Review Article - Genomics of Periodontal Disease and Tooth Morbidity

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1. Introduction

The existence of innate susceptibility and heritability of oral health and disease traits is well‐established. In fact, scholarly work discuss‐ ing possible hereditary components of dental caries was published as early as the 1920s. It was several decades later, and as a result of continued progress in the basic sciences, breakthroughs in the supporting technologies, and substantial investments in effort and resources, that dentistry began to enter the “genome era”. The first genome‐wide association studies of periodontitis and dental car‐ ies were published in 20102 and 2011,3 respectively. Nevertheless, other lines of research (including investigations among twins and families, and many candidate‐gene studies) have helped to build a solid case for the putative role of genetic factors in periodontal dis‐ ease and dental caries. Excellent reviews and comprehensive sum‐ maries of the body of evidence supporting heritable components of oral disease have been published previously...

2. Genomic s of Traditional Clinic Al Definitions of or Al and Dental Disease

2.1 Periodontal disease The genome‐wide association study of aggressive periodontitis re‐ ported by Schaefer et al2 marked the field's entry into the genome era. In that study, the investigators discovered and subsequently replicated the association of rs1537415, located in the glycosyltrans‐ ferase gene (GLT6D1), with aggressive periodontitis. More recently, Sanders et al reported a significant association of a relatively rare TSNAX‐DISC1 noncoding RNA polymorphism (rs149133391) with chronic periodontitis among Hispanic/Latino people and sub‐ sequently replicated it among an independent sample of African‐ Americans. Other studies24-29 have implicated numerous loci without reaching genome‐wide statistical significance levels and/or demonstrating replication in an independent cohort. For example, a recent study among a small Italian population reported associations between EFCAB4B polymorphisms (rs242016 showing the strongest evidence of association) and localized periodontitis...

2.2 Dental caries The first genome‐wide association study for dental caries, published in 2011, was carried out for “childhood caries”, namely dental caries lesions manifested in the primary dentition. A subsequent report comprising five independent cohorts investigated dental caries in the permanent dentition and was published 1 year later. None of these investigations detected significant genome‐wide signals, al‐ though several loci had suggestive evidence of an association or had emerged from stratified analyses...

3. Genomics of Composite , Intermediate , and Biologic Ally Informed Traits of or Al Health and Disease

3.1 Tooth morbidity Tooth loss is the most common type of oral impairment and dis‐ ability, with 79% of American adults aged 50 years and older having lost one or more teeth and 11?ing edentulous. Apart from the obvious functional, biologic, and psychosocial consequences, edentulism (partial and complete) is associated with substantial re‐ habilitation costs and affects quality of life. In terms of etiology, tooth loss is attributed predominantly to the two most common oral diseases, caries and periodontitis. Accurate estimates of the individual contributions of caries and periodontitis to tooth loss are lacking and are probably heterogeneous across populations and between study samples...

3.2 The oral microbiome and inflammatory mediators Understanding the genomic basis of clinical traits and directly ob‐ servable health and disease end points is of natural interest to both clinicians and investigators. In the context of common complex diseases, such as periodontitis and tooth morbidity, it is expected that several loci contribute to disease development. Different loci and environmental factors are also probably involved, driv‐ ing the disease incidence among different population subgroups. Theoretically, the presumably weak association signals of these loci should be detectable in clinical traits if large sample sizes are available...

3.3 Biologically informed, complex traits A logical extension of the genomic interrogation of dental and periodon‐ tal endophenotypes is the combination of these biologic intermediates with clinical measures of health and disease, to create “biologically in‐ formed” complex traits. Therefore, our group recently combined clini‐ cal (ie, periodontal) and biologic (ie, subgingival periodontal pathogen colonization and gingival crevicular fluid interleukin‐1beta expression) data, using a principal components approach, to create six periodontal complex traits. This methodology has been used previously in ge‐ nome‐wide association studies of complex facial morphology96 and bone traits...

3.4 “Precision” periodontal traits To address the limitations imposed by the influence of tooth loss on disease measurement, the need to facilitate clinical data har‐ monization across studies and the opportunity to capitalize on all available (eg, tooth‐level) clinical information, our group recently embarked upon a novel, latent class analysis99 approach to derive a new classification system for periodontitis. In brief, the approach is analogous to an unsupervised clustering procedure, where individuals and teeth are placed within mutually exclusive categories – periodontal profile classes and tooth profile classes, respectively. Our group identified seven distinct periodontal profile classes and seven distinct tooth profile classes that aid in patient stratification,59 are predictive of periodontitis progres‐ sion and tooth loss...

4. Potential Utility of Genome‐ Wide Association Study Findings For the Construction of a Periodontitis Genetic Risk Score

Our genome‐wide association study of periodontitis (as defined by the Centers for Disease Control and Prevention/American Academy of Periodontology classification criteria) demonstrated that considerable proportions of the phenotypic variance can be explained by genome‐wide association study single nucleotide polymorphisms. This proportion can be interpreted as heritabil‐ ity and was (standard error = 0.19) for severe periodontitis. Interestingly, the heritable variance increased to  (standard error = 0.35) when a genome × smoking interaction term was considered. Naturally, once risk loci and specific risk markers have been discovered and confirmed for a disease or condition, questions regarding their predictive ability, and ultimately utility, emerge...

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