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An Official Publication of the Indian Association of Oral and Maxillofacial Pathologists


 
REVIEW OF SCIENTIFIC ARTICLES Table of Contents   
Year : 2005  |  Volume : 9  |  Issue : 1  |  Page : 44-45
 

Review of Scientific Articles


Department of Oral and Maxillo Facial Pathology, Meenakshi Ammal Dental College and Hospital, Chennai, India

Correspondence Address:
B Kavitha
Department of Oral and Maxillo Facial Pathology, Meenakshi Ammal Dental College and Hospital, Chennai
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-029X.39063

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How to cite this article:
Kavitha B. Review of Scientific Articles. J Oral Maxillofac Pathol 2005;9:44-5

How to cite this URL:
Kavitha B. Review of Scientific Articles. J Oral Maxillofac Pathol [serial online] 2005 [cited 2019 Jul 23];9:44-5. Available from: http://www.jomfp.in/text.asp?2005/9/1/44/39063


Functional genotype in matrix metalloproteinases - 2 promoter is a risk factor for oral carcinogenesis

J ORAL PATHOL MED 2004, 33: 405 - 9

Matrix metalloproteinases (MMPs) is a super family of proteolytic enzymes capable of degrading extracellular matrix and basement membrane. Over expression of MMPs in carcinomas was found to be important for tumour invasion and metastasis. Recent studies have also indicated that MMPs are involved in early tumorigenesis, modulating proliferation, apoptosis, and angiogenesis. MMP - 2 primarily hydrolyzes type IV collagen, which is a key clement of basement membrane and MMPs can cleave growth factors in extra cellular matrix involved in tumorigenesis and tumor progression. MMP-2 overexpression or activity has been considered as a marker to predict tumour progression.

A -1306 C → T polymorphism in the MMP- 2 promoter disrupts Sp1 - binding site. This study is aimed to assess the association of such genotype with the risk of oral squamous cell carcinoma (OSCC).

This study has provided evidence for the first time that -1306 → T polymorphism in MMP - 2 promoter is a susceptibity factor for the development of OSCC, with the CC genotype being associated with the increase of risk (two fold), particularly for the subsets occurring on non - buccal sites (four fold).

It is assumed that subjects carrying the CC genotype would have increased expression of this enzyme for long period and they may be more susceptible to cancer.

Identification of RANKL in osteolytic lesions of the facial skeleton

J DENT RES 2004, 83(4): 349 - 353

The precise mechanism of bone remodeling in highly coordinated fashion between osteoblasts and osteoclasts was elucidated with the discovery of the RANKL/RANK/OPG system. This cytokine system consists of a ligand, receptor activator of nuclear factor κB ligand (RANKL), a cell bound receptor, receptor activator of nuclear factor κB (RANK), and a secreted decoy receptor, osteoprotegerin (OPG).

RANKL and OPG were implicated as the essential cytokine systems regulating tumor-bone interactions in a range of diseases. In this study, the role of RANKL in the osteolytic processes in bone - resorbing cysts and tumors of the facial skeleton was elucidated.

There was positive immunoreactivity to RANKL, and TRAP (Tartrate - Resistant Acid phosphatase) in specimens of ameloblastomas, dentigerous cysts, odontogenic keratocysts, and radicular cysts. RANKL activates the osteoblasts in the connective tissue stroma of these lesions causing hone destruction.

The author suggests that agents inhibiting RANKL activity may be therapeutic and also, soluble RANK and OPG, which inhibit osteoclast formation by blocking RANKL - RANK interaction, has therapeutic potential.

Intraepithelial expression of perlecan, a basement membrane - type heparan sulfate proteoglycan reflects dysplastic changes of the oral mucosal epithelium

J ORAL PATHOL MED 2004, 33:87 - 95

One of the 13 major histological characteristics of the oral epithelial dysplasia listed in the WHO Histological Typing of Cancer and Precancer of the oral mucosa is "reduction of cellular cohesion", which was thought to be able to make epithelial cells behave autonomously. However, the reduction of cellular cohesion, in other words, the enlargement of the intercellular space, has neither been of concern pathologically not been investigated to a great extent.

It is viewed that the enlarged intercellular space results froth accumulation of proteoglycans. For the first time, the author has confirmed the presence of ECM molecule such as perlecan (a heparan sulfate proteoglycan, HSPG) in the intercellular space of the epithelium that serves as stroma in individual epithelial cells and that the overexpression of perlecan in dysplastic epithelial cells causes reduction of cellular adhesion. In this study the expression of perlecan was studied by immunohistochemistry as well by in situ hybridization in normal epithelium, dysplastic epithelium, and in oral squamous cell carcinoma.

In this study, the author has found that in the normal epithelium, perlecan was localized to parabasal cells. With severity of dysplastic changes. the perlecan expression extended From basal to prickle cell layer. In squamous Cell carcinoma (poorly differentiated), perlecan was immunolocalized in both carcinoma cells and stromal spaces with myxoid appearance.

The author suggests the presence of other ECM molecules within the epithelium, though presently perlecan is the only ECM molecule confirmed to exist in epithelium.

Alterations of gene expression in human neutrophils induced by smoking cessation

J CLIN PERIODONTAL 2004, 31:1110 -1116

There is evidence that smoking is one of the most significant factor in the development and progression of periodontal disease and that smokers respond poorly to a variety of periodontal therapies. Smoking cessation returns the periodontal healing response to the same level as in non- smokers and the responses of former smokers are comparable with those of non - smokers.

Although evidence of epidemiological studies on smoking cessation is available, little information is available about the biological effects of cigarette smoking cessation on the immune system. In the present study, the effect of smoking cessation on the peripheral neutrophil mRNA expression levels for inflammatory cytokines: chemokines, growth factor, and (IL-1β, TNF-α, IL-8, VEGF) matrix metalloproteinase (MMP-8) was investigated. These have been known to he produced by neutrophils and could be the representative cytokines or enzymes reflecting various neutrophil functions in periodontal diseases.

This experiment was performed in sixteen male smokers before (baseline) and 1, 4 and 8 weeks after smoking cessation, and in eleven non-smoking controls- The status of smoking cessation was verified by exhaled CO concentration and serum cotinine concentration. The mRNAexpression levels from the isolated and stimulated neutrophils were analyzed by semi-quantitative RT-PCR.

The analyzed low mRNA expression levels of neutrophils thorn smokers when compared to non smokers were statistically significant, which could be related to an impairment of' neutrophils by smoking. There was statistically significant increase in MMP-8 levels at 8 weeks after smoking cessation compared with the baseline. Though the other rnRNA expression levels elevated gradually from the baseline, they were not statistically significant. As these neutrophil products (IL-1β, TNF-α, IL-8, VEGF and MMP-8) are related to periodontal pathogenesis, the author finds it surprising that all these mRNA levels in smokers were found to be low. In this study, the author discusses various possible mechanisms behind these decreased rnRNA expression in neutrophils and insists on clarifying the mechanisms of cytokine networks and regulation of immune response between neutrophils and local environment.

In vitro cultured autologous pre - confluent oral keratinocytes for experimental prefabrication of oral mucosa

INT J ORAL MAXILLOFAC SURG 2004, 33: 476 - 485

Skin-bearing composite flaps are usually chosen for reconstruction of large tissue defects after tumor surgery in the oropharyngeal region. The use of these skin-bearing flaps frequently causes unwanted hair growth and excessive keratinization in the oropharyngeal recipient site resulting in compromised aesthetic and functional impairment. Similarly, tissue engineered mucosa grafts, with long culture periods (3 -4 wks) have limited use in large oropharyngeal cancer defects.

To overcome both complications of conventional skin - bearing flaps and tissue engineered mucosa grafts, the author comes LIP with a new tissue engineering technique, in which pre - confluent oral keratinocyte grafting (PCOK) has been addressed based on the fact that relatively undifferentiated keratinocytes are sufficient to achieve subsequent epidermal reconstruction in vivo. In contrast to the clinical reports of an in vitro cultivation of oral keratinocytes for oral mucosa replacement over a period of 3 weeks, the concept of a 48 - h in vitro cultivation of PCOK may result in a reduction of the treatment period.

In this study, oral keratinocytes from 30 winstar rats were isolated and then seeded on a hydrophilic PTFE membrane. After 48 hr, the membrane together with the PCOK was transplanted onto the gracilis muscle and wound bed closed primarily. Biopsies carried out at 1, 2, 3 & 4 weeks post - transplantation were evaluated immunohistochemically for cytokeratins, collagen IV, laminin, lectin - specific labeling of N - acetyl glucosamine oligomeres of endothelial cells to assess the grail acceptance, keratinocyte lining, expression of basement membrane components and vascularization. The success rate (91 %) of graft acceptance is significantly higher than that of conventional cultured epithelial sheets in previous studies (15 -75%).

Based on this animal study, the author concludes that PCOK grafts on muscle in vivo can achieve uniform multi - layered oral epithelial coverage in a short period of time and could he used as an alternative tool for oropharyngeal reconstructive surgery.




 

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