Genetic approaches in the study of periodontal diseases

Sofaer, Joanna

doi:10.1111/j.1365-2710.1992.tb01208.x

Cited by 26 publications

(36 citation statements)

References 83 publications

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“…In the latter case, these rapidly progressing forms often occur within families, raising the possibility that there is a genetic component (213). For some rare inherited and chromosomal disorders, such as Papillon-Lefevre syndrome, Ehlers-Danlos syndromes, and Chédiak-Higashi syndrome, severe early-onset forms of periodontal disease are often characteristic of the syndrome and reflect a fundamental defect in epithelial cell, connective tissue, or leukocyte function (109,287). Such enhanced deterioration is seen in other conditions with a genetic component, such as Down syndrome (4,16,49) and diabetes (219,248,250), especially diabetes among the Pima Indians (206).…”

Section: Host Responsementioning

confidence: 99%

Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment

Loesche

Grossman²

2001

Clin Microbiol Rev

413

338

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Periodontal disease is perhaps the most common chronic infection in adults. Evidence has been accumulating for the past 30 years which indicates that almost all forms of periodontal disease are chronic but specific bacterial infections due to the overgrowth in the dental plaque of a finite number of mostly anaerobic species such as Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola. The success of traditional debridement procedures and/or antimicrobial agents in improving periodontal health can be associated with the reduction in levels of these anaerobes in the dental plaque. These findings suggest that patients and clinicians have a choice in the treatment of this overgrowth, either a debridement and surgery approach or a debridement and antimicrobial treatment approach. However, the antimicrobial approach, while supported by a wealth of scientific evidence, goes contrary to centuries of dental teaching that states that periodontal disease results from a “dirty mouth.” If periodontal disease is demonstrated to be a risk factor for cardiovascular disease and stroke, it will be a modifiable risk factor since periodontal disease can be prevented and treated. Since the antimicrobial approach may be as effective as a surgical approach in the restoration and maintenance of a periodontally healthy dentition, this would give a cardiac or stroke patient and his or her physician a choice in the implementation of treatment seeking to improve the patient's periodontal condition so as to reduce and/or delay future cardiovascular events

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Section: Host Responsementioning

confidence: 99%

Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment

Loesche

Grossman²

2001

Clin Microbiol Rev

413

338

View full text Add to dashboard Cite

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“…The reader is referred to these excellent papers. Here, we will assess several selected aspects of heredity in periodontology, which should complement other recent reviews, including an earlier treatise by Sofaer (1990).…”

Section: Periodontal Diseasesmentioning

confidence: 99%

Genetic Influences in Caries and Periodontal Diseases

Hassell

Harris

1995

Critical Reviews in Oral Biology & Medicine

116

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Deciphering the relative roles of heredity and environmental factors ("nature vs. nurture") in the pathogenesis of dental caries and diseases of the periodontium has occupied clinical and basic researchers for decades. Success in the endeavor has come more easily in the case of caries; the complex interactions that occur between host-response mechanisms and putative microbiologic pathogens in periodontal disease have made elucidation of genetic factors in disease susceptibility more difficult. In addition, during the 30-year period between 1958 and 1987, only meager resources were targeted toward the "nature" side of the nature/nurture dipole in periodontology. In this article, we present a brief history of the development of genetic epistemology, then describe the three main research mechanisms by which questions about the hereditary component of diseases in humans can be addressed. A critical discussion of the evidence for a hereditary component in caries susceptibility is next presented, also from a historical perspective. The evolution of knowledge concerning possible genetic ("endogenous", "idiotypic") factors in the pathogenesis of inflammatory periodontal disease is initiated with an analysis of some foreign-language (primarily German) literature that is likely to be unfamiliar to the reader. We identify a turning point at about 1960, when the periodontal research community turned away from genetics in favor of microbiology research. During the past five years, investigators have re-initiated the search for the hereditary component in susceptibility to common adult periodontal disease; this small but growing body of literature is reviewed. Recent applications of in vitro methods for genetic analyses in periodontal research are presented, with an eye toward a future in which persons who are at risk-genetically predisposed-to periodontal disease may be identified and targeted for interventive strategies. Critical is the realization that genes and environment do not act independently of each other; the appearance or magnitude of heritability may differ with various environments.

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“…Studies involving monozygotic and dizygotic twins have suggested that about half of the population variance in disease could be accounted for by genetic factors (8,24). Increased susceptibility to periodontal disease is found in conjunction with several inherited diseases (10,28). Very recently, an interleukin-1 polymorphism has been reported to be a predictor of future severity in adult periodontal disease (19).…”

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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Genetic approaches in the study of periodontal diseases

Cited by 26 publications

References 83 publications

Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment

Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment

Genetic Influences in Caries and Periodontal Diseases

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

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