Osteocyte regulation of orthodontic force-mediated tooth movement via RANKL expression.

Orthodontic tooth movement is achieved by the remodeling of the alveolar bone surrounding roots of teeth. Upon the application of orthodontic force, osteoclastic bone resorption occurs on the compression side of alveolar bone, towards which the teeth are driven. However, the molecular basis for the regulatory mechanisms underlying alveolar bone remodeling has not been sufficiently elucidated. Osteoclastogenesis is regulated by receptor activator of nuclear factor-κB ligand (RANKL), which is postulated to be expressed by the cells surrounding the tooth roots. Here, we show that osteocytes are the critical source of RANKL in alveolar bone remodeling during orthodontic tooth movement. Using a newly established method for the isolation of periodontal tissue component cells from alveolar bone, we found that osteocytes expressed a much higher amount of RANKL than other cells did in periodontal tissue. The critical role of osteocyte-derived RANKL was confirmed by the reduction of orthodontic tooth movement in mice specifically lacking RANKL in osteocytes. Thus, we provide in vivo evidence for the key role of osteocyte-derived RANKL in alveolar bone remodeling, establishing a molecular basis for orthodontic force-mediated bone resorption.

[The relationship of molecular genetic markers with clinical signs and risk factors of periodontitis]. / Vzaimosvyaz' molekulyarno-geneticheskikh markerov s klinicheskimi priznakami i faktorami riska razvitiya parodontita.

The study revealed positive correlation between bleeding on probing and teeth loss risk with periodontal hypercolonization by Porphyromonas gingivalis, Prevotella intermedia and Treponema denticola. Pathological tooth mobility was associated with hypercolonization by P. intermedia and Tannerella forsythensis. Expression of IL8, TNF-α, MMP8 and MMP9 genes was also assessed in patient groups divided according to the depth of periodontal pockets and-the severity of chronic periodontitis revealing IL8 as positive diagnostic marker.

Expression of HMGB1 in the periodontal tissue subjected to orthodontic force application by Waldo's method in mice.

Recent studies indicate that high mobility group box protein 1 (HMGB1) originating from periodontal ligament (PDL) cells can be a potential regulator in the process of orthodontic tooth movement and periodontal tissue remodeling. The aim of this study is to investigate HMGB1 expression in periodontal tissue during orthodontic tooth movement in mice according to Waldo's method. Six 7-week-old C57BL6 mice were used in these experiments. The elastic band was inserted into the teeth space between the right first and second maxillary molars. After 3 days of mechanical loading, mice were fixed with transcardial perfusion of 4 % paraformaldehyde in 0.1 M phosphate buffer (pH 7.4), and the maxillary was extracted for histochemical analyses. The histological examination revealed local PDL tear at the tension side and the formation of extensive cell-free hyaline zones at the compression side. The immunolocalization of HMGB1 was significantly presented at tension side of PDL, apical area and dental pulp, whereas at the compression side of PDL, the labeling of HMGB1 was almost undetectable as the presence of hyaline zone. Taken together, we concluded that the orthodontic tooth movement by Waldo's method leads to histological changes and HMGB1 expression pattern that differ from those of coil spring method, including PDL tear and extensive hyaline zone which may severely destroy periodontal tissue and in turn impede tooth movement.

[Tooth and bone research using genetically modified mice].

Teeth and bone are both hard tissues and composed of hydroxyapatite. Tooth development initiates with the invasination of oral epithelium, followed by aggregation of supporting ectomesenchymal cells. From mouse study, numbers of molecules have been discovered to relate tooth development. These discoveries have helped to clarify the responsible genes of human genetic disorders with abnormal tooth number and structure. During tooth development, teeth erupt into the outer environment, oral cavity. From this point, teeth are completely different from bone which is always covered by soft tissues. Tooth eruption is composed of two different processes, that is, eruption pathway formation and vertical tooth movement. In this review, mutant mice with abnormal tooth development and eruption are introduced, and molecular mechanism required for this process is discussed.

Assessment of single nucleotide polymorphism at IL-1A+4845 and IL-1B+3954 as genetic susceptibility test for chronic periodontitis in Maharashtrian ethnicity.

BACKGROUND: The inflammatory response that is directed in large part by proinflammatory cytokine interleukin (IL)-1 is genetically determined, with some people having a more vigorous response than others to the same stimulus. The reason for this is speculated that the dysregulated production of IL-1 in some individuals overrides the feedback mechanisms that normally master the dose of inflammation to a level sufficient to fight microbial invasion without long-lasting damage to the tissues involved. The aims of the present study were to determine the distribution of IL-1 gene polymorphism (IL-1A+4845 and IL-1B+3954) and their association with periodontal disease severity and to determine the significance of detecting the composite genotype (IL-1A allele2+IL-1B allele2) versus detecting either of them alone. METHODS: A total of 120 subjects were included and divided into four groups of 30 subjects each, namely, healthy, mild, moderate, and severe periodontitis groups. After a complete clinical examination, DNA was isolated from 0.5 ml blood. Specific primers were used to detect the presence of IL-1 gene polymorphism with the help of polymerase chain reaction (PCR) and subsequent allele detection with restriction fragment length polymorphism (RFLP) and separation by gel electrophoresis. RESULTS: The distribution of the allele1 homozygous genotype was 3% in the severe periodontitis group, and the distribution for the allele2 genotype was 30%. A higly significant difference (Wilcoxon signed-rank test; P<0.001) was seen between subjects positive and negative for the composite genotype. CONCLUSIONS: Results of the present study reinforced the association of the IL-1 genotype as a risk factor for severe chronic periodontitis. Positivity for the composite genotype was found to be significantly associated with severe chronic periodontitis (odds ratio [OR]=12.42).

Periodontal therapy in siblings with Papillon-Lefèvre syndrome and tinea capitis: a report of two cases.

OBJECTIVE: Report of clinical and microbiological periodontal findings before and 6 months after treatment of two siblings with Papillon-Lefèvre syndrome (PLS) and tinea capitis. METHODS: Two brothers, RG 3 years and NG 5 years of age, were referred for treatment due to premature mobility of their deciduous teeth. Probing depths (PPD), attachment levels (PAL-V), and furcation involvements were examined clinically. Panoramic radiographs were taken. Subgingival plaque samples within the deepest pocket of each tooth were taken and analysed by real-time polymerase chain reaction (PCR) for Actinobacillus actinomycetemcomitans (AA), Porphyromonas gingivalis, Tannerella forsythensis, Treponema denticola, Fusobacterium nucleatum, and Prevotella intermedia. One-stage full-mouth scaling and extraction of hopeless teeth were performed under general anaesthesia, followed by systemic amoxicillin and metronidazole for 7 days. Clinical and microbiological analyses were performed 6 months after treatment. RESULTS: Before treatment, both siblings had exhibited PPD of up to 13 mm, Class III furcation defects at four teeth, and marginal suppuration. AA was detected in both patients and at all teeth at levels ranging from 3.0 x 10(2) to 5.1 x 10(6). Both patients exhibited palmar and plantar hyperkeratosis. Seven teeth were extracted from RG, and nine from NG. Six months after treatment, PPD had been reduced to

Papillon Lefevre syndrome.

Papillon-Lefevre syndrome is a very rare autosomal recessive condition characterised by pronounced palmoplantar hyperkeratosis and severe early onset periodontitis, leading to early loss of teeth. Here, we report a case of Papillon-Lefevre syndrome with a brief discussion on treatment aspect.

Expression of mRNAs encoding for alpha and beta integrin subunits, MMPs, and TIMPs in stretched human periodontal ligament and gingival fibroblasts.

The biological mechanisms of tooth movement result from the cellular responses of connective tissues to exogenous mechanical forces. Among these responses, the degradation of the extracellular matrix takes place, but the identification of the molecular basis as well as the components implicated in this degradation are poorly understood. To contribute to this identification, we subjected human fibroblasts obtained from the periodontal ligament (PDLs) and from the gingiva (HGFs) to a continuous stretch to quantify the mRNAs encoding for various metalloproteinases (MMPs), their tissue inhibitors (TIMPs), and alpha and beta integrin subunits. Both cell lines reacted by inducing the expression of the mRNAs encoding for MMP-1, MMP-2, TIMP-1, and TIMP-2, while other mRNAs did not vary (MT1-MMP, TIMP-3) or were not expressed (MMP-9). PDLs expressed selectively the mRNAs encoding for alpha4 and alphav, with no difference measurable under stretching, while the mRNAs encoding for alpha6 and beta1 were increased and the one encoding for alpha5 was decreased. HGFs increased the mRNAs encoding for alpha2, alpha6, beta1, and beta3 and decreased the one encoding for alpha3. Analysis of our data indicated that stretched HGFs and PDLs induced the same pattern of mRNAs encoding for MMPs and TIMPs but differed for those encoding various integrin subunits, known to act as protein receptors in mechanotransduction.

Orthodontic, genetic, and periodontal considerations in the treatment of impacted maxillary central incisors: A study of twins.

Treatment of twins each with one impacted maxillary central incisor and a mesiodens is described. Treatment included rapid expansion, extraction of the mesiodens, surgical exposure of the impacted central incisor, and its forced eruption. The impacted incisor was brought into functional position in one patient but was lost in the other because of insufficient root length and high mobility. Orthodontic, genetic, and periodontal considerations of these 2 cases are evaluated.

Familial ogee roots, tooth mobility, oligodontia, and microdontia.

The term ogee is proposed to describe dome or onion-shaped incisor roots as presented in a family study. A case of ogee permanent upper incisor teeth associated with microdontia, oligodontia, and tooth mobility is described. Forty-seven members of the proband's family were examined. The dental abnormalities were found to be of an autosomal dominant pattern of inheritance.

Papillon-Lefevre syndrome: report of two brothers.

Papillon-Lefevre syndrome was observed in two boys in the same family, and the topic of this report, the second to appear in the Greek dental literature. Both patients presented with hyperkeratosis of the palms and soles and severe periodontal destruction; the latter was more prominent in the younger boy. The children will lose their teeth before reaching maturity.