Antibiotic Exposure Reshapes Oral Microbiome and Host Immunity, Hypothesized to Increase Periodontal Susceptibility

Periodontitis is a chronic inflammatory disease driven by dysbiotic oral biofilms, leading to alveolar bone resorption and tooth loss. While traditionally viewed as a host-mediated response to pathogens, emerging evidence highlights microbial homeostasis as critical for tissue integrity. Current treatments often target pathogens directly, but the broader impact of systemic factors like antibiotic exposure on this delicate balance is a significant gap. This paper explores how antibiotics might disrupt both microbial and host immune defenses, predisposing individuals to periodontitis.

This paper presents a comprehensive hypothesis regarding the mechanisms by which systemic antibiotic exposure may increase periodontitis susceptibility. The authors synthesized evidence from existing literature, integrating findings on antibiotic-induced changes in the oral and gut microbiomes, host immune modulation, and direct effects on bone cell function. They propose a multi-faceted model where antibiotics disrupt microbial homeostasis, weaken colonization resistance, and alter host inflammatory responses, thereby predisposing individuals to chronic periodontal inflammation.

The authors hypothesize that repeated or prolonged systemic antibiotic exposure contributes to periodontitis susceptibility through several interconnected pathways. They propose that antibiotics destabilize the oral and gut microbiomes, reducing protective commensals and microbial diversity, which creates niches for opportunistic pathogens and weakens colonization resistance. Beyond microbial effects, certain antibiotic classes are proposed to directly modulate host immune responses, altering neutrophil activity, cytokine signaling, and antimicrobial peptide balance. This impairs the host's capacity to regulate inflammation against dental plaque. Furthermore, antibiotics may interfere with osteoblast and osteoclast function, modifying bone cell viability and disturbing remodeling dynamics. This indirect route could shape alveolar bone responsiveness during inflammatory challenges, making it more vulnerable to resorption. Collectively, these microbial, immune, and tissue-level effects provide a biologically coherent framework for how antibiotics could modify periodontal susceptibility. > Antibiotics destabilize the oral and gut microbiomes, reducing protective commensals and microbial diversity, which creates niches for opportunistic pathogens and weakens colonization resistance.