Associations between dental treatment in the primary and permanent dentitions using insurance claims data

PURPOSE: The purpose of this study was to assess the associations between dental treatment in the early primary dentition and later treatment in the primary and permanent teeth. METHODS: Delta Dental Plan of Michigan insurance claims data on 9,886 children who were born in 1990 and were covered by dental insurance from 1990-1998 were used. Risk ratios (RR), screening test measures of sensitivity (SN) and specificity (SP), and evidence-based dentistry research measures of Likelihood Ratio (LR) and Number Needed to Treat (NTT) were calculated. RESULTS: Primary anterior tooth treatment at ages 0-3 was weakly associated (RR = 1.43, 95% C.I. = 1.23, 1.65) with treatment of the permanent first molars at ages 6-8 and had SN, SP, LR, and NNT values of 7.4, 95.3, 1.57, and 12 respectively. Primary posterior tooth treatment at ages 4-8 was more strongly associated with future permanent first molar treatment with a RR of 2.44 (95% C.I. = 2.26, 2.64) and SN, SP, LR, and NNT values of 65.9, 61.7, 1.72, and 6. CONCLUSIONS: For this population, early childhood treatment in the primary anterior teeth was a weak predictor of future permanent first molar treatment. Primary posterior teeth treatment, while still not a strong predictor, was better than primary anterior teeth in predicting permanent tooth treatment. Caries treatment at ages 4-8 in the primary teeth was better than treatment at ages 0-3 in predicting permanent first molar treatment.     

Primary migration of a mini-implant under a functional orthodontic loading

Objectives

The objective of this study was to examine whether cortical bone thickness and bone mineral density (BMD) can explain the primary migration of a mini-implant under a functional orthodontic tangential loading at the early stage following implantation.

Materials and methods

Mini-implants were installed in human mandibular sections. A constant tangential load (2 N) was applied to the mini-implant under hydration. Creep, which is a time-dependent viscoelastic displacement in the bone surrounding the mini-implant, was assessed as the change in displacement during 2 h of loading. The total migration was measured as a maximum displacement that combined an initial elastic displacement and creep. After removal of the mini-implant, all specimens were scanned together by cone beam computed tomography. Cortical bone thickness and BMD were measured for the bone voxels surrounding the implant site.

Results

BMD had significant correlations with the displacement parameters (p?<?0.019), but the cortical bone thickness did not (p?>?0.272). Permanent bone deformation adjacent to the implant was observed to be resulting from substantial creep development under the orthodontic functional loading level.

Conclusions

BMD controls the primary migration of the mini-implant system in mandibular bone. Viscoelastic creep can develop at a small constant functional loading level, leading to migration of the mini-implant.

Clinical relevance

The current results indicated that mini-implant migration can develop under the small level of functional orthodontic load used in clinic. If the active bone remodeling around the mini-implant accelerates the migration, the risk of causing damage in vital organs next to the mini-implant increases.     

Involvement of the PVN and BST in 1K1C hypertension in the rat

The paraventricular nucleus of the hypothalamus (PVN) and the bed nucleus of the stria terminalis (BST) are two sources of central nervous system (CNS)-derived arginine vasopressin (AVP), a nonapeptide that has been implicated in central autonomic regulation and in particular in cardiovascular regulation, through its actions within the CNS. These experiments were designed to determine if either the PVN or the BST were involved in the development of Goldblatt one-kidney one-clip (1K1C) hypertension in the rat. In order to test this hypothesis, ibotenic acid lesions of the PVN or electrolytic lesions of the BST were undertaken in both normotensive (sham-operated) rats and in 1K1C rats. In both cases the development of 1K1C hypertension was inhibited over the 18–21 days following surgery. Lesions of the PVN did not alter normal blood pressure regulation in the sham-operated animals, whereas lesions to the BST did affect normal blood pressure regulation, resulting in a dramatic increase in blood pressure during the initial days following surgery. These studies suggest that the PVN and BST are involved in the development of 1K1C hypertension in the rat, moreover the BST may also play a role in central cardiovascular control.     

Preliminary evidence of cannabinoid effects on brain-derived neurotrophic factor (BDNF) levels in humans

Background  Acute and chronic exposure to cannabinoids has been associated with cognitive deficits, a higher risk for schizophrenia and other drug abuse. However, the precise mechanism underlying such effects is not known. Preclinical studies suggest that cannabinoids modulate brain-derived neurotrophic factor (BDNF). Accordingly, we hypothesized that Δ⁹-tetrahydrocannabinol (Δ⁹-THC), the principal active component of cannabis, would alter BDNF levels in humans. Materials and methods  Healthy control subjects (n = 14) and light users of cannabis (n = 9) received intravenous administration of (0.0286 mg/kg) Δ⁹-THC in a double-blind, fixed order, placebo-controlled, laboratory study. Serum sampled at baseline, after placebo administration, and after Δ⁹-THC administration was assayed for BDNF using ELISA. Results  Δ⁹-THC increased serum BDNF levels in healthy controls but not light users of cannabis. Further, light users of cannabis had lower basal BDNF levels. Δ⁹-THC produced psychotomimetic effects, perceptual alterations, and “high” and spatial memory impairments. Implications  The effects of socially relevant doses of cannabinoids on BDNF suggest a possible mechanism underlying the consequences of exposure to cannabis. This may be of particular importance for the developing brain and also in disorders believed to involve altered neurodevelopment such as schizophrenia. Larger studies to investigate the effects of cannabinoids on BDNF and other neurotrophins are warranted.     

Vocalizations of infants with hearing loss compared with infants with normal hearing: Part I--phonetic development

OBJECTIVE: Infants with hearing loss are known to be slower to develop spoken vocabulary than peers with normal hearing. Previous research demonstrates that they differ from normal-hearing children in several aspects of prelinguistic vocal development. Less is known about the vocalizations of early-identified infants with access to current hearing technologies. This longitudinal study documents changes in prelinguistic vocalizations in early-identified infants with varying degrees of hearing loss, compared with a group of infants with normal hearing. It was hypothesized that infants with hearing loss would demonstrate phonetic delays and that selected aspects of phonetic learning may be differentially affected by restricted auditory access. DESIGN: The vocalizations and early verbalizations of 21 infants with normal hearing and 12 early-identified infants with hearing loss were compared over a period of 14 mo (from 10 to 24 mo of age). Thirty-minute mother-child interaction sessions were video recorded at 6- to 8-wk intervals in a laboratory playroom setting. Syllable complexity changes and consonantal development were quantified from vocalizations and early verbalizations. Early behaviors were related to speech production measures at 36 mo of age. Participants with hearing loss were recruited from local audiology clinics and early intervention programs. Participants with normal hearing were recruited through day care centers and pediatrician offices. RESULTS: Relative to age-matched, normal-hearing peers, children with hearing loss were delayed in the onset of consistent canonical babble. However, certain children with moderately-severe losses babbled on time, and infants with cochlear implants babbled within 2 to 6 mo of implantation. The infants with hearing loss had smaller consonantal inventories and were slower to increase syllable shape complexity than age-matched normal-hearing peers. The overall pattern of results suggested that consonant development in infants with hearing loss was delayed but not qualitatively different from children with normal hearing. Delays appeared to be less pronounced than suggested by previous research. However, fricative/affricate development progressed slowly in infants with hearing loss and divergence from the patterns of normal-hearing children was observed. Six children (2 with normal hearing; 4 with hearing loss) were identified as atypical, based on their rates of development. At 24 mo of age, these children persisted in producing a high proportion (0.59) of vocalizations lacking consonants, which was negatively correlated with Goldman-Fristoe scores at 36 mo (r = -0.60). CONCLUSIONS: Results suggest that early-identified children are delayed in consonant and syllable structure development, which may influence early word learning rates. Fricative/affricate development appears to be challenging for some infants with hearing loss. This may be related to the effects of sensorineural hearing loss on high-frequency information, restricted bandwidth provided by amplification, and reduced audibility in contexts of noise and reverberation. Delayed fricative use may have implications for morphological development. Atypically slow rates of change in syllable development may indicate that a child is at risk for delayed speech development.     

Autophagy and oxidative stress in gliomas with IDH1 mutations

IDH1 mutations in gliomas associate with longer survival. Prooxidant and antiproliferative effects of IDH1 mutations and its d-2-hydroxyglutarate (2-HG) product have been described in vitro, but inconsistently observed. It is also unclear whether overexpression of mutant IDH1 in wild-type cells accurately phenocopies the effects of endogenous IDH1-mutations on tumor apoptosis and autophagy. Herein we investigated the effects of 2-HG and mutant IDH1 overexpression on proliferation, apoptosis, oxidative stress, and autophagy in IDH1 wild-type glioma cells, and compared those results with patient-derived tumors. 2-HG reduced viability and proliferation of U87MG and LN18 cells, triggered apoptosis in LN18 cells, and autophagy in U87MG cells. In vitro studies and flank xenografts of U87MG cells overexpressing R132H IDH1 exhibited increased oxidative stress, including increases of both manganese superoxide dismutase (MnSOD) and p62. Patient-derived IDH1-mutant tumors showed no significant differences in apoptosis or autophagy, but showed p62 accumulation and actually trended toward reduced MnSOD expression. These data indicate that mutant IDH1 and 2-HG can induce oxidative stress, autophagy, and apoptosis, but these effects vary greatly according to cell type.     

Identity exploration in the dating domain: The role of attachment dimensions and parenting practices

We examined relations among perceived parenting practices (support and psychological control), attachment dimensions for romantic relationships (anxiety and avoidance) and exploration of the dating identity among actively dating adolescents in two high school aged samples. In the all female sample of Study 1 (n = 653) and the gender balanced sample of Study 2 (n = 1003), parenting practices contributed to adolescent exploration of the dating identity. Parent psychological control, but not parental support, also contributed to elevated feeling of avoidance and anxiety in romantic relationships. Avoidance, in turn, was related to less exploration of the dating identity while anxiety seemed to increase it. Gender moderated the model, with parenting practices predicting exploration only for girls and with the links for avoidance and anxiety with exploration stronger for boys than girls. Indirect effects for parenting practices through attachment dimensions on exploration of the dating identity were also noted.