Oral Microbiome

Background 

The human microbiome is composed of various microorganisms: archaea, bacteria, viruses, and various eukaryotes. Through coevolution, these organisms inhabit different sites both inside and on our bodies, where they play specific roles (Ogunrinola et al., 2020). In humans, the largest concentration and diversity of microorganisms is in the gastrointestinal tract (GIT), followed by the oral cavity (which itself is part of the gastrointestinal tract). The oral environment — the mouth — contains multiple niches, such as the teeth and the oral mucosa, that create a complex habitat for microbial colonies (Deo & Deshmukh, 2019). Notably, microbiome composition is distinct for every individual. From birth, this dynamic and symbiotic relationship allows us to maintain a balanced physiology. 

Normal Microbiome 

The microbiome plays a critical role in protecting the host against invading pathogens and preventing the overgrowth of potentially pathogenic microorganisms already present at low levels — a process known as colonisation resistance. This protection occurs across both the internal environments and external surfaces, including the skin and mucosal membranes, through combination of barrier and immune-mediated functions (Caballero-Flores et al., 2022; Lee & Kim, 2022). Colonisation resistance is a multifactorial process involving both microbe-microbe and microbe-host interactions (Siguenza et al., 2025). Microbe-microbe interactions include competition for binding sites and nutrients, as well as the production of antimicrobial compounds that attenuate pathogen virulence, their growth, or their direct elimination (Lawing & Bleich, 2025). In parallel, microbe-host interactions enhance defence by modulating immune responses, such as through immunoregulatory species, and by strengthening epithelial barriers via improved tight junction integrity and increased mucus production (Parker et al., 2017). Collectively, these mechanisms act to prevent pathogen colonisation and maintain microbial homeostasis. 

The microbiome also plays a key role in our diet, through the breakdown of complex dietary fibres. Because humans lack the enzymes required for process, microbes provide degradative/metabolic capabilities that we have not evolved independently (Fu et al., 2022). During this process, microbes produce short chain fatty acids (SCFAs), such as acetate and butyrate, which are absorbed by the gut epithelium and used by host cells as an energy source for cellular growth. These acids also support several physiological processes, including regulating inflammation, influencing gut hormones and satiety, and further protection against pathogens (Besten et al., 2013; Sankarganesh et al., 2025). 

Moreover, the development and efficacy of our immune systems are deeply associated with the gut microbiota. SCFAs produced by the microbiota moderate anti-tumour immune responses by adjusting CD8 T-cell responses (which eliminate infected or tumour cells) (Shim et al., 2023). The gut microbiota also has a role in immune cell differentiation. For example, influencing T-helper cell differentiation and maturation through the JAK/STAT signalling pathway (Wu et al., 2025), which is key for the functioning of the adaptive immune system. The microbiome also carries out many other important functions, however, these are beyond the scope of this summary. 

Dysbiosis 

Alterations in the microbial communities (dysbiosis) can have significant impacts on the host immune systems and metabolic processes (Hrncir, 2022). For example, a reduction in beneficial microbes and an increase in pro-inflammatory species can disrupt the intestinal barrier (mucosa), allowing pathogenic bacteria to come into direct contact with the underlying tissue (Armstrong et al., 2018). An overgrowth of pathogenic bacteria can also result in increased release of lipopolysaccharide (LPS) into circulation. LPS, also known as endotoxins, present in the outer-membrane of gram-negative bacteria, are immunogenic molecules which can activate several inflammatory pathways. This is especially significant at LPS concentrations which maintain low-grade, persistent inflammation (Arya et al., 2025; Skrzypczak-Wiercioch & Sałat, 2022). This can then lead to chronic inflammation and general immune dysfunction, resulting in illnesses such as inflammatory bowel disease (IBD), metabolic and cardiovascular disease, life-threatening bacterial infections, and various cancers (Shen et al., 2025; Ogunrinola et al., 2020). 

Microbiome dysbiosis can occur from a range of factors. Diet is a major contributor, as nutritional patterns can shape the various microbial compositions and their metabolic activity (Mansour et al., 2021). The use of pharmacological agents, specifically broad-spectrum antibiotics and immune-regulating drugs such as steroids, can significantly impact the microbial communities by reducing beneficial species, or creating an environment where opportunistic species proliferate. Immune dysfunctions can both be a driver and a result of microbial dysbiosis, creating a self-sustaining feedback loop that maintains an imbalance (Rojo et al., 2015; Rojo et al., 2016). Lifestyle factors, such as chronic stress and poor sleep, further contribute to imbalances through the modification of immune and metabolic pathways that can affect microbial homeostasis (Gupta & Gaur, 2025). 

Additionally, a constricted maxilla and resultant mouth breathing greatly alter the oral, pharyngeal and nasal microbiomes. In opposition to nasal breathing, mouth breathing increases oxygen exposure and dryness while altering airflow, thereby affecting local humidity, temperature and pH (Fan et al., 2020). These environmental changes can reshape microbial communities, impacting specific species and/or leading to large-scale shifts in bacterial composition and diversity. Rather than representing a beneficial increase in diversity, these changes are associated with ecological destabilisation, or dysbiosis, characterised by a depletion of beneficial bacteria and an augmentation of pathogenic species (Vrankova et al., 2024).

Consistent with this, Fan et al., (2020) demonstrated that mouth breathing alters the upper airway microbiome in a site-specific manner, with effects becoming more pronounced over time. Mouth breathing was associated with increased diversity and a shift towards more aerobic, opportunistic, and inflammation-associated species. Compared to nose breathers, mouth breathers exhibit increased microbial diversity, suggesting a less tightly regulated environment. Furthermore, it is disrupted normal site specialisation. Whereas nose breathers maintained distinct microbial communities across different airway niches (particularly within the nasal cavity), mouth breathers exhibited greater similarity between sites, indicating a loss of spatial compartmentalisation and increased mixing of microbial niches. 

Tonsils and Adenoids

These microbiome alterations are particularly relevant when considering the function of the tonsils and adenoids. As components of Waldeyer’s ring, these tissues form part of the mucosa-associated lymphoid tissue (MALT) located in the pharynx, at the intersection between the digestive and respiratory systems (Arambula et al., 2021; Kwok et al., 2022). They serve as key immune-inductive sites acting as the first line of immune surveillance against airborne and ingested antigens (Hellings et al., 2000; Samara et al., 2023). They contain specialised compartments, such as germinal centers and T-cell zones, allowing them to facilitate the activation of T-cells and the clonal expansion, affinity maturation, and differentiation of B-cells into plasma and memory cells (Brandtzaeg, 2003; Morris et al., 2015). In addition, they contribute to broader mucosal immunity by supplying immune cells to other mucosal sites, including the nasal and airway mucosa (Brandtzaeg, 2003).

Disruption of the local microbiome may therefore have direct consequences for these lymphoid tissues. Chronic exposure to dysbiotic microbial communities can drive persistent immune activation, leading to ongoing stimulation of both cell-mediated (T-cell) and humoral (B-cell) responses. This sustained inflammatory state promotes hypertrophy of the tonsillar and adenoidal tissue, which underlies clinical manifestations such as sore throat, sleep apnoea, upper airway obstruction, and recurrent tonsillitis (Zautner, 2012). In current clinical practice, these manifestations are frequently managed through the surgical removal of these tissues. Tonsillectomies and adenoidectomies remain one of the most commonly performed procedures worldwide, particularly in children  (Arambula et al., 2021).

Traditionally, enlarged or inflamed tonsils and adenoids are viewed as a primary cause of mouth breathing and related conditions, such as sleep apnoea (Sjöblom et al., 2022). However, emerging  evidence suggests that this relationship may, in some cases, operate in the reverse direction. Mouth breathing-induced microbial dysbiosis of the upper airway may act as a driver of persistent, heightened, immune activation, and subsequent inflammation, contributing to the enlargement of the tonsils and adenoids. This may, in turn, establish a self-persisting cycle, whereby airway obstruction from tissue hypertrophy promotes continued mouth breathing, further exacerbating microbial imbalance and inflammation. From this perspective, surgical removal of these tissues may not address the underlying cause and could have significant implications for immune function (Radman et al., 2020), given the important role of the tonsils and adenoids as lymphoid organs. 

References

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