Download rajiv gandhi university of health sciences

yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
1. Name of Candidate and Address
#1852/3, 1st Cross, Prakashnagar,
3. Course of the study and subject
M.R. Ambedkar Dental College &
Hospital, #1/36, Cline Road, Cooke
Town, Bangalore:560 005
M.D.S. Periodontics
4. Date of admission to course
5. Title of the topic
“Estimation of the level of soluble inter
cellular adhesion molecule -1 (sICAM-1)
in gingival crevicular fluid from healthy
and diseased periodontium”
2 Name of the Institution.
6. Brief resume of intended work:
6.1 Need for study:
Periodontal diseases are chronic inflammatory diseases that are characterized
by destructive inflammatory processes affecting the supporting structures of the teeth,
Resorption of alveolar bone and formation of periodontal pockets1,2. .The central focus
of research on periodontal diagnosis has been the methods that attempt to identify high
risk subjects or high risk sites within subjects before extensive damage to the tissues has
occurred2. Traditional method of diagnosis such as clinical attachment level and probing
pocket depth are deficient with respect to accuracy and their ability to predict disease
activity Therefore considerable attention has been directed towards the measurement of
site specific by-products of the disease process in the gingival tissues or in the adjacent
Crevicular fluid. These site directed measurements may allow for a more definitive
identification of susceptible individuals and may also allow for the evaluation of
responsiveness to therapy2.
Leukocyte migration into tissues is particularly prominent during
inflammatory responses and results from cytokine induced expression of adhesion
molecules on the surface of vascular endothelial cells 3 Cell interactions that occur in
gingival tissues have a significant impact on the disease process. The cells in different
tissues of the body, either in the normal traffic pattern or into inflammatory lesions,
involve a complex family of adhesion molecules2.
Cell adhesion molecules are cell surface proteins involved in the binding of cells, usually
leukocytes to each other, to endothelial cells or to the extra cellular matrix. specific
signals produced in response to infection control their expression and activation, and
binding of CAMS(cell adhesion molecules) to their receptors/ligands play an important
role in inflammatory and immune reaction.2 A number of Cell adhesion molecules have
been detected as soluble circulatory forms in human serum and other body fluids. These
sCAMS may influence cell interaction within gingival tissues and may also influence the
interactions between the bacteria and cells in the gingival crevice / periodontal pocket2.
These CAMS may be released as a consequence of cell damage possibly
arising from cytokine induction. Soluble ICAM-1 belongs to the immunoglobulin
superfamilly. It is elevated in inflammation, infection and cancer indicating that sICAM1, may be a useful parameter for diagnosis, and evaluation of these pathological
conditions. sICAM-1 is expressed by Junctional epithelial cells in health and the
majority of pocket epithelium in disease and shed in gingival crevicular fluid 2, 4
In the present study, GCF will be analysed in order to estimate the level of
sICAM-1 from healthy gingiva, gingivitis and periodontitis sites.
6.2 review of literature:
Diseases of the periodontium are chronic inflammatory diseases
characterized by loss of alveolar bone, periodontal ligament leading to pocket formation
and tooth mortality.1
Studies showed the involvement of inflammatory mediators like sICAM-1
which is increased in sites with periodontitis.and their elevated level reflects the
increased cellular damage2.
Studies have reported that expression of ICAM-1 may be enhanced in
vitro by the action of cytokines and this is reflected in vivo by a greater intensity of
expression on endothelial cells at sites of inflammation.3.
A study conducted in Rheumatoid arthritis patients showed a significant
elevation of serum sICAM-1, sICAM-3, sVCAM-1, sL-Selectin and sP-Selectin but not
e-selectin.Hence the sP-Selectin was found to Co-relate with disease activity in the
In a review, the structure, distribution and function of cell adhesion
molecules involved in inflammatory/immune response are summarized. The Data
demonstrate the distribution of CAMS in gingival tissue is consistent with other
inflammatory lesions. Distribution of E-Selectin and V-CAM-1 on gingival blood vessel
and ICAM-1 on junctional epithelium and pocket epithelium is clearly selective and
interference with CAM function may prove to be a useful approach in the future
management of periodontal disease5.
6.3 Objectives of the study
1. To understand the role of sICAM-1 in the pathogenesis of periodontal disease.
2. To estimate the level of sICAM-1 in periodontal health and disease.
3. To correlate the clinical parameters like bleeding index, plaque index, probing depth,
clinical attachment loss in periodontal health and disease.
7. Methodology
7.1. Source of data
The study population will consists of 90 systemically healthy subjects belonging to both
the sexes and will be selected are from M.R. Ambedkar Dental College and HospitalOPD, Bangalore, Karnataka, India.
7.2. Methods of collection of data
The 90 subjects will be divided into 3 groups of 30 subjects each as follows:1. Healthy group – No bleeding on probing,no signs of inflammation, no attachment
2. Gingivitis group –Probing pocket depth < 3 mm, no attachment loss, bleeding on
probing present, clinical sign of inflammation present.
3.Periodontitis group – clinical sign of inflammation present, presence of bleeding on
probing Probing pocket depth > 5mm, , clinical attachment loss > 3mm,.
Written informed consent will be taken from all subjects. Bleeding index (Ainamo &
Bay) plaque index (Sillness and Loe), probing depth and attachment loss are recorded in
all subjects. Gingival crevicular fluid is collected from healthy, gingivitis, periodontitis
sites by placing microcapillary pipettes using extra crevicular method. All samples will
be stored and subjected to ELISA for estimating soluble intercellular cell adhesion
molecule-1( sICAM-1). Values obtained will be statistically analysed using ANOVA test
with SPSS computer software.
7.3. Does the study require any investigations or interventions to be conducted on
patients or other human or animals?
7.4. Has ethical clearance been obtained from your institution in case of 7.3?
8. List of References
1.Williams.R.C.Periodontal disease,N.Engl.J.Med 1990;322;373-376
2. E.Hannigan, D.P O’Connell, A Hannigan, L.A Buckley” Soluble Cell Adhesion
Molecules in Gingival Crevicular Fluid in Periodontal Health and Disease” J Periodontol
2004 ;75; 546-550.
3. N.A. Moughal, E Adonogianaki, M.H Thornhill and D.F. Kinane "Endothelial cell
leukocyte adhesion molecule (ELAM-1) and intercellular adhesion molecule-1 (ICAM-1)
expression in gingival tissue during health and experimentally induced gingivitis". J
periodont res 1992; 27, 623 – 630.
4. Litter AJ, Buckley CD, Wordworth P, Collins I, Matrison J, Simmons DL. "A
distinct profile of six soluble adhesion molecules (ICAM-1, VCAM-1, E-selectin, Lselectin and P-selectin) in rheumatoid arthritis”. British Journal of Rheumatology; 1997,
36, 164 – 169
5. Crawford JM, Watanabe K "Cell Adhesion Molecules in inflammation and immunity"
Critical Review in Oral Biology and Medicine, 5(2); 91-123 (1994).
6. Gemell E, Walsh LJ, Savage, NW, Seymour GJ, "Adhesion molecular expression in
chronic inflammatory periodontal disease tissue”. J. Periodont Res 1994; 29; 46 – 53.
7. Krugluger W, Nell A, Solar P, Metejka M, Boltz Nitulescu "Influence of SE – selectin
and L-selectin on the regulation of cell migration during chronic periodontitis". J
Periodont Res 1995; 30; 198 – 203.
8. G.J. Seymour, E. Gemell, R.A. Reinhardt, J. Eastcatt, M.A. Taubman,
"Immunopathogsenesis of chronic inflammatory periodontal diseases cellular and
molecular mechanisms", J Periodont res 1993; 28; 478 – 486.