The DOI matches its Crossref record; 134 of the 134 references it cites were found in a registry or an index.
The effects of smoking on bone metabolism
Abstract
Osteoporosis is a common, morbid and costly disorder characterized by deterioration in bone strength. Cigarette smoking is associated with reduced bone mineral density (BMD) and increased fracture risk. There are basic, clinical, and observational studies that define several of the underlying pathophysiologic mechanisms that predispose smokers to bone loss. Such mechanisms include alterations in calciotropic hormone metabolism and intestinal calcium absorption, dysregulation in sex hormone production and metabolism, alterations in adrenal cortical hormone metabolism and in the receptor activator of nuclear factor kappa-B (RANK), receptor activator of nuclear factor kappa-B ligand (RANKL), and osteoprotegerin (OPG) system (RANK-RANKL-OPG system), and direct cellular effects of cigarette use on bone cells. In addition, there is evidence of reversibility in the aforementioned mechanisms with smoking cessation. In summary, cigarette smoking is a reversible risk factor for osteoporosis and osteoporotic fractures through diverse pathophysiologic mechanisms.
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In the citing paper
“Similar to women, the mechanism of aromatase inhibition was reported in men; this mechanism suppressed production of estradiol from testosterone [16].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [16]
In the citing paper
“which may be related to the decreased intake of vitamin D or the induction of the liver enzyme that enhances hepatic metabolism of vitamin D metabolites [5], or via suppression of parathyroid hormone (PTH) release [16].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [16]
In the citing paper
“Bone is dynamic tissue undergoing continuous remodeling via bone formation and resorption [16, 68].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [16]
In the citing paper
“The activities of both are regulated by several factors, including the RANKL-RANK-OPG pathway, estradiol, various cytokines, and calciotropic hormones [16, 45, 69].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [16]
In the citing paper
“Nicotine has an inhibitory effect on osteogenesis and on angiogenesis that play key roles in bone metabolism [16].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [16]
In the citing paper
“After bone reaches peak mass, it undergoes constant remodeling via resorption followed by formation [16, 68].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [16]
In the citing paper
“Laboratory studies found rats exposed to smoke inhalation had higher levels of RANKL/OPG ratio compared to control rats not exposed to smoke [16, 90].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [16]
In the citing paper
“Several studies have indicated that smoking downregulates vitamin D serum levels [42,43] and inhibits the production of PTH [44].”
From An Overlooked Bone Metabolic Disorder: Cigarette Smoking-Induced Osteoporosis (2022) · cites this paper as [44]
In the citing paper
“Cigarette smoking is also considered one of the main social risk factors for developing metabolic bone diseases (such as osteoporosis, Paget’s disease, osteomalacia, and diabetic osteopathy), which compromise bone remodeling for a variety of reasons, including altered bone formation by osteoblasts, increased bone degradation by osteoclasts, or a combination of both [12,14,15].”
From Skeletal System Biology and Smoke Damage: From Basic Science to Medical Clinic (2021) · cites this paper as [14]
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Metadata
- Authors
- Yoon, V., Maalouf, N. M., & Sakhaee, K.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Sakhaee, K.
- Venue
- Osteoporosis International
- Published
- 2012-02-21
- Volume
- 23
- Issue
- 8
- Pages
- 2081-2092
- ISSN
- 0937-941X (ISSN-L)
- 1433-2965
- OpenAlex
- W2142262092
- Cited by
- 268
- References
- 134
- Citations by year
- 2026: 14 · 2025: 25 · 2024: 20 · 2023: 25 · 2022: 26 · 2021: 18 · 2020: 21 · 2019: 23 · 2018: 15 · 2017: 13 · 2016: 13 · 2015: 14 · 2014: 18 · 2013: 16 · 2012: 7
- FWCI
- 3.12
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Osteoporosis International (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Amgen
- Topics
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
- Keywords
- cigarette smoking, osteoporosis, bone metabolism, bone mineral density, fracture risk, sex hormones, RANK/RANKL/OPG system, calcium absorption, smoking cessation, bone loss
- MeSH terms
- Adrenal Cortex Hormones, Adult, Aged, Aged, 80 and over, Animals, Bone and Bones, Calcitriol, Female, Humans, Male, Middle Aged, Osteoblasts, Osteoclasts, Osteoporosis, Parathyroid Hormone, Gonadal Steroid Hormones, Smoking, Bone Density, Smoking Cessation, Intercellular Signaling Peptides and Proteins, Young Adult, Osteoporotic Fractures
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