1. Introduction
The elderly population is increasing in the world. The 2014 US census reported that elderly citizens comprised 20% of the population in the United States [
1]. In Taiwan, people aged
> 65 years of age will reach 30% in 2039, according to a report by the National Development Council. Moreover, chronic rhinosinusitis (CRS) represents one of the most prevalent chronic conditions [
2]. It is estimated that the condition affects between 14–16% of Americans and 10.9% of Europeans [
3]. CRS is reportedly the sixth most-prevalent disease impacting the elderly population [
4].
The etiology of CRS is attributed to multiple factors [
5]. These include bacterial and fungal infections or colonization, allergies, anatomical abnormalities, and a genetic predisposition [
2,
6,
7]. CRS has been classified based on the existence or non-existence of nasal polyps as CRS with nasal polyps (CRSwNP) or CRS without nasal polyps (CRSsNP) [
8]. It is believed that bacteria play a significant role in the development of CRS [
9,
10], and the formation of biofilms, the secretion of superantigens, and the disruption of the nasal microbiota’s balance may all contribute to CRS [
11,
12]. Comparisons between CRSwNP and CRSsNP have been made regarding their bacteriology. Niederfuhr et al. [
13] and Liu et al. [
14] found no difference in microbiological features between CRSwNP and CRSsNP, whereas Stern et al. [
15] discovered that CRSwNP is linked to a greater presence of Gram-negative bacteria compared to CRSsNP.
When studying CRS in older adults, it is essential to take into account the impact of natural aging on the immune system in order to understand the causes of geriatric CRS [
16]. Factors that increase the risk of geriatric CRS include changes to the nasal and paranasal mucosa, including atrophy of the nasal mucosa, reduced mucus production, and impaired mucociliary clearance. The fibro-fatty tissues supporting the nose can degenerate, leading to potential loss of support for nasal structures and associated nasal blockage [
17]. People over a certain age with reduced immunity to infections and a higher number of co-existing health conditions typically experience a more severe clinical manifestation of CRS [
16]. Despite a lack of investigation, age-related variations in nasal colonization are particularly unclear in elderly patients with or without nasal polyps. We hypothesized that elderly patients with chronic rhinosinusitis would have higher nasal bacterial culture positivity rates compared to adults due to decreased mucosal immunity and microbiome alteration with age. In this investigation, we attempted to explore the bacteriology of geriatric chronic rhinosinusitis (CRS), comparing geriatric cases with and without nasal polyps to those of adults in order to determine the role of bacteria in the development of CRS in the elderly population.
4. Discussion
Several factors contribute to the elderly being predisposed to CRS [
23]. Changes in the nasal and paranasal mucosa with age involve: (1) a rise in volume coupled with a drop in elasticity of the nasal mucosa; (2) a diminished or non-existent nasal cycle, partly resulting from a decrease in ciliary effectiveness; (3) atrophy of the supporting tissues of the nose and a potential loss of support for nasal structures, leading to increased nasal obstruction; (4) a higher frequency of rhinorrhea with more mucus due to heightened glandular activity and more viscous secretions; and (5) excessive mucus crusting [
24,
25].Therefore, it is assumed that geriatric CRS has different pathophysiology and clinical presentations from adult CRS [
26]. Nasal polyps were reported to be more prevalent in patients with geriatric CRS compared to those with adult CRS and that CT scan scores of patients with geriatric CRS were significantly worse than those with adult CRS [
27,
28,
29]. In contrast, our results showed nasal polyps were not more prevalent in patients with geriatric CRS than in those with adult CRS, and CT scan scores of patients with geriatric CRS were not significantly worse than those with adult CRS. However, the CT and endoscopic scores of our geriatric patients with CRSwNP were significantly worse than those of our adult patients with adult CRSwNP.
Because innate and adaptive immune responses may be altered in geriatric people, the susceptibility to infection and bacterial colonization increases [
30]. Beyond this general statement, age-related immunologic remodeling also affects hypersensitivity mechanisms that participate in CRS pathophysiology. Aging is associated with progressive impairment of epithelial barrier integrity, reduced antigen presentation, and dysregulated T helper cell polarization. These changes can modify the balance among Th1, Th2, and Th17 pathways, resulting in altered hypersensitivity profiles. In particular, age-related reductions in IgE synthesis and eosinophil recruitment may attenuate classical type I hypersensitivity, whereas diminished regulatory T-cell activity and persistent low-grade inflammation (“inflammaging”) can enhance non-IgE-mediated chronic inflammation of the sinonasal mucosa.
In elderly patients with CRSsNP, the higher bacterial culture rate observed in our study may reflect a shift from an eosinophilic-dominant to a neutrophilic-dominant inflammatory pattern, driven by immunosenescence and mucociliary dysfunction. This shift could favor persistent bacterial colonization and biofilm formation rather than eosinophil-mediated mucosal inflammation typically seen in adults. Clinically, this suggests that infection control and microbiome-targeted therapies—such as prolonged low-dose macrolides, topical antiseptics, or mucociliary clearance enhancement—might be more beneficial in geriatric CRSsNP than solely anti-inflammatory regimens. These findings highlight that age-related immune remodeling not only increases infection susceptibility but also alters the inflammatory landscape of CRS, underscoring the need for age-specific management strategies.
Analysis of the bacterial culture results detailed in
Table 1 revealed distinct patterns of colonization across the four patient subgroups. Specifically, patients with adult CRSwNP (59.6%) demonstrated a significantly higher rate of positive cultures compared to those with adult CRSsNP (29.6%) (
p < 0.05), establishing an association between nasal polyps and increased bacterial colonization in the adult population; conversely, no statistically significant difference in culture positivity was observed between geriatric CRSwNP (54.3%) and geriatric CRSsNP (57.6%) patients. Crucially, geriatric CRSsNP patients exhibited a significantly higher rate of positive bacterial cultures than their adult CRSsNP counterparts (
p < 0.01), which represents a key finding, though no difference was detected when comparing the two CRSwNP groups. This indicated that bacteria played a different role between geriatric CRS and adult CRS, especially in CRSsNP. Therefore, the treatment of geriatric patients with CRS may require different or additional therapeutic approaches [
4,
26].
Proteus spp. and
Pseudomonas aeruginosa were reported to be more common in patients with geriatric CRS than those with adult CRS [
16]. However, the occurrence of bacteria was not significantly different between patients with geriatric CRSwNP and those with geriatric CRSsNP, and between patients with adult CRSwNP and those with adult CRSsNP. Our results also showed that the occurrence of bacteria was not significantly different between patients with geriatric CRSwNP and those with geriatric CRSsNP, and between patients with adult CRSwNP and those with adult CRSsNP. In another study, less occurrence of Actinobacteria but greater abundance of Fusobacteria and Staphylococcus aureus were found in patients with geriatric CRSwNP than those with adult CRSwNP [
30]. Conversely, our results did not show any difference in the occurrence of bacteria between patients with geriatric CRSwNP and those with adult CRSwNP.
When CRS was phenotypically classified into CRSwNP and CRSsNP, in this study, the culture specimen was taken from each nostril. Therefore, it was assumed that the culture results might be different between nostrils with nasal polyps and those without nasal polyps. However, our results showed that the comparison between CRSwNP and CRSsNP was not different from the comparison between nostrils with nasal polyps and those without nasal polyps.
Beyond bacterial infection, allergic mechanisms may also contribute to the development of CRS, particularly in the elderly. While our initial discussion referred to “allergic rhinitis” as a possible comorbidity, this term may be too narrow to capture the full range of allergic and hypersensitivity disorders recognized today. “Allergic disease,” as currently defined, includes multiple phenotypes that extend beyond nasal mucosal inflammation alone. A representative example is Central Compartment Atopic Disease (CCAD)—a recently characterized subtype of CRS localized to the central nasal compartment and strongly associated with inhalant allergy [
31]. Unlike typical allergic rhinitis, CCAD demonstrates localized sinus involvement and a distinct immunopathologic profile.
Furthermore, according to the recent EAACI Position Paper on the Nomenclature of Allergic Diseases and Hypersensitivity Reactions [
32], allergic diseases should be defined primarily by their underlying immune mechanisms rather than by the clinical site of manifestation. This modern framework conceptualizes allergic diseases as a continuum of hypersensitivity conditions affecting multiple organ systems, including both upper and lower airways. Within this perspective, chronic rhinosinusitis—including atopic subtypes such as CCAD—can be regarded as part of the broader allergy–disease spectrum. Integrating this immunologic framework into the interpretation of geriatric CRS highlights that immune senescence not only impairs host defense against pathogens but also reshapes hypersensitivity responses, thereby influencing disease expression in older adults.
This study has several limitations. First, this is a retrospective study, and comorbidities related to allergic or hypersensitivity diseases—such as allergic rhinitis, asthma, and specific phenotypes like CCAD—were not systematically evaluated. According to the updated EAACI position paper [
32], allergic diseases encompass a wide range of immune mechanisms beyond allergic rhinitis; our design did not allow for differentiation according to this modern classification. We acknowledge that these unmeasured factors may have influenced the clinical and microbiological patterns observed, particularly in elderly patients where immune aging could modulate both allergic and infectious inflammation. Second, only patients with CRS who received a bilateral primary functional endoscopic sinus for treatment were enrolled in the study; therefore, our results might not be generalized to all patients with CRS or specific types of CRS. Finally, we did not classify our patients with CRSwNP as eosinophilic CRSwNP and non-eosinophilic CRSwNP. Hirotsu et al. [
33] investigated the differences in bacteria between eosinophilic and non-eosinophilic CRSwNP cases. They found no difference in bacteriology between patients with eosinophilic CRSwNP and those with non-eosinophilic CRSwNP. In contrast, Liu et al. [
14] isolated significantly more Gram-negative aerobic and facultative anaerobic bacteria from patients with CRSwNP who had normal blood eosinophil counts than from those with elevated blood eosinophils. Future prospective studies incorporating allergy testing, eosinophilic biomarkers, and molecular microbiome analysis may clarify these relationships.
Although this study used conventional bacterial culture to evaluate microbial colonization, it is important to acknowledge the methodological limitations of culture-based techniques. Many bacterial species inhabiting the sinonasal mucosa are non-culturable or require specific growth conditions that are not replicated in standard laboratory media. Recent advances in molecular microbiology—such as next-generation sequencing (NGS) and 16S rRNA gene analysis—have enabled a more comprehensive characterization of the nasal microbiome and revealed significant differences in microbial diversity among CRS phenotypes and endotypes [
34,
35]. These molecular approaches have shown that alterations in microbial community structure, rather than the presence of a single pathogen, may play an important role in the pathogenesis of CRS.
Therefore, while our culture-based results provide insight into the presence of viable bacterial species and their relative frequency across age groups, they cannot fully capture the complexity of the sinonasal microbiota. Integrating traditional culture methods with DNA-based or sequencing technologies in future studies would provide a more accurate picture of microbial–host interactions in geriatric CRS and may clarify whether age-related immune changes influence microbiome composition.