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Notes: Background: Genetic polymorphisms for cytokines and their receptors have been proposed as potential markers for periodontal disease. Tumor necrosis factor receptor 2 (TNFR2) is one of the cell surface receptors for TNF-α. Recent studies have suggested that TNFR2 gene polymorphism is involved in autoimmune and other diseases.Objectives: The aim of the present study is to evaluate whether TNFR2(+587T/G) gene polymorphism is associated with chronic periodontitis (CP).Methods: One hundred and ninety-six unrelated subjects (age 40–65 years) with different levels of CP were identified according to established criteria, including measurements of probing pocket depth (PPD), clinical attachment level (CAL), and alveolar bone loss (BL). All subjects were of Japanese descent and non-smokers. Single nucleotide polymorphism at position +587(T/G) in the TNFR2 gene was detected by a polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) method.Results: The frequency and the positivity of the +587G allele were significantly higher in severe CP patients than in controls (p=0.0097; odds ratio=2.61, p=0.0075; odds ratio=3.06). In addition, mean values of PPD, CAL, and BL were significantly higher in the +587G allele positive than in the negative subjects (p=0.035, 0.022, and 0.018, respectively).Conclusions: These findings suggest that the TNFR2(+587G) polymorphic allele could be associated with severe CP in Japanese.

Notes: Background/Aims: Early onset periodontitis (EOP), newly ‘aggressive periodontitis’, is considered to have genetic basis, which have not been clearly defined. The interleukin-1 (IL-1) gene cluster polymorphism as one of genetic factors may influence the expression of several chronic inflammatory diseases. The aim of this study is to investigate the frequency of single nucleotide polymorphisms (SNPs) in the genes encoding IL-1α, IL-1β and a variable number of tandem repeat (VNTR) polymorphisms in the IL-1 receptor antagonist gene (IL-1RN) in 47 generalized EOP (G-EOP) patients and 97 periodontally healthy controls.Material and methods: All subjects were of Japanese descent and systemically healthy. They were identified according to established clinical criteria. SNPs in the IL-1α (+ 4845) and IL-1β (− 511, + 3954) genes were analyzed by amplifying the polymorphic region using polymerase chain reaction (PCR), followed by restriction-enzyme digestion and agarose gel electrophoresis. IL-1RN (VNTR) polymorphisms were then detected by PCR amplification and fragment size analysis.Results: There was no significant difference in the IL-α (+ 4845) and IL-1β (− 511, + 3954) genotypes and allele frequencies between G-EOP patients and healthy controls. However, the frequency of IL-1RN (VNTR) polymorphic alleles was found to be significantly increased in G-EOP patients (χ2 test, P = 0.007; odds ratio = 3.40). Additionally, the carriage rate of IL-1RN (VNTR) polymorphisms was significantly higher in G-EOP patients than in healthy controls (χ2 test, P = 0.005; odds ratio = 3.81).Conclusion: These findings suggest that IL-1RN (VNTR) polymorphisms are associated with G-EOP in Japanese.

Notes: A 58-year-old Japanese man visited our clinic in December 2000 with a complaint of an erythematous plaque with reddish papules and pigmentation on the penis shaft and glans. He noticed the lesion 1 month before his visit. He denied any previous homosexual activity. His wife denied any genital skin lesion or gynecologic abnormality. No history of human immunodeficiency virus infection could be obtained.Physical examination of the skin lesion revealed an asymptomatic, flat-topped, approximately 10-mm-sized, reddish-brown keratotic plaque on the penis shaft. It showed an irregular surface, irregular border, and color variegation. Multiple, small, reddish-brown papules and plaques were distributed on the surrounding penis shaft and glans (〈link href="#f1"〉Fig. 1). The patient had no symptomatic signs. No lymphadenopathy was noted in the inguinal area.〈figure xml:id="f1"〉Figure 1 〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD1307_1:IJD_1307_f1"/〉Clinical features of BP lesions on the penis. A keratotic plaque shows an irregular surface, irregular border, and color variegation, and is surrounded by small, reddish-brown papulesA biopsy specimen revealed parakeratosis and an irregularly acanthotic epidermis composed of abnormal keratinocytes exhibiting cellular atypia and mitotic figures. The tumor cells had large, hyperchromatic, and pleomorphic nuclei (〈link href="#f2"〉Fig. 2). These lesions were diagnosed as bowenoid papulosis (BP). For treatment, an operative excision with a 3 mm margin was performed.〈figure xml:id="f2"〉2〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD1307_1:IJD_1307_f2"/〉Histologic features of the BP lesion. A parakeratotic and irregularly acanthotic epidermis is composed of abnormal keratinocytes exhibiting cellular atypia and mitotic figures. The tumor cells have large, hyperchromatic, and pleomorphic nucleiDNA was extracted from blocks of BP and non-BP, normal-looking skin tissue. Polymerase chain reaction (PCR) was performed utilizing L1 consensus primer set MY09 and MY11 (Bernard HU, Chan SY, Manos MM, et al. Identification and assessment of known and novel human papillomaviruses by polymerase chain reaction amplification, restriction fragment length polymorphisms, nucleotide sequence, and phylogenetic algorithms. J Infect Dis 1994; 170: 1077–1085). MY09/11 consensus PCR generated an approximately 450-base-pair fragment from all of the samples (〈link href="#f3"〉Fig. 3). Nucleotide sequencing revealed that the amplified L1 sequences were identical to that of human papillomavirus (HPV) type 16 (nucleotide positions 6582–7018). All of the L1 sequences from the BP lesion and the normal regions were identical. Our case contained the prototype sequence reported by Dürst et al. (Dürst M, Gissmann L, Ikenberg H, zur Hausen H. A papillomavirus DNA from a cervical carcinoma and its prevalence in cancer biopsy samples from different geographic regions. Proc Natl Acad Sci USA 1983; 80: 3812–3815).〈figure xml:id="f3"〉3〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD1307_1:IJD_1307_f3"/〉Amplification of the L1 sequence from a BP lesion and surrounding tissues. The polymerase chain reaction was carried out using MY09 and MY11 consensus primers. Lanes from left to right: M, 1-kilobase ladder marker; N, negative control (H2O); P, positive control (HPV16 DNA); 1, DNA from BP lesion; 2 and 3, DNA from surrounding tissues consisting of normal skin. An arrow indicates the 450-base-pair bands