Periodontal disease appears to be an independent risk factor for PLBW. Periodontal therapy significantly reduces the rates of PLBW in this population of women with periodontal disease.

Pregnant women with periodontal disease (PD) may be at increased risk for having preterm low-birth-weight (PLBW) children. We investigated whether the maintenance of the mothers' periodontal health after 28 weeks' gestation reduces the risk of PLBW. Of the 639 women studied, 406 had gingivitis and received treatment before 28 weeks' gestation, and 233 had PD and were treated after delivery. Data about previous and current pregnancies and known risk factors were obtained from patients' medical records. Primary outcomes were delivery before 37 weeks' gestation or an infant with birth weight below 2500 g. The incidence of PLBW was 2.5% in periodontally healthy women, and 8.6% in women with PD (p = 0.0004, relative risk = 3.5, 95% CI, 1.7 to 7.3). Risk factors significantly associated with PLBW were previous PLBW, PD, fewer than 6 pre-natal visits, and low maternal weight gain. PD was associated with both preterm birth and low birth weight, independent of other risk factors.

Principal cells in the medial nucleus of the trapezoid body (MNTB) are believed to be critical components in the circuit subserving sound localization. These cells, located in the superior olivary complex, convert excitatory inputs, arriving from the contralateral cochlear nucleus by way of large somatic synapses (the calyces of Held), to inhibitory projections onto principal cells in the ipsilateral lateral superior olive (LSO). We have characterized a population of cells in the rat MNTB using intracellular recording and labeling techniques in a brain slice preparation. MNTB principal cells had spherical or ellipsoid somata that gave rise to single large-diameter dendrites, which branched extensively and often extended beyond the borders of MNTB. Commonly observed axonal projection targets included LSO, the superior paraolivary nucleus, and the medial superior olive, and occasionally the lateral nucleus of the trapezoid body. The projections of individual MNTB cells showed an orderly topography that is consistent with the known tonotopic maps of the nuclei. In response to current injection, principal cells exhibited several nonlinearities, including rectification for depolarizing currents and a "sag" in the membrane potential for hyperpolarizing currents. Superthreshold depolarizing currents elicited transient firing behavior. Application of the potassium channel blocker 4-aminopyridine reduced or eliminated the rectification in the current-voltage relationships and caused depolarizing currents to elicit repetitive firing. Stimulation of afferent inputs elicited short-latency spikes, presumably driven by calyceal synaptic inputs; long-latency, presumably polysynaptic, EPSPs; and short- and long-latency IPSPs. The duration of synaptic events was strongly dependent on membrane potential, and this effect was probably due to the intrinsic membrane properties of the cell. In all cases tested, EPSPs were blocked by CNQX or DNQX, and IPSPs were blocked by strychnine. Two injected non-principal cells differed from principal cells in their morphologies and physiological characteristics.

Aim: To review the burden of caries and periodontitis in the elderly, changes with age that can explain this burden, and the vulnerability to disease of elderly populations. Methods: An assessment of surveys in two populations was conducted. Indicators for caries were identified by updating a systematic review. Secular trends for smoking and type 2 diabetes were discussed. Results: Changes in the susceptibility to periodontitis with age may be explained by exposure to pro-inflammatory conditions and changes in the healing capacity of cells and tissues. Due to accumulated periodontal destruction, the number of surfaces at risk for caries increases. The sequels of restorative treatment contribute to an increased susceptibility for caries development. Population-based surveys in the United States and Germany demonstrate a high caries experience among elderly people. A comparison of surveys demonstrates a relative improvement of periodontal health among elderly during the last few decades. Nevertheless, prevalence estimates for periodontitis remain high. Risk indicators for root caries include caries experience, the number of surfaces at risk and poor oral hygiene. Secular trends of main risk factors for periodontitis and their likely influence on the future periodontitis burden in the elderly are discussed. Conclusion: Caries and periodontitis burden in the elderly remain high.

We report a 5-year-old girl with a large rapidly growing giant cell tumor of the mandible that recurred 2 months after the first surgical excision and 3 months after a second resection. An angiogenic protein, (bFGF), was abnormally elevated in her urine. The patient was treated with interferon alfa-2a for 1 year because this agent inhibits angiogenesis by suppressing bFGF overexpression in infantile hemangiomas and in other human tumors. During this time the bone tumor regressed and disappeared, the urinary bFGF fell to normal levels, and the mandible regenerated. She has remained tumor-free and has been off therapy for 3 years at this writing. This first successful use of interferon alfa-2a to treat a mandibular tumor in a child demonstrates: 1) low grade tumors that overexpress bFGF may respond to interferon alfa-2a, in a manner similar to life-threatening infantile hemangiomas; 2) antiangiogenic therapy, given without interruption for 1 year, was safe and effective in this patient; and 3) treatment may be continued for 1 year without the development of drug resistance.

Platelet degranulation allows the release of a large amount of soluble mediators, is an essential step for wound healing initiation, and stimulates clotting, and angiogenesis. The latter process is one of the most critical biological events observed during tissue repair, increasing the growth of blood vessels in the maturing wound. Angiogenesis requires the action of a variety of growth factors that act in an appropriate physiological ratio to assure functional blood vessel restoration. Platelets release main regulators of angiogenesis: Vascular Endothelial Growth Factors (VEGFs), basic fibroblast growth factor (FGF-2), and Platelet derived growth factors (PDGFs), among others. In order to stimulate tissue repair, platelet derived fractions have been used as an autologous source of growth factors and biomolecules, namely Platelet Rich Plasma (PRP), Platelet Poor Plasma (PPP), and Platelet Rich Fibrin (PRF). The continuous release of these growth factors has been proposed to promote angiogenesis both in vitro and in vivo. Considering the existence of clinical trials currently evaluating the efficacy of autologous PRP, the present review analyses fundamental questions regarding the putative role of platelet derived fractions as regulators of angiogenesis and evaluates the possible clinical implications of these formulations.

After injury to periodontal tissues, a sequentially phased healing response is initiated that enables wound closure and partial restoration of tissue structure and function. Wound closure in periodontal tissues involves the tightly regulated coordination of resident cells in epithelial and connective tissue compartments. Multiple cell populations in these compartments synergize their metabolic activities to reestablish a mucosal seal that involves the underlying periodontal connective tissues and the attachment of these tissues to the tooth surface. The formation of an impermeable seal around the circumference of the tooth is of particular significance in oral health since colonization of tooth surfaces by pathogenic biofilms promotes inflammation, which can contribute to periodontal tissue degradation and tooth loss. The reformation of periodontal tissue structures in the healing response centrally involves fibroblasts, which synthesize and organize the collagen fibers that link alveolar bone and gingiva to the cementum covering the tooth root. The synthesis and remodeling of nascent collagen matrices are of fundamental importance for the reestablishment of a functional periodontium and are mediated by diverse, multi-functional fibroblast populations that reside within the connective tissues of gingiva and periodontal ligament. Notably, after gingival wounding, a fibroblast sub-type (myofibroblast) arises, which is centrally involved in collagen synthesis and fibrillar remodeling. While myofibroblasts are not usually seen in healthy, mature connective tissues, their formation is enhanced by wound-healing cytokines. The formation of myofibroblasts is also modulated by the stiffness of the extracellular matrix, which is mechanosensed by resident precursor cells in the gingival connective tissue microenvironment. Here, we consider the cellular origins and the factors that control the differentiation and matrix remodeling functions of periodontal fibroblasts. An improved understanding of the regulation and function of periodontal fibroblasts will be critical for the development of new therapies to optimize the restoration of periodontal structure and function after wounding.

Aging may negatively affect gingival wound-healing. However, little is known about the mechanisms underlying this phenomenon. The present study examined the cellular responses associated with gingival wound-healing in aging. Primary cultures of human gingival fibroblasts were obtained from healthy young and aged donors for the analysis of cell proliferation, cell invasion, myofibroblastic differentiation, and collagen gel remodeling. Serum from young and old rats was used to stimulate cell migration. Gingival repair was evaluated in SpragueDawley rats of different ages. Data were analyzed by the Mann-Whitney and Kruskal-Wallis tests, with a p value of .05. Fibroblasts from aged donors showed a significant decrease in cell proliferation, migration, Rac activation, and collagen remodeling when compared with young fibroblasts. Serum from young rats induced higher cell migration when compared with serum from old rats. After TGF-beta1 stimulation, both young and old fibroblasts demonstrated increased levels of alpha-SMA. However, alpha-SMA was incorporated into actin stress fibers in young but not in old fibroblasts. After 7 days of repair, a significant delay in gingival wound-healing was observed in old rats. The present study suggests that cell migration, myofibroblastic differentiation, collagen gel remodeling, and proliferation are decreased in aged fibroblasts. In addition, altered cell migration in wound-healing may be attributable not only to cellular defects but also to changes in serum factors associated with the senescence process.