Researchers have known that smoking increases one’s risk of developing osteoporosis, a bone condition characterized by deteriorating bones. Despite noting a relationship between smokers and bone loss, researchers have not identified a biological explanation as to why smoking might lead to osteoporosis. In a new study conducted by a joint research team from the University of Pennsylvania and the Mount Sinai Medical Center, researchers believe that chemicals in cigarettes trigger bone loss to happen faster than usual.
“It has been known from many epidemiological studies that smokers usually show bone loss, and their bone density is much lower than non-smokers’ bone density,” said Narayan Avadhani, Harriet Ellison Woodward Professor of Biochemistry and chair of the Department of Animal Biology in Penn’s School of Veterinary Medicine reported by Medical Xpress. Avadhani is one of the authors of this study. “What we show here is that excessive formation of osteoclasts by cigarette chemicals causes bone loss.”
The researchers know that the bones in the human body naturally regenerate all the time. As time passes and bones age, the rate of deterioration speeds up, which could lead to chronic bone diseases, such as osteoporosis. In this study, the research team studied the effects of smoking on the process of bone remodeling in mouse models. The researchers found that cells in the body that are responsible for creating new bones are known as osteoblasts. The cells that are responsible for breaking down bones are called osteoclasts. When osteoclasts break down bones, the process releases minerals and other molecules. Both osteoblasts and osteoclasts appear to be regulated by RANK liquid, a protein molecule.
The researchers observed that the chemicals found in cigarettes tend to bind to AH – Receptors, also known as cellular aryl hydrocarbon receptors. When these chemicals and the receptors bond, it triggers the production of more osteoclasts, which then leads to a faster bone deterioration rate.
“Our study implicates a number of poly aryl hydrocarbons and dioxins found in tobacco smoke,” Mone Zaidi, a professor of medicine and of structural and chemical biology and director of the Mount Sinai Bone Program, said. Zaidi co-authored this study. “[The study] clarifies how those toxins enhance active bone breakdown to make the skeleton more fragile. It is our hope that these findings provide the conceptual framework for the design of novel therapies to help prevent and treat osteoporosis.”
The researchers hope that this finding could help with future research looking into ways of preventing bone loss in smokers. The study, “Smoke Carcinogens Cause Bone Loss Through the Aryl Hydrocarbon Receptor and Induction of Cyp Enzymes,” was published in Proceedings of the National Academy of Sciences.
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