A new study about the side effects of antibiotic treatment reveals that it may dysregulate postpubertal skeletal development by interfering with gut bacteria.

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A new study examines bone health, antibiotics, and the immune system.

The trillions of bacteria living in our bodies are crucial for our health.

They support the gastrointestinal and immune systems.

They also help the body absorb nutrients from foods and supplements.

People often call the “good” bacteria within us “commensal,” because they live together in harmony without causing any harm.

However, we often treat the “bad” microbes that cause disease using antibiotics.

Some researchers from the Medical University of South Carolina (MUSC) in Charleston specialize in osteoimmunology, the “interface of the skeletal and immune systems.” The scientists analyzed the impact of antibiotics on postpubertal skeletal development and published their results in The American Journal of Pathology.

The study demonstrated that antibiotic disruption of the gut microbiota causes a pro-inflammatory response that may lead to less bone resorption, a process by which osteoclasts, or large bone cells, release the minerals and transfer them to the blood.

According to Chad M. Novince, Ph.D. — who studies the link between microbiome and skeletal health — the study “introduces antibiotics as a critical exogenous modulator of gut microbiota osteoimmune response during postpubertal skeletal development.”

The postpubertal phase of development supports the accumulation of about 40 percent of peak bone mass. Previous research by Novince and team had already shown that the gut microbiota contributes to skeletal health.

To determine the impact of antibiotics on the gut microbiota in postpubertal skeletal development, Novince conducted a new study. He did so in collaboration with microbiome scientist Alexander V. Alekseyenko, Ph.D., founding director of the MUSC Program for Human Microbiome Research.

The scientists treated mice with a cocktail of three antibiotics. Their findings showed that antibiotic treatment caused disruption in the gut microbiota. Following these results, Novince demonstrated that there were also significant changes to the trabecular bone. This is the spongy part crucial for metabolism.

The delicate balance of bone resorption by osteoclasts and bone-building by osteoblasts control bone metabolism.

The team saw that although there were no changes to the osteoblasts, the number of osteoclast cells, as well as their size and activity levels, was increased. This affects the process of bone resorption.

The scientists found that levels of osteoclastic signaling molecules were increased in the circulation of animals that they had treated with antibiotics. These findings led them to believe that increased osteoclast activity may be the result of a specific immune response to changes in the microbiota.

Further analysis of immune cells in the bone marrow confirmed this theory, revealing a significant increase in myeloid-derived suppressor cells (MDSCs) of antibiotic-treated animals. MDSCs are cells that regulate the immune response during the course of various conditions.

Our study is actually able to dive into specific adaptive and innate immune cell mechanisms within the bone marrow environment to show that there is an effect on the bone cells.”

Study co-author Jessica D. Hathaway-Schrader, Ph.D.

This study demonstrated that antibiotic disruption of the gut microbiota has a significant impact on the communication between the immune system and bone cells. Its findings may lead to clinical trials “aimed at defining the impact of specific antibiotics on the gut microbiome.”

The objective of the research is to support the development of noninvasive therapeutic interventions in the microbiome to prevent and treat skeletal deterioration.