Multiple Choice Questions Test - VI (Basic Periodontology).
Pellicle formation starts within seconds of a clean surface being exposed to the oral environment. An equilibrium between adsorption and desorption of salivary molecules occurs after 90–120 minutes. The thickness of the pellicle is influenced by the shear forces at the site of formation. After 2 hours, the pellicle on lingual surfaces is 20–80 nm thick whereas buccal pellicles can be 200–700 nm deep.
Reference: Oral Microbiology Fifth Edition Professor Philip D Marsh.
Upon cleavage, the released TNF-α forms a bioactive homotrimer, which then exerts its effects in an
autocrine and/or paracrine manner. The pleiotropic actions of TNF-α are mediated through two distinct cell surface receptors: TNF-α receptor-I (TNFR-I /p55) and TNF-α receptor-II (TNFR-II/p75). Only TNFR1 contains a cytoplasmic death domain and may directly induce apoptosis. TNF-α induces leukocyte adhesion molecules on endothelial cells (ECs), which mediate 3 defined steps of the inflammatory response; namely, leukocyte rolling, firm adhesion, and transmigration.
Reference: Chandrashekharan et al. Tumor necrosis factor α (TNF-α) receptor-II is required for TNF-α induced leukocyte-endothelial interaction in vivo. Blood. 2007 March 1; 109(5): 1938–1944.
Human neutrophil elastase is found as two isozymes named E1 and E2. These isozymes degrade Type IV collagen, laminin, fibronectin, and heparan sulfate proteoglycan similarly to each other. The degradation of such basement membrane components by elastase may assist the extravasation of neutrophils in the process of inflammation. Only type V collagen, which is susceptible to neutrophil gelatinase, is resistant to elastase. This broad substrate specificity of the enzyme may also contribute to tissue destruction at the sites of inflammation.
Reference: Hideto Watanabe et al. Human Neutrophil Elastase: Degradation of Basement Membrane Components and Immunolocalization in the Tissue. J Biochem (1990) 108 (5): 753-759.
There is synergistic relationship among various micro-organisms in a biofilm. In dental plaque we can see this relationship among various micro-organisms. Most common of these are:
- Protoheme produced by campylobacter rectus functions as a growth factor for P. Gingivalis.
- Formate produced by Prevotella melaninogenica which stimulates the growth of C. Rectus.
Reference: Carranza`s Clinical Periodontology By Michael G. Newman, Henry Takei, Perry R. Klokkevold, Fermin A. Carranza
Tissue macrophages, mast cells and immature dendritic cells are important in initiation of immune response. Stimulation of macrophages or mast cells through their Toll-like receptors leads to the synthesis and secretion of proinflammatory cytokines and lipid mediators, thereby initiating the inflammatory response that recruits both soluble immune components and immune cells from the blood. TLR stimulation of dendritic cells induces the initiation of an adaptive immune response.
Genetic Polymorphism is a difference in DNA sequence among individuals, groups, or populations. When a mutation increases to a level involving more than 1% of population, it is referred to as Polymorphism. Sources include SNPs, sequence repeats, insertions, deletions and recombination. (e.g. a genetic polymorphism might give rise to blue eyes versus brown eyes, or straight hair versus curly hair). Genetic polymorphisms may be the result of chance processes, or may have been induced by external agents (such as viruses or radiation). If a difference in DNA sequence among individuals has been shown to be associated with disease, it will usually be called a genetic mutation. Changes in DNA sequence which have been confirmed to be caused by external agents are also generally called "mutations" rather than "polymorphisms."
Reference: PHRMA Genomics Lexicon.
Definition of Candidate gene: Any gene thought likely to cause a disease. The gene may be a candidate because it is located in a particular chromosome region suspected of being involved in the disease or its protein product may suggest that it could be the disease gene in question.
Efficient leukocyte recruitment to sites of inﬂammation requires the selectin family of adhesion molecules. E-, P-, and L-selectin mediate leukocyte capture and rolling on the inﬂamed vessel wall. Selectin-mediated leukocyte capture and rolling has been a generally accepted prerequisite for ﬁrm leukocyte adhesion and subsequent transmigration. Firm leukocyte adhesion is mediated primarily through β2 (CD18)-integrins. β2-Integrins are a family of four hetero dimers, CD11a/CD18 (LFA-1), CD11b/CD18 (Mac-1), CD11c/CD18 (p150,95), and CD11d/CD18. LFA-1 is the predominant β2-integrin on lymphocytes and neutrophils. Neutrophils also express Mac-1. Both LFA-1 and Mac-1 can interact with intercelular cell adhesion-1 (ICAM-1) expressed on resting and inﬂamed endothelial cells.
Reference: S. Bradley Forlow And Klaus Ley. Selectin-independent leukocyte rolling and adhesion in mice deﬁcient in E-, P-, and L-selectin and ICAM-1. Am J Physiol Heart Circ Physiol 280: H634–H641, 2001.
P. gingivalis becomes more proteolytic (e.g. higher gingipain activity) in response to an increase in haemin availability, and an increase in environmental pH results in further upregulation of gingipain activity. In contrast, a high temperature results in P. Gingivalis down regulating protease activity.
Reference: Philip D. Marsh, Annette Moter & Deirdre A. Devine Dental plaque biofilms: communities, conflict and control. Periodontology 2000, Vol. 55, 2011, 16–35.