Detection of high‐risk groups and individuals for periodontal diseases

Johnson, Newell W.; Griffiths, Gareth; Wilton, James; Maiden, M. F. J.; Curtis, Michael A.; Gillett, I. R.; Wilson, David T.; Sterne, J. A. C.

doi:10.1111/j.1600-051x.1988.tb01584.x

Cited by 166 publications

(92 citation statements)

References 36 publications

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“…Risk for periodontitis is not shared equally by the population. It is clear that periodontitis severely affects a high-risk group representing around 10-15% of the population, in whom the disease quickly progresses from chronic gingivitis to destructive periodontitis (Johnson et al, 1988;Jenkins and Kinane, 1989). This differential risk for periodontitis is consistent with heritable ele-ments of susceptibility, but direct evidence for a differential genetic contribution to periodontitis comes from several sources.…”

Section: (Iv) Evidence For the Role Of Genetic Variants In Periodontimentioning

confidence: 97%

“…Risks for many diseases, including periodontal diseases, are not borne equally by all individuals (Johnson et al, 1988;Jenkins and Kinane, 1989). A variety of microbial, environmental, behavioral, and systemic disease factors is reported to influence risk for moderate to severe periodontitis (Page and Beck, 1997).…”

Section: (Ii) Genetic Disease Paradigms (A) Genetic Variancementioning

confidence: 99%

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Genes and Gene Polymorphisms Associated with Periodontal Disease

Kinane

Hart

2003

Critical Reviews in Oral Biology & Medicine

293

252

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ABSTRACT:The scientific literature during the last ten years has seen an exponential increase in the number of reports claiming links for genetic polymorphisms with a variety of medical diseases, particularly chronic immune and inflammatory conditions. Recently, periodontal research has contributed to this growth area. This new research has coincided with an increased understanding of the genome which, in turn, has permitted the functional interrelationships of gene products with each other and with environmental agents to be understood. As a result of this knowledge explosion, it is evident that there is a genetic basis for most diseases, including periodontitis. This realization has fostered the idea that if we can understand the genetic basis of diseases, genetic tests to assess disease risk and to develop etiology-based treatments will soon be reality. Consequently, there has been great interest in identifying allelic variants of genes that can be used to assess disease risk for periodontal diseases. Reports of genetic polymorphisms associated with periodontal disease are increasing, but the limitations of such studies are not widely appreciated. While there have been dramatic successes in the identification of mutations responsible for rare genetic conditions, few genetic polymorphisms reported for complex genetic diseases have been demonstrated to be clinically valid, and fewer have been shown to have clinical utility. Although geneticists warn clinicians on the over-enthusiastic use and interpretation of their studies, there continues to be a disparity between the geneticists and the clinicians in the emphasis placed on genes and genetic polymorphism associations. This review critically reviews genetic associations claimed for periodontal disease. It reveals that, despite major advances in the awareness of genetic risk factors for periodontal disease (with the exception of periodontitis associated with certain monogenetic conditions), we are still some way from determining the genetic basis of both aggressive and chronic periodontitis. We have, however, gained considerable insight into the hereditary pattern for aggressive periodontitis. Related to our understanding that it is autosomal-dominant with reduced penetrance comes a major clinically relevant insight into the risk assessment and screening for this disease, in that we appreciate that parents, offspring, and siblings of patients affected with aggressive periodontitis have a 50% risk of this disease also. Nevertheless, we must exercise caution and proper scientific method in the pursuit of clinically valid and useful genetic diagnostic tests for chronic and aggressive periodontitis. We must plan our research using plausible biological arguments and carefully avoid the numerous bias and misinterpretation pitfalls inherent in researching genetic associations with disease.

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Section: (Iv) Evidence For the Role Of Genetic Variants In Periodontimentioning

confidence: 97%

Section: (Ii) Genetic Disease Paradigms (A) Genetic Variancementioning

confidence: 99%

Genes and Gene Polymorphisms Associated with Periodontal Disease

Kinane

Hart

2003

Critical Reviews in Oral Biology & Medicine

293

252

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“…Adult periodontitis is the most common form, but not all individuals are equally susceptible (7,17). Attachment and bone levels decrease with age, but only 7 to 13% of individuals progress to advanced loss (15,17,21).…”

mentioning

confidence: 99%

“…Again, not all individuals are equally susceptible to bone resorption when they are infected with this bacterium (17,25), suggesting that host factors are important in the onset and progression of this disease.…”

mentioning

confidence: 99%

Genetic Control of Susceptibility toPorphyromonas gingivalis-Induced Alveolar Bone Loss in Mice

2000

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Periodontal disease affects a large percentage of the human population. Resorption of the alveolar bone of the jaw is a pivotal sequela of periodontal disease, because this bone is the attachment site for the periodontal ligaments that anchor the teeth. Using a murine model in which alveolar bone loss is induced by oral infection with Porphyromonas gingivalis, a gram-negative bacterium associated with human adult periodontal disease, we provide evidence suggesting that susceptibility to such bone loss is a genetically determined trait. AKR/J, DBA/2J, and BALB/cByJ or BALB/cJ mice were highly susceptible, while A/J, A/HeJ, 129/J, SJL/J, and C57BL/6J mice were much more resistant. When susceptible BALB/cJ and BALB/cByJ mice were crossed to resistant strains, two patterns were observed. (BALBc/ByJ ؋ C57BL/6J)F 1 offspring were susceptible, suggesting C57BL/6J has recessive resistance alleles, while (BALB/cJ ؋ A/J)F 1 mice were all resistant, suggesting that A/J mice have dominant resistance alleles. These results suggest a tractable genetic basis for P. gingivalisinduced alveolar bone loss and open the possibility of exploiting the mouse model to identify loci important for host susceptibility and resistance to periodontal disease.

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“…Periodontal disease is a spectrum of different diseases for which certain individuals are at relatively high risk [1]. Periodontitis is defined as a bacterial disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment and bone loss [2].…”

Section: Introductionmentioning

confidence: 99%

Syndromes That Include Both Palmoplantar Keratoderma And Severe Periodontitis: A Review

Dababneh¹

2013

Dentistry

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Palmoplantar keratodermas (PPK) include a heterogeneous group of disorders with overlapping clinical features. The main aspect of PPK is thickening and hyperkeratosis of the palmar and plantar skin, that may be hereditary or acquired; diffuse, focal, or punctuate; and transgrediens or progrediens. PPKs are further distinguished by their mode of inheritance and by the presence of certain associated clinical features. Periodontitis was reported in association with more than one syndrome characterized by PPK. An extensively reported one is the Papillon-Lefévre syndrome (PLS) which is characterized by early onset of PPK and periodontitis affecting the primary and secondary dentitions. In addition to PLS, Haim-Munk, HOPP, Variant Carvajal and Weary-Kindler are other syndromes manifested by PPK and reported in association with severe periodontitis. Atypical cases of PLS were also reported, such as partial expression or a late presentation of the syndrome. The aim of this article is to critically review the literature concerned with Papillon-Lefévre syndrome in its typical and atypical clinical presentation, in addition to other syndromes manifested at the same time by PPK and severe periodontitis.Thorough history and medical examination, together with periodontal, dermatologic, and genetic counseling, are important to exclude other existing medical conditions or other syndromes that might need special attention and care.

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Detection of high‐risk groups and individuals for periodontal diseases

Cited by 166 publications

References 36 publications

Genes and Gene Polymorphisms Associated with Periodontal Disease

Genes and Gene Polymorphisms Associated with Periodontal Disease

Genetic Control of Susceptibility toPorphyromonas gingivalis-Induced Alveolar Bone Loss in Mice

Syndromes That Include Both Palmoplantar Keratoderma And Severe Periodontitis: A Review

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