The findings indicate that angiogenic factors are differentially expressed in oral lichen planus compared with inflamed controls, with increased expression of pro-angiogenic factors and decreased anti-angiogenic expression.

There is a global increase in the prevalence of human papillomavirus (HPV)‐driven oropharyngeal squamous cell carcinoma (OPSCC) in Australia and New Zealand. Risk factors for HPV‐positive OPSCC are male gender, white race, age older than 40 but younger than 59 years old, having multiple lifetime sex partners, having oro‐genital and oro‐anal sex. High‐risk HPV subtypes play a major role in the pathogenesis of OPSCC, however, they play a much lesser role in oral squamous cell carcinoma (OSCC). Among the laboratory tests used to detect oncogenic HPV infection, polymerase chain reaction is a sensitive method but does not reflect the role of HPV in oncogenesis. While widely used, p16 immunohistochemistry is both a sensitive and a specific surrogate marker for oncogenic HPV infection in OPSCC, but not in OSCC. However, it is a useful prognostic marker in OPSCC. The current gold standard to accurately detect oncogenic HPV infection is E6/E7 mRNAin situ hybridization. Because both HPV‐positive and p16‐positive OPSCC have better short‐term prognoses there is current debate and trials on treatment de‐escalation in HPV‐positive OPSCC. Dental practitioners can play an important role in early diagnosis of HPV‐positive OPSCC.

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Caries results in the demineralization and destruction of enamel and dentine, and as the disease progresses, irreversible pulpitis can occur. Vital pulp therapy (VPT) is directed towards pulp preservation and the prevention of the progression of inflammation. The outcomes of VPT are not always predictable, and there is often a poor correlation between clinical signs and symptoms, and the events occurring at a molecular level. The inflamed pulp expresses increased levels of cytokines, including tumour necrosis factor (TNF)a, interleukin (IL)-1a, IL-1b, IL-4, IL-6, IL-8, IL-17 and IL-23, which recruit and drive a complex cellular immune response. Chronic inflammation and sustained cytokine release can result in irreversible pulp damage and a decreased capacity for tissue healing.Other chronic inflammatory diseases, such as psoriasis, inflammatory bowel diseases and rheumatoid arthritis, are also characterized by an dysregulated immune response composed of relatively high cytokine levels and increased numbers of immune cells along with microbial and hard-soft tissue destructive pathologies. Whilst anti-cytokine therapies have been successfully applied in the treatment of these diseases, this approach is yet to be attempted in cases of pulp inflammation. This review therefore focuses on the similarities in the aetiology between chronic inflammatory diseases and pulpitis, and explores how anticytokine therapies could be applied to manage an inflamed pulp and facilitate healing. Further proof-ofconcept studies and clinical trials are justified to determine the effectiveness of these treatments to enable more predictable outcomes in VPT.

Accumulating evidence suggests tumor protein 53 (p53) promotes correct cellular differentiation. Thus, mutant TP53 may be more frequent in tumors with irregular differentiation. This study investigated whether TP53 mutations were more frequent in diffuse large B cell lymphoma (DLBCL) that lacked the B cell lineage marker CD19. Sixteen CD19 negative and 78 CD19 positive DLBCL were sequenced for TP53 mutations. Twenty nine tumors had TP53 mutations and were associated with poorer survival. Mutant TP53 was more frequent in CD19 negative lymphomas (81% versus 21%, p < 0.0001). Analysis of other B cell markers revealed a lack of paired box 5 (PAX5) in CD19 positive lymphomas with mutant TP53 (50%), which was more frequent compared to tumors with wild-type TP53 (15%, p = 0.002). In summary, DLBCL lacking CD19 or PAX5 expression were more likely to have mutant TP53, suggesting irregular B cell marker phenotypes are associated with TP53 mutation.Normal functioning of p53 is critical for preventing cancers. We know this because mice with defects in Trp53 are highly tumor prone; in humans inherited TP53 mutations, Li-Fraumeni Syndrome, is characterized by multiple tumor types, and about half of all human cancers contain TP53 mutations (www.iarc. 5,6 . A poorer prognosis is associated with DLBCL with mutant p53 [5][6][7][8][9][10] . Of interest, 10-12% of DLBCL have lost the B cell lineage marker CD19 11,12 and are also associated with a poor prognosis 5,6,12 . Given this, and the data from the PRD mutant mouse, we were interested to determine if mutant p53 might be driving abnormal B cell differentiation that pre-disposes to malignancy. This study investigated the prevalence of TP53 mutations in DLBCL with irregular expression of B cell markers including those that were CD19 negative. ResultsTP53 mutations are enriched in CD19 negative DLBCL. Ninety-four DLBCL were included in the study. The patient demographics and clinical information are provided in Table 1. Sixteen DLBCL were CD19 negative based on a low expression of CD19 positive cells by flow cytometry (a clear visible shift in fluorescence consistent with reduced expression) based on the initial diagnostic assessment. A lack of CD19 positive cells in