Dental caries is a common dental condition [1] that arises due to interaction between the host, environment, and oral microbiome [2]. A considerable proportion of the oral microbiome is found attached to oral hard and soft tissues in a complex but reproducible arrangement, and embedded in an extracellular matrix, called oral biofilm [3]. Dental caries lesions (cavities) result from a complex interplay between the presence of cariogenic bacteria such as Streptococcus mutans and Streptococcus sorbinus in oral biofilm and the availability of a carbohydrate-rich diet. The metabolic end products of this interplay between specific microbiota and the dietary source are acids capable of demineralizing dental hard tissues [3, 4]. Balance between risk factors (such as reduced salivary flow, frequency and composition of carbohydrate rich foods) and protective factors (such as good oral hygiene and regular dental care visits) determines the extent and severity of dental caries [4].

Several hypotheses attempt to explain the microbial etiopathogenesis of dental caries. The non-specific plaque (biofilm) hypothesis and the specific plaque (biofilm) hypothesis present contrarian views on the role of cariogenic microbiota in oral biofilm. The non-specific plaque hypothesis posits that there is a linear relationship between the quantity of dental biofilm and the resulting dental caries with the inherent assumption that all microbes are participants in disease causation [4, 5]. As more data on the functional heterogeneity of microbes in the dental biofilm have become available, this viewpoint has been refined. The specific plaque hypothesis posits that certain microbiota are crucial in the causation of dental caries (cariogenic bacteria) [4, 6]. An additional hypothesis, the ecological plaque hypothesis, emphasizes the role of environmental factors and considers them to be driving factors for the selection of bacteria in a biofilm population [7, 8]. Conversely, there will be bacteria that do not thrive in particular environments and as such the environment controls the selection of a disease-specific biofilm. Similarly, in the extended ecological plaque hypothesis, it is proposed that pathogenic microbiota, selected by the environment, can further shape the disease-specific biofilm and therefore, the environment and microbiota act synergistically to shape the disease process [9]. This evolution of theories to explain the etiopathogenesis of dental caries emphasizes the role of three elements: host, environment, and microbes.

Dental caries management in routine clinical practice includes control of active carious lesions by removal of infected and affected tooth structures, restoration of carious defects, and prevention regimens to eliminate or reduce the development of new carious lesions [10]. Current terminologies and ontologies, however, do not accurately represent the important role that the microbiome has in the formation of carious lesions. Rather, they focus on the anatomical features of carious lesions, such as being demineralized or cavitated, and often obfuscate the distinctions between dental caries as a disease affecting a tooth, as lesions that are produced as a result of the disease, and as lesions produced as a result of dysbiosis in the oral microbiome. As our understanding of caries associated with the dysbiotic microbiome develops, precision approaches to modulate host immunity and microbiome will certainly follow [11]. In this regard, there has been considerable progress in in vitro systems and in vivo animal models. Directed approaches to modulate the dysbiotic microbiome may include vaccines, probiotics, and small molecules (synthetic or natural) [12–15]. To capture the current state of evidence and provide flexibility for evolving literature on host-environment-microbiome interactions, there is a need to revise and expand the ontological framework for dental caries. In this manuscript, we review how dental caries is classified in several prominent terminologies and ontologies, and based on our review, we discuss the modifications made to the Oral Health and Disease Ontology (OHD) [16] to more accurately represent the scientific understanding of the role the oral microbiome has in dental caries.

Our research team, which included two experienced ontologists, a microbiome researcher, and three dentists, analyzed several prominent biomedical terminologies and ontologies. To find these ontologies, we searched Google Scholar and PubMed for relevant articles, and we searched the ontology browsing services Ontology Lookup Service [17], Bioportal [18], Ontobee [19], and Aber-OWL [20] for relevant ontologies.

Our searches in Google Scholar and PubMed did not find any ontologies for relating dental caries to oral microbial dysbiosis. On Google Scholar, we used the query ((ontology and caries and microbiome) -"gene ontology" -"Antibiotic Resistance Ontology"). In order to exclude a large number of false positives, we had to exclude the terms “gene ontology” and "Antibiotic Resistance Ontology". The query returned 259 results, but these articles mentioned ontologies in context of data analysis and were not about developing an ontology for representing how dental caries is related to imbalances within the oral microbiome. On PubMed, we used the query (ontology and caries and microbiome). This returned five results in the last ten years. Again, these articles were not about developing an ontology for relating dental caries and oral microbial dysbiosis.

On the ontology services we searched for the terms ‘caries’ or ‘dental caries’. This returned 25 ontologies on the Ontology Lookup Service, 31 ontologies on Bioportal, 12 ontologies on Ontobee, and 23 ontologies on Aber-OWL. After reviewing the results, we focused on analyzing the Systematized Nomenclature of Medicine - Clinical Terms (SNOMED CT) [21], The International Classification of Diseases, 11th ed. (ICD-11) [22], Medical Subject Headings (MeSH) [23], NCI Thesaurus (NCIt) [24], Human Disease Ontology (DO) [25], Monarch Disease Ontology (MONDO) [26], and the Human Phenotype Ontology (HPO) [27]. Several ontologies were excluded from our analysis because they were very similar, and some cases had identical branches, to the other select ontologies. ICD-11 was selected because of the substantial role it has in providing medical diagnosis codes, and MeSH was chosen because of its importance for searching PubMed. After identifying the deficiencies in the selected terminologies and ontologies, we added terms and relations to the Oral Health and Disease Ontology (OHD) that more accurately represent how oral microbial dysbiosis influences the development of dental caries.

Our analysis of the selected ontologies (below) determined that they did not accurately represent the complex multi-factor etiology of dental caries: interactions of the host, environment and microbiome. Based on these deficiencies, in this iteration, we expanded the OHD to provide a more comprehensive representation of the role of the microbiome in dental caries. The emphasis on microbiome is considered first due to the rapid development of knowledge in this field. Note, to improve readability, bold text is used for classes and italics text is used for relations.

In recent years, there has been a paradigm shift in cariology. It now stresses the complexity of the development and progression of the disease with many conjoint elements that depend largely on host-microbe interaction [36]. Furthermore, treatment for dental caries has shifted from a surgical-restorative model to a preventive and disease management-based model [37].

Our review revealed broad shortcomings across existing ontologies and terminologies, underscoring their inability to fully capture the multifactorial nature of dental caries. Clinical classification systems like SNOMED CT and ICD‑11, for example, define caries strictly as a lesion or disorder of tooth hard tissues, with no links to the oral microbiome or biofilm dysbiosis. This narrow, anatomy-centric focus means key etiological factors – such as microbial imbalances, dietary sugars, or omits saliva-mediated effects. Research vocabularies like MeSH and NCIt likewise exhibit conceptual inconsistencies, often conflating the disease process with its outcomes (e.g. treating “dental caries” as both the decay process and the cavity lesion) or using ambiguous definitions that blur whether caries is a pathological process or a physical structure. Meanwhile, disease ontologies in the OBO Foundry (including DO, MONDO, and HPO) adopt a formal disease model (inspired by OGMS) but still lack explicit representations for oral biofilm dysbiosis, acid-driven demineralization processes, or the resulting tooth lesions. In their current state, none of these resources can represent the full etiologic network of caries – they cannot relate a dysbiotic microbiome to caries onset, nor incorporate the myriad risk and protective factors that modulate disease progression. Additional host and environmental variables (for instance, high-sugar diets, medications, smoking, saliva flow, or even stress) are largely ignored [38], even though such factors can aggravate or attenuate dysbiosis and enamel degradation.

These gaps highlight an urgent need for ontologies to evolve beyond static lesion descriptors. Future ontology development should integrate host–microbe–environment interactions and acknowledge the spectrum from healthy homeostasis to dysbiosis [39]. Notably, a consensus in cariology now views dental caries as a “community-scale metabolic disorder” driven by complex microbial communities rather than a single pathogen [40]. This perspective implies that ontologies must be flexible and extensible – capable of linking dysbiotic states to downstream pathological processes, modeling preventative or aggravating factors, and accommodating new discoveries – so that our representations of oral health keep pace with emerging scientific understanding.

The OHD’s framework representing dental caries is a significant advance over current ontologies and terminologies. However, there are still areas that need to be addressed. To fully represent the etiology of oral microbial dysbiosis, it is necessary to represent the factors that impact the host-microbiome interaction. These include, among others, how host-derived factors, such as medication history, smoking status, and diet, interact with (or impact) the oral microbiome environment. Moreover, we have not included particular species of microbes often found in the oral microbiome. Adding terms for these microbes as well the particular functions they serve within the microbiome is potential future enhancement of the OHD.

In this paper, we demonstrated that current medical ontologies and terminologies have not kept pace with the recent shift in understanding the etiology of caries. Instead, they remain focused on the development or existence of lesions and lack the expressiveness to describe the role of biofilm ecology and microbiome imbalance during the caries disease course. These deficiencies motivated us to restructure the OHD to include terms that represent oral microbial dysbiosis and disease processes that arise from an imbalanced microbiome. This restructuring is advantageous for two reasons. First, it aligns the OHD with modern cariology. Keeping pace with scientific advances is critical for ensuring that an ontology’s terms remain relevant to the scientific community, and, as a result, the OHD is an advance over the aforementioned ontologies. Second, the OHD provides a semantic framework for including more dysbiosis-related terms, such as specific kinds of oral microbial dysbiosis and dysbiosis treatment, and, hence, can more easily incorporate new findings in the field of cariology.