1. Bansal R, Bansal R. Regenerative endodontics: A state of the art. Ind J Dent Res 2011;22:122-131.

Abstract – p.122//Bansal et al 2011	Abstract – p.255//Murray et al 2004
Scientific advances in the creation of restorative biomaterials, in vitro cell culture technology, tissue grafting, tissue engineering, molecular biology and the human genome project provide the basis for the introduction of new technologies into dentistry.	Scientific advances in the creation of restorative biomaterials, in vitro cell culture technology, tissue grafting, tissue engineering, molecular biology, and the human genome project provide the basis for the introduction of new technologies into dentistry.
http://www.google.co.in/search?sourceid=navclient&ie=UTF-8&rlz=1T4DKUS_enUS264IN313&q=Scientific+advances+in+the+creation+of+restorative+biomaterials%2c+in+vitro+cell+culture+technology%2c+tissue+grafting%2c+tissue+engineering%2c+molecular+biology+and+the+human+genome+project+provide+the+basis+for+the+introduction+of+new+technologies+into+dentistry. Assessed: June 18, 2011
Abstract – p.122//Bansal et al 2011	Jhaveri A, 2009//DrBicuspid.com**
Non-vital infected teeth have long been treated with root canal therapy (for mature root apex) and apexification (for immature root apex), or doomed to extraction.	Nonvital infected teeth have long been treated with root canal therapy and apexification, or doomed to extraction.
** http://www.drbicuspid.com/index.aspx?sec=sup&sub=rst&pag=dis&ItemID=301812 Assessed: June 19, 2011 http://www.google.co.in/search?sourceid=navclient&ie=UTF-8&rlz=1T4DKUS_enUS264IN313&q=Non-vital+infected+teeth+have+long+been+treated+with+root+canal+therapy+%28for+mature+root+apex%29+and+apexification+%28for+immature+root+apex%29%2c+or+doomed+to+extraction. Assessed: June 18, 2011
Abstract – p.122//Bansal et al 2011	Jhaveri A, 2009//DrBicuspid.com**
Although successful, current treatments fail to re-establish healthy pulp tissue in these teeth. But, what if the non-vital tooth could be made vital once again?	Although largely successful, current treatments fail to re-establish healthy pulp tissue in these teeth. But what if the nonvital tooth could be made vital once again?
** http://www.drbicuspid.com/index.aspx?sec=sup&sub=rst&pag=dis&ItemID=301812 Assessed: June 19, 2011 http://www.google.co.in/search?sourceid=navclient&ie=UTF-8&rlz=1T4DKUS_enUS264IN313&q=Although+successful%2c+current+treatments+fail+to+re-establish+healthy+pulp+tissue+in+these+teeth.+But%2c+what+if+the+non-vital+tooth+could+be+made+vital+once+again%3f . Assessed: June 18, 2011
Abstract – p.122//Bansal et al 2011	Jhaveri A, 2009//DrBicuspid.com**
That is the hope offered by regenerative endodontics, an emerging field focused on replacing traumatized and diseased pulp with functional pulp tissue.	That's the hope offered by regenerative endodontics, an emerging field focused on replacing traumatized and diseased pulp with functional pulp tissue.
** http://www.drbicuspid.com/index.aspx?sec=sup&sub=rst&pag=dis&ItemID=301812 Assessed: June 19, 2011
Abstract – p.122//Bansal et al 2011	p.711//Nakashima M et al 2005
The purpose of this article is to review these biological procedures and the hurdles that must be overcome to develop regenerative endodontic procedures.	The purpose of this article is to review the biological principles of tissue engineering and the hurdles that must be overcome to develop regenerative endodontic procedures.
http://www.google.co.in/search?sourceid=navclient&ie=UTF-8&rlz=1T4DKUS_enUS264IN313&q=The+purpose+of+this+article+is+to+review+these+biological+procedures+and+the+hurdles+that+must+be+overcome+to+develop+regenerative+endodontic+procedures. Assessed: June 18, 2011

Oral Lichen Planus

HOW TO WRITE  "ABSTRACT AND CONCLUSION FOR A REVIEW."

Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;350-365.	Roopashree MR et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734.	Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;350-365.
ABSTRACT: Both antigen-specific and non-specific mechanisms may be involved in the pathogenesis of oral lichen planus (OLP). Antigen-specific mechanisms in OLP include antigen presentation by basal keratinocytes and antigen-specific keratinocyte killing by CD8+ cytotoxic T-cells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase (MMP) activation in OLP lesions. These mechanisms may combine to cause T-cell accumulation in the superficial lamina propria, basement membrane disruption, intra-epithelial T-cell migration, and keratinocyte apoptosis in OLP. OLP chronicity may be due, in part, to deficient antigen-specific TGF-b1-mediated immunosuppression. The normal oral mucosa may be an immune privileged site (similar to the eye, testis, and placenta), and breakdown of immune privilege could result in OLP and possibly other autoimmune oral mucosal diseases. Recent findings in mucocutaneous graft-versus-host disease, a clinical and histological correlate of lichen planus, suggest the involvement of TNF-a, CD40, Fas, MMPs, and mast cell degranulation in disease pathogenesis. Potential roles for oral Langerhans cells and the regional lymphatics in OLP lesion formation and chronicity are discussed. Carcinogenesis in OLP may be regulated by the integrated signal from various tumor inhibitors (TGF-b1, TNFa, IFN-g, IL-12) and promoters (MIF, MMP-9). We present our recent data implicating antigen-specific and non-specific mechanisms in the pathogenesis of OLP and propose a unifying hypothesis suggesting that both may be involved in lesion development. The initial event in OLP lesion formation and the factors that determine OLP susceptibility are unknown.	ABSTRACT: Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory oral mucosal disease of unknown etiology. OLP presents as white striations, white papules, whiteplaques, erythema, erosions, or blisters affecting predominantly the buccal mucosa, tongue and gingiva. Both antigen-specific and non-specific mechanisms are hypothesized to be involved in the pathogenesis of oral lichen planus (OLP). Antigen-specific mechanisms in OLP include antigen presentation by basal keratinocytes and antigen-specific keratinocyte killing by CD8+ cytotoxic Tcells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase activation in OLP lesions. These mechanisms may combine to cause T cell accumulation in the superficial lamina propria, basement membrane disruption, intra-epithelial T cell migration and keratinocyte apoptosis in OLP. The various hypotheses proposed for pathogenesis of oral lichen planus are discussed in this review.	Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory oral mucosal disease of unknown etiology. OLP presents as white striations, white papules, white plaques, erythema, erosions, or blisters affecting predominantly the buccal mucosa, tongue, and gingivae (Vincent et al., 1990; Silverman et al., 1991).
Ismail SB et al. Oral lichen planus and lichenoid reactions: etiopathogenesis, diagnosis, management and malignant transformation. J Ora Sci 2007;49:89-106.	Roopashree MR et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734.	Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;350-365.
As many studies are being performed to understand the pathogenesis, potential biomarkers are being proposed to predict the onset and severity of OLP in individuals, which include CD 275 (77), serum autoantibodies to desmogleins 1 and 3 (76), urinary prokallikrein, PLUNC (78), biomarkers to predict the malignant transformation of OLP including 8-nitroguanine (79), and biomarkers to monitor therapeutic response to OLP (80).	Conclusion: Based on the pathogenesis, biomarkers are being proposed to predict the onset and severity of oral lichen planus, like CD2756, desmogleins 1 and 3; detect malignant transformation like PLUNC (Palate, lung and nasal epithelium carcinoma associated protein) and 8-nitoguanine; and monitor the therapeutic response. Analysis of current data suggests that blocking IL-12, IFN-c, TNF-a, RANTES, or MMP-9 activity or upregulating TGF-b1 activity in oral lichen planus may be of therapeutic value. More work is required for a full understanding of the etiology and pathogenesis of Oral lichen planus.	In the meantime, analysis of current data suggests that blocking IL-12, IFN-g, TNF-a, RANTES, or MMP-9 activity or up-regulating TGF-b1 activity in OLP may be therapeutic.

Oral Lichen Planus

Text similarity with different context orientation.

 

Sugarman PB, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;13:350-365.

Roopashree MR, et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734.

THE EPITHELIAL BASEMENT MEMBRANE As discussed above, epithelial basement membrane changes are common in OLP and include breaks, branches, and duplications (Jungell et al., 1989a; Zhou et al., 2001). Keratinocytes contribute to the structure of the epithelial basement membrane by secreting collagen IV and laminin V into the basement membrane zone (Marinkovich et al., 1993). Presumably, apoptotic keratinocytes are no longer able to perform this function. Hence, keratinocyte apoptosis triggered by intra-epithelial CD8+ cytotoxic T-cells may result in epithelial basement membrane disruption in OLP. Conversely, evidence from the involuting mouse mammary gland model suggests that keratinocytes require a basement-membrane-derived cell survival signal to prevent the onset of apoptosis (Pullan et al., 1996). Hence, epithelial basement membrane disruption may trigger keratinocyte apoptosis in OLP. An intriguing question in OLP is which came first — keratinocyte apoptosis or epithelial basement membrane disruption? Both mechanisms may be involved in the pathogenesis of OLP, e.g., basement membrane disruption may trigger keratinocyte apoptosis, and apoptotic keratinocytes may be unable to repair the disrupted basement membrane. Such a cyclical mechanism may underlie disease chronicity.

The epithelial basement membrane Keratinocytes contribute to the structure of the epithelial basement membrane by secreting collagen IV and laminin V into the basement membrane zone. Also evidence from the involuting mouse mammary gland model suggests that keratinocytes require a basementmembrane- derived cell survival signal to prevent the onset of apoptosis (3). Thus basement membrane is required for keratinocyte survival and keratinocyte for normal basement membrane production (Fig. 3). Apoptotic keratinocytes are no longer able to perform this function. Hence, keratinocyte apoptosis triggered by intra-epithelial CD8+ cytotoxic T cells may result in epithelial basement membrane disruption in OLP, which allows the non-specific T lymphocytes present in the sub epithelial zone to migrate into the epithelium. Both keratinocyte apoptosis and basement membrane disruption may be involved in the pathogenesis of OLP, e.g., basement membrane disruption may trigger keratinocyte apoptosis, and apoptotic keratinocytes may be unable to repair the disrupted basement membrane. Such a cyclical mechanism may underlie disease chronicity (3, 5).

Oral Lichen Planus

Same text but with different contextual interpretation.

123

Sugarman PB, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;13:350-365.	Lodi G, et al. Current controversies in oral lichen planus: Report of an international consensus meeting. Part 1. Viral infections and etiopathogenesis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;1:40-51.	Roopashree MR, et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734.
The lichen planus antigen is unknown, although the antigen may be a self-peptide, thus defining lichen planus as a true autoimmune disease. The role of autoimmunity in disease pathogenesis is supported by many autoimmune features of OLP, including disease chronicity, adult onset, female predilection, association with other autoimmune diseases, occasional tissue-type associations, depressed immune suppressor activity in OLP patients, and the presence of auto-cytotoxic T-cell clones in lichen planus lesions (Sugerman et al., 1992, 1993, 2000b). We suggest that keratinocytes express lichen planus antigen but only at the lesion site, i.e., the clinical distribution of lichen planus lesions is determined by the distribution of the lichen planus antigen. Hence, an early event in lichen planus lesion formation may be keratinocyte antigen expression or unmasking at the future lesion site induced by systemic drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), bacterial or viral infection, or an unidentified agent. Subsequently, intra-epithelial CD8+ cytotoxic T-cells recognize the lichen planus antigen associated with MHC class I on lesional keratinocytes and trigger keratinocyte apoptosis.	LP has a well-defined clinical distribution and there is a clear demarcation between lesional and nonlesional tissue. A possible explanation for this pattern of presentation is that keratinocytes express the LP antigen, but only at the lesion site. In other words, the clinical distribution of lichen planus is determined by the distribution of the antigen. Hence, an early event in LP lesion formation may be keratinocyte antigen expression or unmasking at the future lesion site induced by systemic drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), bacterial or viral infection, or an unidentified agent. Following altered keratinocyte antigen expression, antigen-specific CD41 and CD81 T cells may be either (1) on routine surveillance in the epithelium and encounter the keratinocyte antigen by chance (‘‘chance encounter’’ hypothesis) or (2) attracted to the epithelium by keratinocyte-derived chemokines (‘‘directed migration’’ hypothesis). The ‘‘chance encounter’’ hypothesis is supported by findings of CD81 T cells in normal human epidermis141,142 and basal cell degeneration in the absence of a dense inflammatory infiltrate in LP lesions.143 Conversely, the ‘‘directed migration’’ hypothesis is supported by findings of constitutive chemokine receptor expression by naı¨ve T cells144 and a dermal T-cell infiltrate prior to the appearance of intraepithelial lymphocytes and epithelial damage in LP lesions.145 In this context, keratinocyte antigen expression6chemokine production are primary events in oral LP lesion formation, followed by keratinocyte apoptosis triggered by antigen-specific CD81 cytotoxic T cells (Fig 1).	The lichen planus antigen is unknown, although the antigen may be a self-peptide, thus defining lichen planus as a true autoimmune disease. An early event in lichen planus lesion formation may be keratinocyte antigen expression or unmasking at the future lesion site induced by systemic drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), bacterial or viral infection, or an unidentified agent (3).

Plasmablastic lymphoma in a previously undiagnosed AIDS patient: A case report.

Nagpal D, Maralingannavar M, Koshti S. 
 Vieira FO, El Gandour O, Buadi FK, Williams GB, Shires CB, Zafar N. Plasmablastic lymphoma in a previously undiagnosed AIDS patient: A case report. Head and Neck Pathol 2008;2:92-96.

Sarode SC, Sarode GS, Patil A. Plasmablastic lymphoma of the oral cavity: A review. Oral Oncol 2010;46:146-153.

Vieira F, O. et al, 2008

Nagpal D et al, 2010

The epidemiology and prognosis of AIDS has changed tremendously since the first description of disease in 1980 [1]. The introduction of effective therapy and prophylaxis for opportunistic infections has significantly reduced mortality [2, 3]. Highly active antiretroviral therapy (HAART), introduced in 1996, has not only reduced the complications associated with AIDS, but also significantly improved survival [4–6]. However, secondary malignancies continue to be a major cause of AIDS-related morbidity and mortality [5]. Recent reports have shown a significant decrease in the incidence of non-Hodgkin lymphoma (NHL) in AIDS patients on HAART [7, 8], but the incidence still remains much higher than that of the general population [3, 9, 10]. The prevalence of AIDS-related malignancies is expected to increase as AIDS patients continue to live longer [4, 5, 8]. Therefore, PBL is expected to be seen more frequently among the spectrum of AIDS-defining illness [11].

Since its first description in early 1980’s AIDS epidemiology and prognosis has changed drastically due to the effective use of HAART1. After its introduction in 1996 HAART has been demonstrating success in reducing the complications associated with AIDS thus improving the survival. But secondary malignancies are still of concern for the AIDS related morbidity and mortality 2.

Sarode SC et al, 2010	Nagpal D et al, 2010
As per the current view, PBL arising from a post-germinal centre, preterminally differentiated B-cell lineage shows an abrupt dif ferentiation arrest in the plasmablastic stage.20 Oral PBL effaces the mucosal architecture with infiltration of the submucosa and extension to the mucosal surface with ulceration. It is characterised by monomorphic cellular proliferation of large lymphoid cells in a diffuse sheet-like and cohesive growth pattern. Thus as in other forms of NHL, it is likely that EBV has an important role in the pathogenesis of oral PBL, but a similar role for HHV8 is less certain.	PBL arising from post-germinal, preterminally differentiated B-cell lineage with abrupt arrest in the Plasmablastic stage. It is characterized by monomorphic cellular proliferation of large lymphoid cells in a diffuse cohesive or sheet-like pattern 5. Recent reviews have described that EBV has an important role in the pathogenesis of oral PBL, but a similar role for HHV8 is less certain 6.
Vieira FO et al, 2008	Nagpal D et al, 2010
The natural history of PBL without adequate treatment is progression from local to systemic disease and subsequent death.	The natural history of PBL without adequate treatment is progression from local to systemic disease and subsequent death 2.
Vieira FO et al, 2008	Nagpal D et al, 2010
Discussion The World Health Organization (WHO) classifies PBL as a non-Hodgkin B-cell lymphoma, predominantly occurring in HIV-positive patients. Originally PBL was described in the oral cavity region although, many reports of patients without HIV and outside the head and neck area have been recently presented in the literature [10, 13, 16–19]. PBL presents an aggressive behavior mostly in immunosuppressed HIV-positive patients who are co-infected by	Discussion The World Health Organization (WHO) classifies PBL as a non-Hodgkin B-cell lymphoma, predominantly occurring in HIV-positive patients. Originally PBL was described in the oral cavity region although; many reports of patients without HIV and outside the head and neck area have been recently presented in the literature 7-10. PBL has an aggressive nature especially in immunicompromised HIV-positive patients. Once antiretroviral therapy is initiated a

EBV. Interestingly, once antiretroviral therapy is initiated a more favorable and indolent response is observed.	more favorable and indolent response is observed 11.
Sarode SC et al, 2010	Nagpal D, 2010
Oral PBL effaces the mucosal architecture with infiltration of the submucosa and extension to the mucosal surface with ulceration. It is characterised by monomorphic cellular proliferation of large lymphoid cells in a diffuse sheet-like and cohesive growth pattern. The sheets of tumor cells are interspersed with macrophages, resulting in a ‘starry-sky’ appearance on low power examination. The tumor cells are reminiscent of immunoblasts and plasmablastic differentiation in the form of a round to oval shape with either centrally or eccentrically placed nuclei and abundant eosinophilic. cytoplasm (Fig. 2). Dutcher and Russell bodies characteristic of plasma cells are not seen.4 Usually, a single prominent nucleoli is located in the center of the nucleus. Brisk mitotic index, apoptotic bodies and sometimes necrosis has also been reported.	On light microscopy oral PBL shows infiltration of submucosa and extension to mucosal surface with ulceration, this was not found in the present case. It is characterized by monomorphic cellular proliferation of large lymphoid cells in diffuse sheet like and cohesive growth pattern. The sheets of tumor cells are interspersed with macrophages resulting in a ‘starry-sky’ appearance on low power examination. The tumor cells are reminiscent of immunoblasts and Plasmablastic differentiation in the form of round to oval shape with either centrally or eccentrically placed nuclei and abundant eosinophilic cytoplasm. Usually, single prominent nucleolus is located in the center of the nucleus. Brisk mitotic index, apoptotic bodies and sometimes necrosis has also been reported 5.
Vieira FO et al, 2008	Nagpal D et al, 2010
Once PBL is confirmed, work-up tests for HIV should be included due to this strong association [4, 6, 11–13, 20– 22]. In case the test results confirmed PBL-AIDS associated, there is evidence that initiating HAART improves prognosis, decreases incidence of systemic complications, and improves survival [4, 14, 19, 20, 23].	Once PBL is confirmed, work-up tests for HIV should be included due to this strong association 12,13 . In case the test results confirmed PBL-AIDS association, there is evidence that initiating HAART improves prognosis, decreases incidence of systemic complications, and improves survival 4, 10, 14-16.
Sarode SC et al, 2010	Nagpal D et al, 2010
Treatment may consist of chemotherapy, using prednisolone, cyclophosphamide, adriamycin and/or vincristine, or local excision followed by radiation. The final course of therapy is considered on a case-by-case basis depending on the stage of the disease, the presence of systemic symptoms or the association with HIV infection.7 Local radiotherapy has proven successful	Treatment may consist of chemotherapy, local excision followed by radiation. The final course of therapy is considered on case-by-case basis depending on the stage of the disease, the presence of systemic symptoms or the association with HIV infection. Local radiotherapy has proven successful only on gingival lesions. Multidrug chemotherapy with or without radiation therapy is

when only gingival lesions are present. Multi-drug chemotherapy with or without radiation treatment is generally recommended for the disseminated disease.	recommended for disseminated disease 17.
Vieira FO et al, 2008	Nagpal D et al, 2010
Currently there is agreement that HIV-positive patients with PBL must commence HAART [14, 19, 20, 23, 24], since it has shown improvement in survival rates.	Currently there is agreement that HIV-positive patients with PBL must commence HAART since it has shown to improve the survival rate 2,5,14.
Sarode SC et al, 2010	Nagpal D et al, 2010
Conclusion Oral PBL is an uncommon, recently described B-cell derived lymphoma most commonly seen in patients with HIV infection. It is characterised by a diagnostic triad of predilection for gingivo-buccal complex mucosa, classical plasmablastic morphology with the lack of neoplastic plasma cells and a limited immunohistochemical panel consisting of CD20 negativity, LCA (+/_), CD138/ VS38c diffuse positivity, light chain restriction and high Mib-1 index.	Conclusion Oral PBL is not uncommon among HIV-positive individuals, classified under non-hodgkin’s type of lymphoma derived from the B cells 1,2. It is characterized by a diagnostic triad of predilection for gingiva-buccal complex mucosa, classical Plasmablastic morphology with lack of neoplastic plasma cells and limited immunohistochemical panel consisting of CD20 negativity, LCA (+/-), CD138 positivity and high Mib-1 index 5.

Plasmablastic lymphoma in a previously undiagnosed AIDS patient: A case report. International Journal of Contemporary Dentistry 2010;1(3):7-10.