Journal of Bone Research
Open Access

Smoking Effect on Bone Mass and Bone Mineral Density (BMD)

Giorgio Treglia^{* *}Correspondence: Giorgio Treglia, Department of Oncology, Oncology Institute of Southern Switzerland, Bellinzona, Switzerland, Email:

Author info »

Description

The osteocytes, which control this process, are responsible for bone resorption by the osteoclasts and bone synthesis by the osteoblasts in adult bone. Numerous signaling pathways are involved in the intricate regulation of bone metabolism. Bone Turnover Markers (BTMs) in the blood and Bone Mineral Density (BMD) measurements can be used to determine how well these processes are balanced. The carboxyl-terminal crosslinked telopeptide of Type 1 Collagen (CTX-1), a degradation byproduct of type 1 collagen bone resorption, and procollagen type 1 amino-terminal propeptide are the recommended BTMs for assessing resorption and creation, respectively (P1NP).

Numerous chemicals control the production and resorption of bones. Receptor Activator of Nuclear factor ĸB Ligand (RANKL) encourages osteoclastogenesis and bone resorption. TNF- (Tumour Necrosis Factor) plays a significant part in inflammation and, in collaboration with RANKL, induces bone resorption. Osteoprotegerin (OPG) is a protein receptor that binds to RANKL and prevents the development of osteoclasts. Through inhibiting the established WNT signaling pathway, sclerostin and Dickkopf-1 (DKK1) are effective inhibitors of bone formation. The multifunctional adipokine leptin appears to restrict bone growth through a central pathway in addition to stimulating bone formation via a peripheral pathway. Additionally, vitamin D and Parathyroid Hormone (PTH) have direct effects on bones and are critical in controlling serum calcium levels. As a result, measuring these chemicals may provide information about the mechanisms underlying changes in BTM serum levels.

More than 7,000 chemicals are found in tobacco smoke, and research has shown that smoking leads to early death, cancer, and a number of chronic disorders, including coronary heart disease and chronic obstructive pulmonary disease. Numerous studies back up the claim that smoking has an impact on the skeletal system. The Fracture Risk Assessment Tool has been updated to add smoking as a risk factor for fractures and osteoporosis. Three million fractures a year in the United States are predicted to be caused by osteoporosis, with a projected cost of $25.3 billion by 2025. According to recent research, the mechanisms of bone turnover are unbalanced as a result of cigarette use. This results in lower bone mass and Bone Mineral Density (BMD), which makes bones more susceptible to osteoporosis and fracture. The most recent Surgeon General report causally connected tobacco use with a number of skeletal system problems due to the high calibre of the available data (e.g., hip fracture, rheumatoid arthritis, and periodontitis).

The development of numerous cessation programmes has resulted from the realisation that the greatest method to lessen the negative effects and costs of smoking on human health is to stop using tobacco. However, the effectiveness of these programmes is only moderate. The factors that lead people to start smoking again are probably complicated, and the introduction of new smoking devices like water pipes and ecigarettes just adds to the complexity. While programmes are being established to encourage cessation, there is a need to assist people who already experience bone problems as a result of smoking. More research is needed to comprehend the pathophysiologic mechanisms underlying smoking's detrimental effects on bone health.

Bone tissue is directly impacted by smoking. Bone is a dynamic tissue that continuously remodels itself through bone resorption and creation. The two main cells that shape bones are osteoblasts and osteoclasts. The RANKL-RANK-OPG pathway, oestrogen, other cytokines, and calciotropic hormones are a few of the agents that control both of their activities.

Numerous receptors, including nicotinic acetylcholine receptors, androgen receptors, and aryl hydrocarbon receptors in osteoblasts and osteoclasts, are implicated in osteoblast and osteoclast activity. Nicotine, which binds to nicotinic receptors in osteoblasts, is the substance in tobacco that is most prevalent. This binding promotes cell proliferation at low concentrations, but at high concentrations, it prevents the formation of osteoblasts, which leads to cell death. Nicotine inhibits angiogenesis and osteogenesis, two processes important for bone metabolism. A dose-dependent inhibitory effect of nicotine on osteoblast formation and vascular endothelial growth factor, both essential for angiogenesis, was discovered in an in vivo rabbit investigation. Additionally, aryl hydrocarbon receptors in osteoblasts and osteoclasts can be bound by chemical polycyclic aryl hydrocarbon molecules like benzo(a)pyrene, and this constitutive binding to aryl hydrocarbon receptors may be harmful to bone.