Complex hereditary Oral health condition : The 2 most common oral diseases that affect large segments of population are dental caries and periodontal disease.

Dental caries: Dental caries is considered an infectious disease; there are risk factors that are genetically determined including - pit and fissure morphology, enamel structure and composition, tooth eruption time, salivary flow and comparison, arch form, dental spacing, immunologic function and dietary preference. Studies of monozygotic twins suggest that approximately 50% of variance in dental caries can be attributed to hereditary factors. Understanding the human hereditary traits contributing to dental caries coupled with genetic knowledge of virulence of pathologic micro-organisms involved will allow new diagnostic and novel therapeutic approaches to be applied for management of disease.

Periodontal pathology: The importance of a microbial etiology in periodontitis is well established and specific microbes appear to be associated with certain forms of periodontitis. In most cases, micro-organisms alone are not sufficient to cause disease. Significant data now supports an important role of hereditary susceptibility to a variety of types of periodontitis.

Mutations of cathepsin C genes are responsible for Papillon-Lefere Syndrome, Haim Munk syndrome, and to some extent pre-pubertal periodontitis.

CHS-gene mutation causes Chediak Higashi syndrome and beta 2 integrin (a cell surface receptor) gene mutations are responsible for leukocyte adhesion deficiency type 1.

Genetic studies of aggressive forms of periodontitis suggest that susceptibility is inherited by genetic trait, but it is not clear how many genes may be involved in these non-syndrome forms of periodontitis.

Heredity also appears to play a significant role in most common form of chronic periodontitis. It is likely to result from the additive effect of multiple genes, which may each contribute to decrease susceptibility individually as well as through interactive effects with other gene products and through modulation by environmental factors.

Each individual gene polymorphism may contribute a relatively small part of susceptibility, none alone is sufficient to cause nor predictive of disease risk.