Bone loss after ridge expansion with or without reflection of the periosteum.

OBJECTIVE To evaluate the role of the periosteum in preserving the buccal bone after ridge splitting and expansion with simultaneous implant placement. MATERIAL AND METHODS In 12 miniature pigs, the mandibular premolars and first molars were removed together with the interdental bone septa and the buccal bone. Three months later, ridge splitting and expansion of the buccal plate was performed with simultaneous placement of two titanium implants per quadrant. Access by a mucosal flap (MF) was prepared on test sides, while a mucoperiosteal flap (MPF) with complete denudation of the buccal bone was increased on control sides. After healing periods of six and 12 weeks, the animals were sacrificed for histologic and histometric evaluation. RESULTS In the MF group, all 16 implants were osseointegrated, while in the MPF group, four of 16 implants were lost. Noticeable differences of bone levels on the implant surface and of the bone crest (BC) were found between the MF and the MPF group. Buccally after 6 weeks, the median distance between the implant shoulder (IS) and the coronal-most bone on the implant (cBIC) was for the MF group -1.42 ± 0.42 mm and for the MPF group -4.80 ± 2.72 mm (P = 0.15). The median distance between the IS and the buccal BC was -1.24 ± 0.51 mm and -2.78 ± 1.98 mm (P = 0.12) for the MF and MPF group, respectively. After 12 weeks, median IS-cBIC was -2.12 ± 0.84 mm for MF and -7.19 mm for MPF, while IS-BC was -2.08 ± 0.79 mm for MF and -5.96 mm for MPF. After 6 weeks, the median buccal bone thickness for MF and MPF was 0.01 and 0 mm (P < 0.001) at IS, 1.48 ± 0.97 mm and 0 ± 0.77 mm (P = 0.07) at 2 mm apical to IS, and 2.12 ± 1.19 mm and 1.72 ± 01.50 mm (P = 0.86) at 4 mm apical to IS, respectively. After 12 weeks, buccal bone thickness in the MF group was 0 mm at IS, 0.21 mm at 2 mm apical to IS, and 2.56 mm at 4 mm apical to IS, whereas complete loss of buccal bone was measured from IS to 4 mm apical to IS for the MPF group. CONCLUSIONS In this ridge expansion model in miniature pigs, buccal bone volume was significantly better preserved when the periosteum remained attached to the bone.

Alveolar bone regeneration in response to local application of calcitriol in vitamin D deficient rats

AIM Vitamin D deficiency is considered to diminish bone regeneration. Yet, raising the serum levels takes months. A topic application of the active vitamin D metabolite, calcitriol, may be an effective approach. Thus, it becomes important to know the effect of vitamin D deficiency and local application on alveolar bone regeneration. MATERIAL AND METHODS Sixty rats were divided into three groups; two vitamin depletion groups and a control group. Identical single defects (2 mm diameter) were created in the maxilla and mandible treated with calcitriol soaked collagen in one deficiency group while in the other two groups not. Histomorphometric analysis and micro CTs were performed after 1 and 3 weeks. Serum levels of 25(OH)D3 and PTH were determined. RESULTS Bone formation rate significantly increased within the observation period in all groups. Bone regeneration was higher in the maxilla than in the mandible. However, bone regeneration was lower in the control group compared to vitamin depletion groups, with no significant effects by local administration of calcitriol (micro CT mandible p = 0.003, maxilla p < 0.001; histomorphometry maxilla p = 0.035, mandible p = 0.18). CONCLUSION Vitamin D deficiency not necessarily impairs bone regeneration in the rat jaw and a single local calcitriol application does not enhance healing.

Breastfeeding, lung volumes and alveolar size at school-age.

BACKGROUND Previous studies found larger lung volumes at school-age in formerly breastfed children, with some studies suggesting an effect modification by maternal asthma. We wanted to explore this further in children who had undergone extensive lung function testing. The current study aimed to assess whether breastfeeding was associated with larger lung volumes and, if so, whether all compartments were affected. We also assessed association of breastfeeding with apparent diffusion coefficient (ADC), which measures freedom of gas diffusion in alveolar-acinar compartments and is a surrogate of alveolar dimensions. Additionally, we assessed whether these effects were modified by maternal asthma. METHODS We analysed data from 111 children and young adults aged 11-21 years, who had participated in detailed lung function testing, including spirometry, plethysmography and measurement of ADC of (3)Helium ((3)He) by MR. Information on breastfeeding came from questionnaires applied in early childhood (age 1-4 years). We determined the association between breastfeeding and these measurements using linear regression, controlling for potential confounders. RESULTS We did not find significant evidence for an association between duration of breastfeeding and lung volumes or alveolar dimensions in the entire sample. In breastfed children of mothers with asthma, we observed larger lung volumes and larger average alveolar size than in non-breastfed children, but the differences did not reach significance levels. CONCLUSIONS Confirmation of effects of breastfeeding on lung volumes would have important implications for public health. Further investigations with larger sample sizes are warranted.

Clinical presentation, diagnosis, therapy and outcome of alveolar echinococcosis in dogs.

Alveolar echinococcosis (AE), a parasitic disease primarily of the liver caused by the larval stage of Echinococcus multilocularis, is highly endemic in Switzerland. In contrast to well-established management protocols in people, little is known with regard to optimal treatment strategies in dogs. The objective of this study was to describe the clinical signs and diagnostic procedures in dogs with AE and to evaluate outcome following medical treatment alone or surgery and medical treatment. Of 23 putative AE cases between 2004 and 2014, 20 were classified as confirmed (n=18) or probable (n=2) AE, based on abdominal ultrasound, serology, cytology, histology and/or PCR. Most dogs presented with abdominal distension in an advanced stage of disease. Dogs receiving specific treatment (radical or debulking surgery together with medical treatment, or medical treatment alone) survived longer than dogs left untreated, but no difference was found between treatment types. Survival at one year was associated with absence of free abdominal fluid, absence of abdominal distension and treatment of any type. However, dogs treated with debulking surgery all faced relapse. Findings of this study suggest that in AE-affected dogs for which a therapeutic approach is regarded appropriate by owners and veterinarians, radical surgical resection and medical treatment or, if total resection is not possible, medical treatment alone should be considered. However, studies on larger numbers of dogs are necessary before definitive treatment recommendations can be made.

The role of inducible nitric oxide synthase for interstitial remodeling of alveolar septa in surfactant protein D-deficient mice

Surfactant protein D (SP-D) modulates the lung's immune system. Its absence leads to NOS2-independent alveolar lipoproteinosis and NOS2-dependent chronic inflammation, which is critical for early emphysematous remodeling. With aging, SP-D knockout mice develop an additional interstitial fibrotic component. We hypothesize that this age-related interstitial septal wall remodeling is mediated by NOS2. Using invasive pulmonary function testing such as the forced oscillation technique and quasistatic pressure-volume perturbation and design-based stereology, we compared 29-wk-old SP-D knockout (Sftpd(-/-)) mice, SP-D/NOS2 double-knockout (DiNOS) mice, and wild-type mice (WT). Structural changes, including alveolar epithelial surface area, distribution of septal wall thickness, and volumes of septal wall components (alveolar epithelium, interstitial tissue, and endothelium) were quantified. Twenty-nine-week-old Sftpd(-/-) mice had preserved lung mechanics at the organ level, whereas elastance was increased in DiNOS. Airspace enlargement and loss of surface area of alveolar epithelium coexist with increased septal wall thickness in Sftpd(-/-) mice. These changes were reduced in DiNOS, and compared with Sftpd(-/-) mice a decrease in volumes of interstitial tissue and alveolar epithelium was found. To understand the effects of lung pathology on measured lung mechanics, structural data were used to inform a computational model, simulating lung mechanics as a function of airspace derecruitment, septal wall destruction (loss of surface area), and septal wall thickening. In conclusion, NOS2 mediates remodeling of septal walls, resulting in deposition of interstitial tissue in Sftpd(-/-). Forward modeling linking structure and lung mechanics describes the complex mechanical properties by parenchymatous destruction (emphysema), interstitial remodeling (septal wall thickening), and altered recruitability of acinar airspaces.

Correlation between alveolar ventilation and electrical properties of lung parenchyma.

One key problem in modern medical imaging is linking measured data and actual physiological quantities. In this article we derive such a link between the electrical bioimpedance of lung parenchyma, which can be measured by electrical impedance tomography (EIT), and the magnitude of regional ventilation, a key to understanding lung mechanics and developing novel protective ventilation strategies. Two rat-derived three-dimensional alveolar microstructures obtained from synchrotron-based x-ray tomography are each exposed to a constant potential difference for different states of ventilation in a finite element simulation. While the alveolar wall volume remains constant during stretch, the enclosed air volume varies, similar to the lung volume during ventilation. The enclosed air, serving as insulator in the alveolar ensemble, determines the resulting current and accordingly local tissue bioimpedance. From this we can derive a relationship between lung tissue bioimpedance and regional alveolar ventilation. The derived relationship shows a linear dependence between air content and tissue impedance and matches clinical data determined from a ventilated patient at the bedside.

Susceptibility versus resistance in alveolar echinococcosis (larval infection with Echinococcus multilocularis).

Epidemiological studies have demonstrated that the majority of human individuals exposed to infection with Echinococcus spp. eggs exhibit resistance to disease as shown by either seroconversion to parasite--specific antigens, and/or the presence of 'dying out' or 'aborted' metacestodes, not including hereby those individuals who putatively got infected but did not seroconvert and who subsequently allowed no development of the pathogen. For those individuals where infection leads to disease, the developing parasite is partially controlled by host immunity. In infected humans, the type of immune response developed by the host accounts for the subsequent trichotomy concerning the parasite development: (i) seroconversion proving infection, but lack of any hepatic lesion indicating the failure of the parasite to establish and further develop within the liver; or resistance as shown by the presence of fully calcified lesions; (ii) controlled susceptibility as found in the "conventional" alveolar echinococcosis (AE) patients who experience clinical signs and symptoms approximately 5-15 years after infection, and (iii) uncontrolled hyperproliferation of the metacestode due to an impaired immune response (AIDS or other immunodeficiencies). Immunomodulation of host immunity toward anergy seems to be triggered by parasite metabolites. Beside immunomodulating IL-10, TGFβ-driven regulatory T cells have been shown to play a crucial role in the parasite-modulated progressive course of AE. A novel CD4+CD25+ Treg effector molecule FGL2 recently yielded new insight into the tolerance process in Echinococcus multilocularis infection.