Multiple Choice Questions Test - V (Basic Periodontology).
Like all other epithelial tissues, oral sulcular epithelia undergo turnover, which means replacement by cell division in the basal layer and migration of the daughter cells to the surface of the epithelium where they eventually die and are shed into the oral cavity. The turnover rate of the oral sulcular epithelium has been estimated to be 10-14 days.
Reference: Attstrom, R. (1975). "The roles of gingival epithelium and phagocytosing leukocytes in gingival defense." J Clin Periodontol 2: 25-32.
C3 is the most abundant protein of the complement system (~1.3 mg/ml). C4b2b cuts C3 into two major fragments:
C3a bind to receptors on basophils and mast cells triggering them to release their vasoactive contents (e.g., histamine). Because of the role of these materials in anaphylaxis, C3a is called an anaphylatoxin.
C3b as an opsonin. Macrophages and neutrophils have receptors for C3b and they can bind the C3b-coated bacterial cell surface leading to phagocytosis.
Genes for Fcγ receptor are located on chromosome 1 and encode three main receptor classes: FcγRI (CD64), FcγRII (CD32) and FcγRIII(CD16). These classes are further subdivided into subclasses: FcγRIa and b, FcγRIIa, b and c, and FcγRIIIa and b. FcγRIIa is found on all granulocytes, antigen-presenting cells, platelets, endothelial cells and a subset of T cells. FcγRIIIa is present on monocytes and macrophages, NK cells and a subset of T cells. The FcγRIIIb is the major IgG receptor of neutrophils.
Reference: Loos, B. G., Leppers-Van de Straat, F. G., Van de Winkel, J. G. & Van der Velden, U. (2003) Fc gamma receptor polymorphisms in relation to periodontitis. Journal of Clinical Periodontology 30, 595–602.
Quorum sensing is the mechanism by which bacteria from plaque can coordinate their gene expression and communicate with one another in a cell density-dependent manner via small diffusible molecules. In S. mutans, quorum sensing is mediated by a competence stimulating peptide (CSP), which increases the transformation frequency of biofilm-grown S. mutans 10–600-fold.
Reference: Philip D. Marsh, Annette Moter & Deirdre A. Devine Dental plaque biofilms: communities, conflict and control. Periodontology 2000, Vol. 55, 2011, 16–35.
Predominant Periodontal ligament fibers: The predominant collagens of the periodontal ligament are type I, III, and XII, with individual ﬁbrils having a relatively smaller average diameter than tendon collagen ﬁbrils, a difference believed to reﬂect the relatively short half-life of ligament collagen, and hence less time for ﬁbrillar assembly. The vast majority of collagen ﬁbrils in the periodontal ligament are arranged in deﬁnite and distinct ﬁber bundles, and these are termed principal ﬁbers.
Elastic ﬁbers: There are three types of elastic ﬁbers: elastin, oxytalan, and elaunin. Only oxytalan ﬁbers are present within the periodontal ligament; however, elaunin ﬁbers may also be found in association with ﬁber bundles in the gingival ligament.
Reference: Antonio Nanci & Dieter D. Bosshardt. Structure of periodontal tissues in health and disease. Periodontology 2000, Vol. 40, 2006, 11–28.
The prognosis for the older patient should be better as the periodontal disease progression is slow in this case and immune system is competently fighting the disease over a long period of time. Whereas in younger patient same amount of periodontal destruction shows aggressiveness of disease as well as immunological incompetence.
In humans, the MHC complex consists of more than 200 genes located close together on chromosome 6. Genes in this complex are categorized into three basic groups: class I, class II, and class III. There are three main MHC class I genes, known as HLA-A, HLA-B, and HLA-C. The proteins produced from these genes are present on the surface of almost all cells. There are six main MHC class II genes in humans: HLA-DPA1, HLA-DPB1, HLA-DQA1, HLA-DQB1, HLA-DRA1, and HLA-DRB1. MHC class II genes provide instructions for making proteins that are present almost exclusively on the surface of certain immune system cells. Proteins produced from MHC-III are involved in inflammation and other immune system activities.
TLR-2 and TLR-4 are part of innate immunity having important role in the recognition of periodontopathogens such as Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythensis. TLR activation leads to an intracellular signaling cascade is stimulated, leading to the activation of transcription factors and to subsequent inflammatory cytokine expression, leukocyte migration, and osteoclastogenesis.
Reference: G.P. Garlet. Destructive and Protective Roles of Cytokines in Periodontitis: A Re-appraisal from Host Defense and Tissue Destruction Viewpoints. J Dent Res 89(12):1349-1363, 2010.
In humans, the MHC complex consists of more than 200 genes located close together on chromosome 6. Genes in this complex are categorized into three basic groups: class I, class II, and class III. Class I MHC molecules are composed of two polypeptide chains, a long α chain and a short β chain called β2-microglobulin. The α chain has four regions.
- The cytoplasmic region of α chain consists of sites for phosphoylation and binding to cytoskeletal elements.
- The transmembrane region contains hydrophic amino acids by which the molecule is anchored in the cell membrane.
- A highly conserved α3 immunoglubilin-like domain to which CD8 binds.
A highly polymorphic peptide binding region formed from the α1 and α2 domains. The β2- microglobulin associates with the α chain and helps maintain the proper conformation of the molecule.
There are two types of complement regulators:
Fluid-phase regulators of complement:
Because the complement system has tendency for rapid activation and amplify its own activation, the complement system needs to be well controlled in the ﬂuid phase. The relatively short half-life and continuous decay-dissociation of the bimolecular complement enzyme complexes naturally restrict complement activation. These include C1 inhibitor (C1 INH), C4b-binding protein (C4bp), factor H, clusterin (apo-J) and S protein (vitronectin).
Membrane regulators of complement:
Three of the regulators, C3b receptor (CR1, CD35), membrane cofactor protein (MCP, CD46) and decay-accelerating factor (DAF, CD55) act as inhibitors of the C3/C5 convertases whereas protectin (CD59) is an inhibitor of MAC.