. Diabetes, cigarette smoking and aging enhance the pathologic processes to increase bone resorption and inhibit coupled bone formation to accelerate bone loss. Other bone pathologies such as rheumatoid arthritis, post-menopausal osteoporosis and bone unloading/disuse also affect osteoblast lineage cells and participate in formation of osteolytic lesions by promoting bone resorption and inhibiting coupled bone formation. Thus, periodontitis involves the activation of an inflammatory response that involves a large number of cells to stimulate bone resorption and limit osseous repair processes.

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Section: Periodontal Diseasementioning

confidence: 99%

Section: Periodontal Diseasementioning

confidence: 99%

Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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“…140 The rationale behind this clinical observation is that smoking increases the number of osteoclasts by inhibiting osteoclast apoptosis via the mitochondrial reactive oxygen species and cytochrome C-caspase-3 pathway, also affecting bone marrow cells, leading to an increased formation of osteoclasts. 141 It is encouraged, therefore, to restrict smoking for at least 3 months before vertical ridge augmentation. 4 Moreover, other conditions affecting wound healing such as diabetes mellitus have been identified as detrimental factors for vertical ridge augmentation.…”

Section: Fac Tor S Influen Cing the Outcome S Of Verti C Al Ridg E Au...mentioning

confidence: 99%

“…A smoking habit has been suggested to limit the extent of vertical ridge augmentation, 4 to lead to a higher risk of postoperative complications, 36,66 and to increase the rate of implant failure in regenerated bone 140 . The rationale behind this clinical observation is that smoking increases the number of osteoclasts by inhibiting osteoclast apoptosis via the mitochondrial reactive oxygen species and cytochrome C‐caspase‐3 pathway, also affecting bone marrow cells, leading to an increased formation of osteoclasts 141 . It is encouraged, therefore, to restrict smoking for at least 3 months before vertical ridge augmentation 4 .…”

Section: Factors Influencing the Outcomes Of Vertical Ridge Augmentat...mentioning

confidence: 99%

Minimal invasiveness in vertical ridge augmentation

Urban

Montero

Sanz‐Sánchez

et al. 2023

Periodontology 2000

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Vertical ridge augmentation is one of the most challenging procedures in implant dentistry because of the advanced skills required by the operator and the fact that bone augmentation is aimed outside the bony contour, in an environment of reduced blood supply. What is more, the flap management required to ensure soft tissue closure frequently leads to associated comorbidities in terms of swelling and hematomas. For these reasons, and even if autologous onlay block grafts are still the gold standard, new techniques and biomaterials have favored the development of potentially less invasive approaches. The present work evaluates the most recent strategies in vertical ridge augmentation to reduce invasiveness and complications, including diagnostic/treatment planning considerations, surgical techniques, digital tools (eg, customized titanium meshes/membranes or bone blocks), and future trends in the field of tissue engineering and cell therapy.

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“…In excess, mtROS can contribute to mitochondrial dysfunction and in many diseases [74][75][76] . This undeniable influence of mtROS on other signaling pathways is a key mechanism often implicated by inhaled toxicants 33,[77][78][79] .…”

Section: Cigarette Smoke (Cs) and Cigarette Smoke Extract (Cse) Trigg...mentioning

confidence: 99%

Alterations of Mitochondrial Network by Cigarette and e-Cigarette Vaping

Kanithi¹,

Junapudi²,

Shah³

et al. 2022

Preprint

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Toxins present in cigarette and e-cigarette smoke constitute a significant cause of illnesses and are known to have fatal health impacts. Specific mechanisms by which toxins present in smoke impair cell repair are still being researched and are of prime interest for developing more effective treatments. Current literature suggests toxins present in cigarette smoke and aerosolized e-vapor trigger abnormal intercellular responses, damage mitochondrial function, and consequently disrupt the homeostasis of the organelle’s biochemical processes by increasing reactive oxidative species. Increased oxidative stress sets off a cascade of molecular events, disrupting optimal mitochondrial morphology and homeostasis. Furthermore, smoking-induced oxidative stress may also amalgamate with other health factors to contribute to various pathophysiological processes. An increasing number of studies show that toxins may affect mitochondria even though exposure to secondhand or thirdhand smoke. This review assesses the impact of toxins present in tobacco smoke and e-vapor on mitochondrial health, networking, and critical structural processes including mitochondria fission, fusion, hyperfusion, fragmentation, and mitophagy. The efforts are focused on discussing current evidence linking toxins present in first, second, and thirdhand smoke to mitochondrial dysfunction

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Cigarette Smoke Exposure Inhibits Osteoclast Apoptosis via the mtROS Pathway

Cited by 13 publications

References 42 publications

Impact of the host response and osteoblast lineage cells on periodontal disease

Impact of the host response and osteoblast lineage cells on periodontal disease

Minimal invasiveness in vertical ridge augmentation

Alterations of Mitochondrial Network by Cigarette and e-Cigarette Vaping

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