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Related Concept Videos

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Principles of Pharmacogenetics: Types of Genetic Variants01:27

Principles of Pharmacogenetics: Types of Genetic Variants

The human genome is over 99.9% identical between individuals, yet genetic differences exist at millions of bases. The human genome contains approximately 3 million variant positions per individual, many of which are heterozygous, contributing to genetic diversity and individual traits. Genetic variations include single-nucleotide polymorphisms (SNPs), insertions, deletions, and copy number variations (CNVs).SNPs, the most common variation, involve single-base changes in DNA. These can be...
Single Nucleotide Polymorphisms-SNPs01:05

Single Nucleotide Polymorphisms-SNPs

A single nucleotide polymorphism or SNP is a single nucleotide variation at a specific genomic position in a large population. It is the most prevalent type of sequence variation found in the human genome. Point mutations that occur in more than 1% of the population qualify as SNPs. These are present once every 1000 nucleotides on an average in the human genome. Replacement of a purine with another purine (A/G) or a pyrimidine with another pyrimidine (C/T) is known as a transition. In contrast,...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Pharmacogenetics of Drug Metabolism: Overview01:27

Pharmacogenetics of Drug Metabolism: Overview

Genetic polymorphism in drug metabolism is crucial to the inter-individual variability observed in drug responses. Drug metabolism primarily involves the chemical modification of drugs and other xenobiotics to enhance their elimination by increasing their polarity. Two main classes of enzymes mediate this biotransformation process: Phase I enzymes, primarily cytochrome P450s, catalyze oxidation and reduction reactions, while other enzymes, such as esterases, mediate hydrolysis, and Phase II...
Pharmacogenomics: Identification of New Drug Targets01:29

Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...

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Related Experiment Video

Updated: Jun 14, 2026

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
07:15

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

Gene polymorphisms in chronic periodontitis.

Marja L Laine1, Bruno G Loos, W Crielaard

  • 1Department of Oral Microbiology, Academic Center for Dentistry Amsterdam (ACTA), University of Amsterdam and Vrije University, 1081 BT Amsterdam, The Netherlands.

International Journal of Dentistry
|March 27, 2010
PubMed
Summary

Genetic variations in genes like IL1 and IL6 may influence chronic periodontitis (CP) susceptibility. However, current studies on gene polymorphisms require larger sample sizes and better controls for conclusive evidence.

Related Experiment Videos

Last Updated: Jun 14, 2026

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
07:15

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

Area of Science:

  • Genetics
  • Periodontology
  • Immunology

Background:

  • Chronic periodontitis (CP) is a prevalent inflammatory condition affecting periodontal tissues.
  • Genetic factors are increasingly recognized for their role in CP susceptibility and progression.

Purpose of the Study:

  • To review existing literature on gene polymorphisms associated with chronic periodontitis susceptibility.
  • To identify specific genes and their polymorphisms potentially linked to CP risk.

Main Methods:

  • Comprehensive literature search using keywords: periodontitis, periodontal disease, genes, mutation, polymorphism.
  • Review of candidate gene polymorphism studies with case-control designs and reported genotype frequencies in CP patients.

Main Results:

  • Evidence suggests polymorphisms in IL1, IL6, IL10, vitamin D receptor, and CD14 genes may be associated with CP in specific populations.
  • Significant variability in rare allele carriage rates and underpowered studies were noted.
  • Most studies did not adequately control for other known risk factors for CP.

Conclusions:

  • Gene polymorphisms in IL1, IL6, IL10, VDR, and CD14 show potential links to CP susceptibility.
  • Further research with larger cohorts, well-defined phenotypes, and control for confounding factors is necessary.
  • Investigating multiple genes within the same pathway is crucial for a comprehensive understanding of genetic contributions to CP.