No abstract

Inflammation is a defense strategy against invading agents and harmful molecules that is activated immediately following a stimulus, and involves the release of cytokines and chemokines, which activate the innate immune response. These mediators act together to increase blood flow and vascular permeability, facilitating recruitment of effector cells to the site of injury. Following resolution of the injury and removal of the stimulus, inflammation is disabled, but if the stimulus persists, inflammation becomes chronic and is strongly associated with cancer. This is likely to be due to the fact that the inflammation leads to a wound that does not heal, requiring a constant renewal of cells, which increases the risk of neoplastic transformation. Debris from phagocytosis, including the reactive species of oxygen and nitrogen that cause damage to DNA already damaged by the leukotrienes and prostaglandins, has an impact on inflammation and various carcinogenic routes. There is an association between chronic inflammation, persistent infection and cancer, where oncogenic action is mediated by autocrine and paracrine signals, causing changes in somatic cells under the influence of the microbial genome or of epigenetic factors. Among the infectious agents associated with cancer, certain genotypes of human papillomavirus (HPV) stand out. HPV is responsible for virtually all cases of cervical cancer and a lower proportion of cancers of the vagina, vulva, anus, penis and a number of extragenital cancers. In the present review, recent advances in the mechanisms involved in the inflammatory response are presented with their participation in the process of carcinogenesis, emphasizing the role of chronic inflammation in the development of HPV-induced cervical cancer.

Age, multiple sexual partners, and infection with HPV-16 increased the risk of having LSILs or HSILs. Early onset of sexual activity and smoking only increased the risk of having HSILs.

No abstract

Low-level laser therapy (LLLT) induces anti-inflammatory and angiogenic activities in wound healing. However, the mechanism of action and optimal parameters require further clarification. In this study, we investigated the effects of LLLT on wound healing matrix metalloproteinase (MMP)-2 immunoexpression and angiogenic processes. Twenty female Wistar rats were randomly divided into four groups (n = 5) according to the treatments as follows. CG7 and CG14 were control groups at days 7 and 14, respectively, which received physiological saline (0.9 % NaCl daily). LG7 and LG14 were laser therapy groups at days 7 and 14, respectively, which received two (LG7) or four (LG14) LLLT applications (40 mW; 660 nm; 4 J/cm). A dorsal skin sample in the wound area (measuring 2 cm) was removed after the experimental period, and then the animals were euthanized. The specimens were processed for qualitative and quantitative histological analyses and measurement of MMP-2 expression in the dermis and epidermis. A persistent crust and moderate number of inflammatory cells were found in CG7 and CG14 groups. In the LG14 group, wounds demonstrated complete re-epithelization at the remodeling phase. Angiogenesis and MMP-2 expression were higher in LLLT-treated groups, particularly the LG14 group, which correlated according to the Spearman correlation test. LLLT improves wound healing by enhancing neocollagenesis, increasing the amount of new vessels formed in the tissue (neoangiogenesis), and modulating MMP-2 expression. Epidermal overexpression of MMP-2 was correlated to angiogenic processes.