Introduction: The aim of this study was to determine 8-OHdG concentration as a biomarker of oxidant-induced DNA damage and to assess total antioxidant status (TAS) in gingival and peripheral blood during periodontal lesion. Materials and Methods: The study included 56 untreated periodontitis patients (26 with aggressive periodontitis, and 30 with chronic periodontitis (CP). The control group consisted of 25 healthy volunteers without pathological changes in the periodontium. Competitive ELISA was used to measure 8-OHdG. A colorimetric method based on the reduction of ABTS
Mandibular prognathism is defined as an abnormal forward projection of the mandible beyond the standard relation to the cranial base and it is usually categorized as both a skeletal Class III pattern and Angle Class III malocclusion. The etiology of mandibular prognathism is still uncertain, with various genetic, epigenetic, and environmental factors possibly involved. However, many reports on its coexistence in both twins and segregation in families suggest the importance of genetic influences. A multifactorial and polygenic background with a threshold for expression or an autosomal dominant mode with incomplete penetrance and variable expressivity are the most probable inheritance patterns. Linkage analyses have, thus far, shown the statistical significance of such loci as 1p22.1, 1p22.3, 1p32.2, 1p36, 3q26.2, 4p16.1, 6q25, 11q22, 12pter-p12.3, 12q13.13, 12q23, 12q24.11, 14q24.3 to 31.2, and 19p13.2. The following appear among candidate genes: MATN1, EPB41, growth hormone receptor, COL2A1, COL1A1, MYO1H, DUSP6, ARHGAP21, ADAMTS1, FGF23, FGFR2, TBX5, ALPL, HSPG2, EVC, EVC2, the HoxC gene cluster, insulin-like growth factor 1, PLXNA2, SSX2IP, TGFB3, LTBP2, MMP13/CLG3, KRT7, and FBN3. On the other hand, MYH1, MYH2, MYH3, MYH7, MYH8, FOXO3, NFATC1, PTGS2, KAT6B, HDAC4, and RUNX2 expression is suspected to be involved in the epigenetic regulations behind the mandibular prognathism phenotype.
Clefts that occur in children are a special topic. Avoiding risk factors, and also an early diagnosis of cleft possibility can result in minimizing or avoiding them. If on the other hand when clefts occur they require a long-term, multistage specialized treatment. Etiology of clefts seems to be related to many factors. Factors such as genetic, environmental, geographic and even race factors are important. Identification of risk factors can lead to prevention and prophylactic behaviors in order to minimize its occurrence. Exposure to environmental factors at home and work that lead to cleft predisposition should not be disregarded. It seems that before planning a family it would be wise to consult with doctors of different specializations, especially in high-risk families with cleft history in order to analyze previous lifestyle. Clefts are very common in hereditary facial malformations and are causing a lot of other irregularities in the head and neck region. In this paper after a brief papers review authors present socio-geographic, environmental and also work place related factors that are influencing pregnant women condition and should be taken under serious consideration.
HPV infections are currently the most frequent cause of genital infections in the USa. Risk factors are early onset of sexual activity, multiple sexual partners, a history STds, an early age of first pregnancy and tobacco use. In the past, HPV viruses were thought to be STds, but it is now known that penetration is not necessary. Skin-to--skin or mucosa-to-mucosa contact is enough to transmit the virus, which presents high tropism for those tissues. The Papillomaviridae family includes over 120 viruses, some of which have high malignant transformation rates. The most common malignancy connected to HPV is uterine cervix cancer and anal canal cancer. The range of morphology of perianal lesions means that a thorough clinical examination is required, including an anoscopy. Therapeutic modalities often seek to eliminate macroscopic changes rather than focus on the cause of the infection, which leads to a high recurrence rate. Externally located changes can be eliminated with patient-applied treatments. Those located in the anal canal and distal end of the rectal ampulla require treatment by a qualified medical provider. due to the high recurrence rate after standard treatment, special attention has been given to vaccinations. The polyvalent vaccine includes HPV viruses with both low and high malignant transformation risk. This has led to a decrease in the rate of malignancies (Adv Clin Exp Med 2014, 23, 2, 307-311). The Epidemiology and Biology of HPV Anal InfectionsThe Human Papilloma Virus (HPV) used to be thought of as one of the most common sexually transmitted diseases (STds) [1]. However, penetrative sexual contact is not in fact necessary to transmit the virus, which is predominantly transmitted by skin-to-skin or mucosa-to-mucosa contact [2]. The HPV family (Papillomaviridae) consists of more than 120 viruses presenting a tropism towards either the cutaneous or mucosa epithelium. The frequency of HPV infection has risen in the past 35 years, and this can be attributed to a decrease in the age of the first sexual contact as well as an increase in the number of sex partners [3]. HPV is the most common genital infection in the US, and the lifetime risk of at least one HPV infection in women is 75% [1,4]. The prevalence of anal HPV infection is very high: about 57% in HIV-negative men who have sex with men (MSM) [5]; and among HIV-positive men the infection rate is about 60 times higher than in the general male population [6]. Several risk factors for HPV infection have been identified: early onset of sexual activity, multiple sexual partners, a history of STds, an early age of first pregnancy and tobacco use [7].HPV penetrates skin or mucosa up to the basal membrane in search of keratinocytes (basal
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