Multiple Choice Questions Test - III (Basic Periodontology).
In response to lipopolysaccharides(LPS) endothelial cells secrete IL-8 which acts as chemoattractant. Mediators that are secreted from activated host cells (e.g., IL-1β, TNF-α, PGE2, and histamine) further assist bacterial virulence factors in the activation of endothelial cells. This leads to secretion of more chemokines (IL-8, MCP-1) and expression of adhesion molecules on the surface of endothelial cells, which are important for leukocyte extravasation (P- and E-selectins as well as ICAM-1 and -2).
Reference: Phoebus N. Madianos, Yiorgos A. Bobetsis, Thomas E. Van DykePeriodontal Disease and Overall Health: A Clinician`s Guide. Infection and Inflammation. Page-24.
Plasma thromboplastin antecedent
Hageman (contact) factor
Prekallikrein (Fletcher factor)
HMWK (Fitzgerald factor)
Normal levels of complement components:
- Total blood complement level: 41 to 90 hemolytic units
- C1 level: 16 to 33 mg/dL
- C3 levels:
- Males: 88 to 252 mg/dL
- Females: 88 to 206 mg/dL
- C4 levels:
- Males: 12 to 72 mg/dL
- Females: 13 to 75 mg/dL
Note: mg/dL = milligrams per deciliter.
The A. actinomycetemcomitans leukotoxin operon consists of four coding genes designated ltxC, ltxA, ltxB and ltxD and an upstream promoter. ltxA encodes the structure of the toxin, ltxC for components required for posttranslational acylation of the toxin and ltxB and D for transport of the toxin to the bacterial outer membrane. The leukotoxin promoter is located upstream of the ltxC gene.
Reference: Anders Johansson. Aggregatibacter actinomycetemcomitans Leukotoxin: A Powerful Tool with Capacity to Cause Imbalance in the Host Inflammatory Response. Toxins 2011, 3, 242-259.
It is a rare disease which was originally described as a disease in which neutrophils lacked specific granules. Specific granule proteins which are missing in Specific granule deficiency (SGD) include lactoferrin, cobalophilin, cytochrome b, the FPR, C5a receptor, and CR3. Further in this condition not only are specific granules affected, but the packaging of defensins into azurophil granules is also defective. Oral manifestations of this disease include severe periodontitis and oral ulceration.
Both Papillon-Lefe`vre syndrome and Haim-Munk syndrome are allelic variants of mutations of the cathepsin C gene.
Papillon-Lefèvre Syndrome (PLS) is an autosomal recessive disorder (gene:11q14.2) that is caused by mutations in cathepsin C (CTSC) (OMIM #245000). PLS is characterized by palmoplantar hyperkeratosis and aggressive periodontitis, has a worldwide prevalence of 1–4 cases per million in the general population, and is often related with consanguinity. In this condition Aggressive periodontitis begins with the primary dentition, leading to periodontium destruction, and the premature loss of deciduous teeth by age of 6 years; afterwards gums heal, until the development of the permanent dentition, when periodontitis reappears and teeth are prematurely lost by the age of 16-years. Besides these basic features, PLS patients can present with liver abscesses, increased incidence of pyogenic infections or mental retardation.
Haim-Munk syndrome: In 1965, Haim and Munk described an unusual syndrome in four sibs of a Jewish religious isolate from Cochin, India. It is an extremely rare autosomal recessive disorder of keratinization characterized clinically by palmoplantar hyperkeratosis, severe early onset periodontitis, onychogryphosis, pes planus, arachnodactyly, and acro-osteolysis. Mutations in the lysosomal protease cathepsin C gene have been identified as the underlying genetic defect in Haim-Munk syndrome
Reference: José G Romero-Quintana et al. Identification of novel mutation in cathepsin C gene causing Papillon-Lefèvre Syndrome in Mexican patients. BMC Medical Genetics 2013, 14:7
T C Hart et al. Haim-Munk syndrome and Papillon-Lefèvre syndrome are allelic mutations in cathepsin C. J Med Genet 2000;37:88-94
Hypo-function of lymphocyte-monocyte cytokine system leads to less gingival inflammation because there is suppressed immune response.
Reference: Carranza 8th edition page 146.
Effects of oestrogen on periodontal tissue:
- Decreases keratinization while increasing epithelial glycogen that results in the diminution in the effectiveness of the epithelial barrier.
- Increases cellular proliferation in blood vessels.
- Stimulates PMNL phagocytosis.
- Inhibits PMNL chemotaxis.
- Suppress leukocyte production from the bone marrow.
- Inhibits proinflammatory cytokins released by human marrow cells.
- Reduces T-cell mediated inflammation.
- Stimulates the proliferation of the gingival fibroblasts.
- Stimulates the synthesis and maturation of gingival connective tissues.
- Increases the amount of gingival inflammation with no increase of plaque.
- Increase in gingival crevicular fluid flow.
Reference: GN Güncü et al. Effects of endogenous sex hormones on the periodontium-Review of literature. Australian Dental Journal 2005;50:(3):138-145
Leukotoxin A (LtxA) is a 114-kDa protein toxin that is secreted by Aggregatibacter actinomycetemcomitans. LtxA targets specifically the β(2) integrin, leukocyte function antigen-1 (LFA-1) on white blood cells (WBCs) and causes cell death.
Reference: DiFranco KM et al. Leukotoxin (Leukothera®) targets active leukocyte function antigen-1 (LFA-1) protein and triggers a lysosomal mediated cell death pathway. J Biol Chem. 2012 May 18;287(21):17618-27.
↓sed Bone turnover due to ↓sed Bone resorption.
↓sed Number of new bone multicellular units.
Net positive whole body bone balance
↓sed Osteoclast recruitment
↑sed Osteoclast apoptosis
↓sed Osteoclast adhesion
↓sed Depth of resorption site
↓sed release of cytokines by macrophages.
↑sed Osteoblast differentiation and number
Inhibit mevalonate pathway (that result in perturbed cell activity and induction of apoptosis).
↓sed Post-translational prenylation of GTP—bonding proteins
In 1987, Golub et al. described a new use for the first chemically modified tetracycline (4-dedimethylamino tetracycline or chemically modified tetracycline-1), which is devoid of antibacterial activity due to the removal of the dimethylamino group from the carbon-4 position of the ‘‘A’’ ring of the drug molecule, but which retains its anticollagenase activity. A series of 10 different chemically modified tetracyclines have since been identified, called chemically modified tetracyclines 1–10, nine of which were found to retain their anti-collagenase but to have lost their antimicrobial properties. The one chemically modified tetracycline found to have lost its anti-collagenase property was chemically modified tetracycline-5, or the pyrazole analogue, in which the carbon-11 carbonyl oxygen and carbon-12 hydroxyl groups were replaced by nitrogen atoms, which eliminated this important Zn++ or Ca++ binding site on the tetracycline molecule.
Golub L, McNamara T, D’Angelo G, Greenwald R, Ramamurthy N. A non-antibacterial chemically-modified tetracycline inhibits mammalian collagenase activity. J Dent Res 1987: 66: 1310–1314.
Maria Emanuel Ryan & Lorne M. Golub. Modulation of matrix metalloproteinase activities in periodontitis as a treatment strategy. Periodontology 2000, Vol. 24, 2000, 226–238)
The complement-activated product, C5a, displays powerful biological activities that lead to inflammatory sequelae. C5a is a strong chemoattractant and is involved in the recruitment of inflammatory cells such as neutrophils, eosinophils, monocytes, and T lymphocytes, in activation of phagocytic cells and release of granule-based enzymes and generation of oxidants, all of which may contribute to innate immune functions or tissue damage.
IL-1 and TNF trigger the synthesis of platelet-activating factor (PAF) by endothelial cells.
P N Monk, A-M Scola et al. Function, structure and therapeutic potential of complement C5a receptors Br J Pharmacol. 2007 October; 152(4): 429–448.
the epithelial turnover rate is highest for junctional epithelium. because of the presence of subclinical inflammartion the junctional epithelium is constantly renewing itself.
Fibroblasts play an important role in immuno-inflammatory response. They have important roles like angiogenesis and secretion of fibroblasts derived growth factors which play an important role in wound healing.
IL-1 and TNF are involved in both inflammation and healing and are considered to be important as angiogenic factors. Although TNF-α is known for its cytotoxicity, the molecule can also induce endothelial proliferation. This angiogenic factors are made by cells of the monocyte lineage. The signal to shutdown of angiogenesis in the periodontium is unclear. Recently, a TNF superfamily molecule has been shown to be active in inhibiting angiogenesis in tumors. This factor, vascular endothelial growth inhibitor (VEGI) is a negative regulator of angiogenesis.