Genetic contributions to saliva protein concentrations in adult human twins

Rudney, Joel D.; Michalowicz, Bryan S.; Krig, M.A.; Kane, Patricia K.; Pihlstrom, Bruce Lee

doi:10.1016/0003-9969(94)90148-1

Cited by 13 publications

(11 citation statements)

References 36 publications

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“…A positive correlation was found between increased whole saliva protein levels and gingival inflammation and periodontal disease (Henskens et al, 1993;Rudney et al, 1994). Flow rate did not show significant differences (Henskens et al, 1996a).…”

Section: (D) Cystatins Endogenous Cps and Periodontal Diseasementioning

confidence: 88%

“…Either might be subject to genetic control, or to long-term physiological modulation in response to factors such as diet or oral disease. Total salivary protein does have a genetic component (Rudney et al, 1994). It also increases with gingivitis and periodontal disease (Henskens et al, 1993;Rudney et al, 1994).…”

Section: (Ii) Papain-like Cp Inhibitory Activities Of Human Type 2 Cymentioning

confidence: 99%

“…There are several likely reasons for the disparities among these studies. Criteria for inclusion in control and experimental populations have differed, and there is evidence for population heterogeneity in salivary protein levels in both health and disease that may stem, in part, from genetic differ-ences (Rudney et al, 1993(Rudney et al, , 1994. As an environmental factor, cystatin activity was found to differ between smokers and nonsmokers (Lie et al, 2001).…”

Section: (D) Cystatins Endogenous Cps and Periodontal Diseasementioning

confidence: 99%

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Salivary (SD-Type) Cystatins: Over One Billion Years in the Making—But to What Purpose?

Dickinson

2002

Critical Reviews in Oral Biology & Medicine

103

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The cystatin superfamily is comprised of a large group of ancestrally related proteins, most of which are potent inhibitors of cysteine peptidases (CPs). Human saliva contains relatively abundant proteins that are related ancestrally in sequence to the cystatin superfamily. These proteins are now commonly referred to as 'salivary cystatins', although this is something of a misnomer (see below). It has been several years since the publication of the last comprehensive reviews that focused on the salivary cystatins (Bobek and Levine, 1992;Henskens et al., 1996c). Since then, significant advances have been made regarding the gene organization, protein structure, and properties of human and rat proteins. Therefore, a major purpose of this article is to review this recent work. What is the function of the 'salivary cystatins'? Despite a great deal of research effort, we still do not have a definitive answer to this question. A major impediment is the lack of a disease to associate with a specific defect in a gene: Functionality must be inferred from circumstantial evidence. A central premise of this review is that clues to 'salivary cystatin' function are contained within their phylogenetic history, and that by looking at established or likely functions of their 'siblings' and 'cousins', one can assess the likelihood of this function(s) continuing into the 'salivary cystatins'. A comprehensive review of the large cystatin superfamily is beyond the scope of a single article. This review will aim to outline the main branches of the superfamily and the common elements of their structure and function, but will pay closest attention to the nearest relatives of the 'salivary cystatins'.(1) BACKGROUND Scission of peptide bonds is an essential reaction in living cells, and there is a considerable number of peptidases that catalyze this reaction with various degrees of specificity. CPs use a cysteine residue in the active site as the nucleophile in the reaction (see Dickinson, 2002, and references therein). Release of proteolytic enzymes outside of their normal compartment has the potential to cause serious degradation and pathology-an effect taken advantage of by pathogenic organisms from a wide range of phyla. Therefore, control of proteolytic enzyme activity is mandatory. Building upon a very early report (see Barrett et al., 1986, for a review of this earlier literature) of a bovine trypsin inhibitor in chicken egg white, a search for egg white inhibitors of plant proteinases (the CPs ficin and papain) identified a relatively small (12.7 kDa) protein that was a potent inhibitor (Ki = 10 nM). The term cystatin was coined for this protein, which was shown also to inhibit mammalian CPs of the papain superfamily, including cathepsins B, C, H, and L. Cystatins form 1:1 reversible complexes with CPs, in competition with the substrate, but in some cases the binding is so tight as to be physiologically irreversible. (2) THE CYSTATIN SUPERFAMILYExamination of mammalian tissues and serum revealed several CP inhibitors ranging in si...

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Section: (D) Cystatins Endogenous Cps and Periodontal Diseasementioning

confidence: 88%

Section: (Ii) Papain-like Cp Inhibitory Activities Of Human Type 2 Cymentioning

confidence: 99%

Section: (D) Cystatins Endogenous Cps and Periodontal Diseasementioning

confidence: 99%

See 1 more Smart Citation

Salivary (SD-Type) Cystatins: Over One Billion Years in the Making—But to What Purpose?

Dickinson

2002

Critical Reviews in Oral Biology & Medicine

103

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“…Like many other systemic and dental diseases, it depends on complex interactions between the genetic predisposition of an individual and the environmental (including behavioral) factors. Several genetically controlled factors have previously been identified or implicated to be involved in the susceptibility to dental caries, including salivary proteins, such as LTF [Rudney et al, 1994;Azevedo et al, 2010]. In this study, we evaluated the LTF rs1126478 (140A/G) variant in quite large groups of children with and without dental caries.…”

Section: Discussionmentioning

confidence: 99%

Lack of Association between Lactotransferrin Polymorphism and Dental Caries

et al. 2013

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Objective: Dental caries is a complex, multifactorial disease and one of the most common illnesses worldwide. Its etiology is related to microbial, dietary and host factors. Recent evidence suggests a role of lactotransferrin (LTF) in caries. The purpose of this study was to determine the association between LTF gene polymorphism and dental caries. Methods: In this case-control study, 637 unrelated children, aged 11-13 years, were enrolled. The subjects were divided into two groups, i.e. caries-free (decayed/missing/filled teeth = 0) and caries-affected children (decayed/missing/filled teeth ≥ 1). The LTF rs1126478 (140A/G in exon 2, Lys/Arg) genotypes were determined by PCR with restriction analysis using the EarI enzyme. Results: Of 637 children, 155 (24.3%) were caries free. There were no statistically significant differences between caries levels and allele or genotype distributions in the total cohort. When the caries-affected group (n = 482) was stratified into low (decayed/missing/filled teeth = 1), moderate (2 ≤ decayed/missing/filled teeth ≤ 3) and high (decayed/missing/filled teeth ≥ 4) caries experience, allele and genotype frequencies were similar among all subgroups. Conclusions: The LTF 140A/G (exon 2, Lys/Arg) polymorphism was not associated with the susceptibility to or severity of dental caries in the Czech population.

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“…The periodontitis risk-assessment model should include a pathogen score and the clinical status (DMFT and periodontal status) of the caregiver or parent; the use of such a model could help identify children who face a high risk of periodontal disease and exclude those whose risk of developing the disease is low. An understanding of the risk factors involved in initial periodontitis and the use of an appropriate diagnostic sampling protocol will be invaluable not only in identifying people who face the risk of suffering from periodontitis, but also in developing effective disease intervention measures [36].…”

Section: Discussionmentioning

confidence: 99%

Chair-Side Quantitative Oral-Microflora Screening for Assessing Familial Correlation of Periodontal Status and Caries Prevalence

et al. 2014

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Aim: Our goal was to investigate the relationship between clinical status and the presence of carious or periodontal pathogens among parent-child familial pairs. Clinical practices of risk assessment with consideration of familial pathogen interaction might reduce the need for therapy, improve patient outcomes, and ultimately reduce oral disease burden. Materials and Methods: In this study, we enrolled 30 parent-child pairs, with the children exhibiting complete deciduous dentition or mixed dentition with only permanent first molars. Clinical statuses were evaluated using caries and periodontal disease indicators, including the sum of decay and the number of missing or filled teeth (DMFT) for adults, decay, extraction caused by dental disease, and filled teeth (deft), for children, probing depth, and plaque control record (PCR). Supra- and sub-gingival bacteria were determined based on semi-quantitative measurements of microbial infection by using data from the Dentocult® SM test (caries-related organisms) and the PerioCheck® test (periodontal disease-related organisms). Results: No statistically significant relationship was detected between the prevalence of periodontal pathogens and that of cariogenic pathogens in the oral cavity. However, the clinical status of caries (DMFT) was negatively correlated with the clinical status of periodontal disease (pocket depth) in parents who were infected with dominant periodontal pathogens (r = −0.59, p<0.01). Parents’ DMFT scores were positively correlated with children’s deft and PCR scores. PCR and deft scores of children appeared to decrease significantly with the parent’s pocket depth. Conclusion: The study showed that the quantity of caries pathogens were not significant related to periodontal pathogens, but the caries clinical outcome is negative related with periodontal clinical outcome between familial pairs.

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Genetic contributions to saliva protein concentrations in adult human twins

Cited by 13 publications

References 36 publications

Salivary (SD-Type) Cystatins: Over One Billion Years in the Making—But to What Purpose?

Salivary (SD-Type) Cystatins: Over One Billion Years in the Making—But to What Purpose?

Lack of Association between Lactotransferrin Polymorphism and Dental Caries

Chair-Side Quantitative Oral-Microflora Screening for Assessing Familial Correlation of Periodontal Status and Caries Prevalence

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