Multiple Choice Questions Test - I (Basic Periodontology).
The main components of Basement Membrane are laminin, type IV collagen, fibronectin, type VII collagen and proteoglycans. Laminin, the most abundant noncollagenous extracellular matrix protein in BM, has multiple structural and functional roles in tissue development. Type IV collagen provides the basic, strong membrane while fibronectin plays a key role in tissue development and healing through cell matrix binding sites. Anchoring fibrils in the lamina densa, composed mainly of type VII collagen, are known to maintain the integrity of tissues.
Reference: Pierre Le Bars and Assem Soueidan. Distribution Patterns of E-Cadherin, Type VII Collagen and Fibronectin in Denture-Related Stomatitis: A Preliminary Study. The Open Dentistry Journal, 2012, 6, 14-22.
There are three genes that regulate the production of IL-1: IL1A, IL1B and IL1RN. These genes are located on chromosome 2q13. Genes IL1A and IL1B control the production of the pro-inflammatory proteins, IL-1α and IL-1β, respectively. IL1RN controls the synthesis of an antagonist protein (IL-ra).
Reference: P. S. G. Prakash and D. J. Victor. Interleukin-1b gene polymorphism and its association with chronic periodontitis in South Indian population. International Journal of Genetics and Molecular Biology Vol. 2(8), pp. 179-183, August 2010
NO is generated within biologic tissues via the enzymatic conversion of L-arginine to L-citrulline by nitric oxide synthase (NOS). Nitric oxide synthase (NOS) exists in the body as three distinct isoforms: neuronal (nNOS or NOS-I), inducible (iNOS or NOS-II) and endothelial NOS (eNOS or NOS-III). NO is a short-lived molecule implicated in a wide range of biologics/ processes ranging from immune homeostasis to cancer. While low levels of NO are present in tissue homeostasis, NO is produced at higher concentrations in response to inflammatory stimuli such as bacterial 1,PS via inducible forms of NOS (iNOS). NO is a highly reactive free radical reacting with metal and Oliol residues leading to lipid peroxidation, protein and DNA damages and stimulation of cyrokine release.
Reference: Salvi GE, Lang NP. Host response modulation in the management of periodontal diseases. J Clin Periodontol 2005;32(suppl.6): 108-129.
Bacteria have long been recognized as an essential factor in the etiology and progression of periodontal diseases. Toward the end of the 19th century, oral microbiology was just beginning its integration into the study of dentistry, and the work of American microbiologist Willoughby D. Miller played a key role. In the year 1890, Miller published his pioneering book The Microorganisms of the Human Mouth, in which he describes how the accumulation of many different bacterial species collectively induce inflammation and destruction of periodontal tissue. Miller did not believe that any specific organisms were responsible, but that the virulence factors of the community as a whole produced the observed pathology. His hypothesis was backed by the work of J. Leon Williams of London who described dental plaque as a gelatinous accumulation of bacteria, and the obvious association of plaque build-up and periodontal disease. Studies conducted between 1930 to 1970 failed to identify a specific organism as the etiologic agent of periodontal diseases. These negative findings formed a basic tenet of the non-specific hypothesis which suggested that periodontal disease is due to subgingival accumulation of micro-organisms beyond a threshold that can be limited by mechanisms of host resistance (Theilade, 1986). This theory has subsequently evolved into the specific plaque hypothesis, which postulates that certain bacteria are the etiologic agents of distinct forms of periodontal diseases (Loesche, 1976; Tanner et al, 1979; Slots, 1986). Recently an “ecological plaque hypothesis” has been propose that reconciles the key elements of the earlier two hypothesis:
(a) The selection of "pathogenic" bacteria is directly coupled to changes in the environment.
(b) Diseases need not have a specific etiology; any species with relevant traits can contribute to the disease process.
Newman , Michael G.. Carranza`s Clinical Periodontology, 11th Edition.
Marsh PD: Are dental diseases examples of ecological catastrophes? Microbiology 2003, 149:279-294.
Hypophosphatasia was initially recognized by Rathbun in 1948. It is an inherited disorder that affects the development of bones and teeth. This condition disrupts a process called mineralization, in which minerals such as calcium and phosphorus are deposited in developing bones and teeth. Hypophosphatasia, as well as Ehlers–Danlos syndrome are associated with abnormal collagen formation and periodontal disease.
Reference: Etienne Mornet. Hypophosphatasia. Orphanet J Rare Dis. 2007; 2: 40.
Bone Morphogenetic protein-7 (BMP-7):
Bone Morphogenetic protein 7 (BMP7), also known as osteogenic protein 1 (OP-1) is a multifunctional growth factor belonging to the transforming growth factor beta (TGF-β) super-family. Initially discovered in 1965 by Marshall Urist, BMPs are the only known proteins capable of inducing the formation of new bone.
Bone Morphogenetic protein-8 (BMP-8):
BMP-8 is also known as osteonegenic protein 2 (OP 2). BMP8 Induces cartilage and bone formation. May be the osteoinductive factor responsible for the phenomenon of epithelial osteogenesis. It also plays a role in calcium regulation and bone homeostasis.
Reference: Michael B. Lee. Bone morphogenetic proteins: background and implications for oral reconstruction. Journal of Clinical Periodontology Volume 24, Issue 6, pages 355–365, June 1997.
- Vascular dilation and vasculitis subsequent to the junctional epithelium.
- Infiltration of polymorphonuclear neutrophils (PMNs) into the junction and sulcular epithelium.
- Predominant immune cells are PMNs.
- Perivascular loss of collagen.
- Alteration of the coronal part of the junctional epithelium.
- Vascular proliferation.
- Rete peg formation and atrophic areas in the SE and JE.
- Predominant immune cells are lymphocytes (75% of the infiltrate).
- Increased collagen loss, 70% of collagen destroyed around the cellular infiltrate.
- Vascular proliferation and blood stasis.
- More advanced area of rete-peg formation and atrophic areas in the SE and JE.
- Predominant immune cells are plasma cells.
- Continued collagen loss.
The lesion is considered advanced when the destruction of bone is evident.
One important mechanism of resistance appears to be the slower rate of growth of bacterial species in biofilms, which makes them less susceptible to many but not all antibiotics. Other mechanisms include exopolymer matrix , extracellular enzymes such as β-lactamases, formaldehyde lyase and formaldehyde dehydrogenase, hydrodynamics and super resistant strains.
Reference: Xu KD, McFeters GA, Stewart PS. Biofilm resitance to antimicrobial agents. Microbiology 2000: 146: 547–549.
Gingipains are cysteine proteinases produced by P. Gingivalis which are responsible for about 85% of the general proteolytic activity generated by this bacterium. These enzymes are encoded by three genes (rgpA, rgpB, and kgp). In most P. gingivalis strains the gingipains are associated with the bacterial cell surface. Whereas RgpA and Kgp occur in a form of noncovalent complexes of unique catalytic domains with practically identical hemagglutinin/adhesion domains, RgpB is a single-chain enzyme.
Reference: Katarzyna Popadiak, Jan Potempa, Kristian Riesbeck and Anna M. Blom. Biphasic Effect of Gingipains from Porphyromonas gingivalis on the Human Complement System. J Immunol 2007; 178:7242-7250.
Insertion sequences (IS) are defined as mobile genetic elements that are known to encode only functions involved in insertion events. This is to be contrasted with transposons (Tn) that are mobile genetic elements containing additional detectable genes in addition and unrelated to insertion functions (for example, drug resistance). They constitute an important component of most bacterial genomes. Majority of Insertion sequence elements are between 0.7 and l.8 kb in size and the terminal end is l0 to 40 base pairs in length with perfect or nearly perfect repeats.
Reference: Jacques Mahillon and Michael Chandler I. Insertion Sequences. Microbiol. Mol. Biol. Rev. 1998, 62(3):725.
In diabetic patients the function of cells involved in host response, including neutrophils, monocytes and macrophages is altered. The adherence, chemotaxis and phagocytosis of neutrophils often are impaired. Macrophages and monocytes often exhibit elevated production of proinflammatory cytokines and mediators such as tumor necrosis factor α (TNF-α) in response to periodontal pathogens, which may increase host tissue destruction. Collagen produced by fibroblasts is susceptible to rapid degradation by matrix metalloproteinase enzymes, the production of which is elevated in diabetes. The accumulation of AGEs in patients with diabetes also increases the intensity of the immunoinflammatory response to periodontal pathogens, because inflammatory cells such as monocytes and macrophages have receptors for AGEs. Interactions between AGEs and their receptors on inflammatory cells result in the increased production of proinflammatory cytokines such as IL-1β and TNF-α.
Brian L. Mealey. Periodontal disease and diabetes: A two-way street. The Journal of the American Dental Association October 2006 vol. 137 no. suppl 2 26S-31S
Kornman & Loesch (1980) have reported that the subgingival flora changes to a more anaerobic flora as pregnancy progresses. Microbilogical investigations show that the only microorganism that increases significantly during pregnancy is Prevotella intermedia and this increase is associated with elevations of levels of systemic estradiol and progesterone. These hormones are used as growth factors by these organisms as a substitute for vit. K.
Kornman KS, Loesch WJ. The subgingival microbial flora during pregnancy. J Perio dont Res 1980;15:111.
Kormman S, Loesce J. Effects of estradiol and progesterone on Bacteroides melaninogenicus and Bacteroides gingivalis. Infect Immun 1982; 35: 256-63.
Erythema multiforme (EM) is an acute, self-limited, and sometimes recurring skin condition that is considered to be a type IV hypersensitivity reaction associated with certain infections, medications, and other various triggers.
- Itching of the skin
- Joint aches
- Multiple skin lesions that:
Usually appear as a nodule, papule, or macule and may look like hives
Have a central sore surrounded by pale red rings, also called a "target", "iris", or "bulls-eye"
May have vesicles and blisters of various sizes (bullae)
Are located on the upper body, legs, arms, palms, hands, or feet
May involve the face or lips
Are usually even on both sides (symmetrical)
Cardiac conditions associated with endocarditis
Endocarditis prophylaxis recommended:
Endocarditis prophylaxis not recommended:
Dajani AS, Taubert KA, Wilson W, Bolger AF,Bayer A, Ferrieri P, Gewitz MH, Shulman ST, Nouri S, Newburger JW, Hutto C, Pallasch TJ, Gage TW, Levison ME, Peter G, Zuccaro G : Prevention of bacterial endocarditis. Recommendations by the American Heart Association. JAMA 277 : 1794-1801, 1997.
Blood glucose levels must be held in the range of 4-5 mmoles/l between meals and under 10 mmoles/l after meals. This kind of management requires hormonal regulation of many processes. The main actors here are insulin, glucagon, adrenaline and growth hormone. The "stress" hormones adrenalin, noradrenalin and growth hormone activate lipolysis through a common mechanism.