Topical use of platelet-rich plasma to influence bone volume in maxillary augmentation: a prospective randomized trial.

BACKGROUND AND OBJECTIVES: The atrophic posterior maxilla often requires restoration of the alveolar ridge due to a lack of bone quantity and quality before dental implant placement. The aim of this study was to verify the hypothesis that platelet-rich plasma (PRP) has an influence on bone density in the maxilla after sinus floor elevation in combination with autologous cancellous bone from the iliac crest. Therefore, a randomized, prospective, controlled trial was set up in two centres. STUDY DESIGN AND METHODS: Fifty-three patients who underwent osteoplastic bone grafting for sinus floor elevation were included. The intervention group was treated with defined concentrations of PRP in addition to transplanted bone. Bone biopsy was performed 4 months after augmentation. Bone volume was then measured using the histomorphometric parameter bone volume. RESULTS: The histomorphometric evaluation of the biopsies did not indicate superiority of any of the treatments in terms of bone volume. CONCLUSION: Topical use of PRP did not improve maxillary bone volume either clinically relevant or statistically significant compared to that in conventionally treated patients. The use of PRP to support bone regeneration cannot be recommended as a standard method for maxillary augmentation.

Deposition and spectral performance of an inhomogeneous broadband wide-angular antireflective coating.

Gradient index coatings and optical filters are a challenge for fabrication. In a round-robin experiment, basically the same hybrid antireflection coating for the visible spectral region, combining homogeneous refractive index layers of pure materials and linear gradient refractive index layers of material mixtures, has been deposited. The experiment involved three different deposition techniques: electron-beam evaporation, ion-beam sputtering, and radio frequency magnetron sputtering. The material combinations used by these techniques were Nb(2)O(5)/SiO(2), TiO(2)/SiO(2), and Ta(2)O(5)/SiO(2), respectively. The spectral performances of samples coated on one side and on both sides have been compared to the corresponding theoretical spectra of the designed profile. Also, the reproducibility of results for each process is verified. Finally, it is shown that ion-beam sputtering gave the best results in terms of deviation from the theoretical performance and reproducibility.

[Insufficiency fractures in rheumatology. Case report and overview]. / Insuffizienzfrakturen in der Rheumatologie. Fallbeschreibung und Ubersicht.

Stress fractures occur as insufficiency fractures, with a prevalence of 0.8% in patients with rheumatological illness. The main sites of insufficiency fractures are the pelvis and sacrum, parts of the tibia and fibula that are close to the joints, and the calcaneus and hip. Since the painful symptoms overlap with the clinical picture of the painful joint diseases and because of the low sensitivity of conventional diagnostic X-ray, insufficiency fractures are not diagnosed directly or their diagnosis is delayed. The high sensitivity of computer tomography, skeletal scintigraphy and nuclear magnetic resonance imaging should be exploited in the diagnosis of insufficiency fractures. The case report presented describes insufficiency fractures of the distal right tibia and fibula in an elderly female patient with rheumatoid arthritis being treated with long-term glucocorticoids. In addition to advanced age, female gender, immobility and rheumatoid arthritis requiring long-term cortisone, there are further risk factors for insufficiency fractures: fluoride treatment over many years in the past, hypovitaminosis D3, renal failure. The DXA bone density values of the neck of the femur and the lumbar vertebrae do not show any osteoporosis, and the calcium concentration in the serum is low; phosphate is raised and parathormone is normal; osteocalcin, beta crosslaps and alkaline phosphatase are raised. Bone biopsy specimens taken from the iliac crest and the proximal femur and investigated for the purpose of differential diagnosis revealed renal osteopathy with secondary hyperparathyroidism and osteomalacia. In elderly patients with kidney failure, the possibility of renal osteopathy must be considered as the possible cause of reduced bone quality with a raised risk of insufficiency fractures, even when the parathormone levels are normal. In view of the frequency of osteopathies in rheumatological patients, osteology is of enormous significance in rheumatology.

[Genetics of osteoporosis]. / Genetik der Osteoporose.

Osteoporosis is a disease affecting mainly women but also an increasing number of men. The destruction of the bone microarchitecture and the reduction of bone mass lead to increased fragility and pathologic bone fractures. Family studies and twin studies have shown that peak bone mass, mechanical strength, and physiological bone turnover are subject to genetic control. Vitamin D receptor polymorphisms were one of the first genetic factors suggested to influence bone phenotype, although their impact on bone metabolism was initially overestimated. Meanwhile, polymorphisms in numerous other genes such as collagen I alpha 1, estrogen receptor, transforming growth factor beta (TGF-beta), interleukin-1, interleukin-6, calcitonin, parathyroid hormone, and apolipoprotein E have been found to be associated with bone mineral density. In the interpretation of genetic findings, genetic differences between different ethnic groups, environmental factors such as calcium intake, vitamin D status, hormonal status, body size, and total body bone mineral density have to be considered. Understanding the molecular physiology of the genes described in this article and all genes influencing bone metabolism identified in the future will enable us to identify persons at risk for osteoporosis and to develop more specific therapies.

Sex steroids, biochemical markers, bone mineral density and histomorphometry in male osteoporosis patients.

The present study investigates the role of sex steroids, especially serum estradiol and serum testosterone in male osteoporosis patients and their association to established markers of bone turnover as also to BMD results and histomorphometric findings. Included were patients with secondary osteoporosis due to steroid medication, anticonvulsive medication and alcohol consumption, and heavy smoking patients. 100 males aged from 30 to 78 years were investigated for osteodensitometry (DEXA) and assessment of biochemical bone turnover markers (venous blood samples, 24 hour urine samples). In 40 of these patients bone biopsies were taken for histomorphometry. Laboratory investigations were made for serum Ca, P, parathyroid hormone (PTH), osteocalcin (OC), carboxyterminal extension peptide of type I procollagen (PICP), bone specific alkaline phosphatase (B-ALP), 25OH-vit.D, testosterone, estradiol, gonadotropines, and deoxypyridinoline and hydroxyproline from 24-hour urinary collection. Regions of interest for osteodensitometry with DEXA technique were the lumbar spine L1-L4 and the femoral neck (Ward's triangle). All of the patients examined had low bone mineral density (BMD) values compared to age- and sex-matched controls. Results from descriptive statistics showed hypogonadism in 26.4%, 25 OH-vitamin D deficiency in 26.2% and high serum estradiol in 59.1% of patients, compared to age- and sex-matched controls. 8.5% had elevated PTH levels. Multivariate analysis of data showed no significant correlation between BMD and semiquantitative histomorphometric findings (scaled from 1-5), neither a significant correlation between serum testosterone/estradiol and BMD. A significant correlation was observed between testosterone and estradiol values (r = 0.389, p = 0.008), and between OC and BMD results at ward's triangle (p = 0.008). In steroid treated patients (n = 12) significant differences were found for PTH (P < 0.01), 25 OH-Vit.D (p < 0.05) and urinary deoxypyridinoline (p < 0.05) as compared with the other patient group (n = 88). In summary we found high serum estradiol in 59.1% of our patients collective with low BMD, there was no correlation between BMD and histomorphometric findings. We observe a significant positive correlation between testosterone and estradiol values, but we did not find any association to bone turnover markers or BMD results.

Multiple endocrine neoplasia (MEN)--an overview and case report--patient with sporadic bilateral pheochromocytoma, hyperparathyroidism and marfanoid habitus.

The multiple endocrine neoplasia syndromes are divided into two categories: MEN type I and MEN type II. The MEN type II syndrome is further divided into MEN IIa and MEN IIb. The syndromes are characterized by benign and malignant changes in two or more endocrine organs, as well as incidental changes in nervous, muscular and connective tissue. Two main forms can be distinguished: the MEN-I syndrome with hyperplasia of the parathyroid gland, accompanied by islet cell tumor and pituitary adenoma; the MEN-II syndrome with medullary thyroid carcinoma in combination with bilateral pheochromocytoma and hyperplasia of the parathyroid gland (MEN IIa), while type IIb is characterized by the additional appearance of neurocutaneous manifestations without primary hyperparathyroidism. Characteristics shared by these syndromes include the involved cell type, most of the tumors are composed of one or more specific polypeptide- and biogenic amine-producing cell types (APUD--amine precursor uptake and decarboxylation). The second characteristic is the increased incidence in certain families. The hereditary component is autosomal dominant with variable expression but high penetrance. Mechanisms of tumorigenesis differ in these syndromes. While MEN I is caused by an inherited mutation of a tumor suppressor gene, menin, located on the long arm of chromosome 11, MEN II is caused by activation of the RET proto-oncogene. We have reported the case of a young man exhibiting bilateral pheochromocytoma. In addition, the patient showed mild primary hyperparathyroidism and marfanoid habitus, all these stigmata usually being part of the MEN-II syndrome. Although this described patient showed a phenotypic mixture of the MEN-IIa and MEN-IIb syndrome, the genetic analysis for MEN II and von-Hippel-Lindau gene did not reveal any pathologic mutations, the endocrine disorders described here are not related to multiple endocrine neoplasia syndromes.

MEN1 gene mutation analysis of sporadic adrenocortical lesions.

To clarify the role of the MEN1 gene in the tumorigenesis of sporadic adrenocortical tumors, we performed a molecular study on 35 adrenocortical lesions including 6 hyperplasias, 19 adenomas and 10 carcinomas. Loss of heterozygosity (LOH) of the MEN1 gene was assessed by PCR using an intragenic (D11S4946) and 2 flanking microsatellite markers (D11S4936, PYGM) and/or fluorescence in situ hybridization (FISH) with a 40-kb cosmid probe containing the MEN1 gene. The complete coding sequence of the MEN1 gene was screened for mutations using non-radioactive, PCR-based single-strand conformation polymorphism (SSCP) analysis and MDE heteroduplex gel electrophoresis. PCR-LOH and FISH analyses performed in 29 tumors (PCR-LOH in 4, FISH in 17 and both in 8 tumors) revealed allelic deletion of the MEN1 locus in 8 (27.5%) and at 11q13 in 9 (31%) tumors. Furthermore, the frequency of LOH at 11q13 was significantly higher in adrenocortical carcinomas (60%) than in benign lesions (11%). Mutation analysis of tumor samples revealed 9 polymorphisms in 7 tumors (S145S, R171Q, R171Q together with L432L) but no mutations, with the exception of one adrenocortical adenoma. The latter tumor contained a somatic E109X stop codon mutation in exon 2 and a 5178-9G-->A splice mutation in intron 4, which was also detectable in various nontumorous tissues and blood indicative of a germ-line mutation. The patient, who had no clinical signs or family history of MEN1, later also developed a neuroendocrine carcinoma (atypical carcinoid) of the lung. Our findings indicate that inactivating mutations of the MEN1 tumor-suppressor gene appear not to play a prominent role in the development of sporadic hyperplastic or neoplastic lesions of the adrenal cortex and that the newly reported 5178-9G-->A splice mutation in intron 4 might cause a variant of the MEN1 phenotype.

Mutations and allelic deletions of the MEN1 gene are associated with a subset of sporadic endocrine pancreatic and neuroendocrine tumors and not restricted to foregut neoplasms.

Endocrine pancreatic tumors (EPT) and neuroendocrine tumors (NET) occur sporadically and rarely in association with multiple endocrine neoplasia type 1 (MEN1). We analyzed the frequency of allelic deletions and mutations of the recently identified MEN1 gene in 53 sporadic tumors including 30 EPT and 23 NET (carcinoids) of different locations and types. Allelic deletion of the MEN1 locus was identified in 18/49 (36.7%) tumors (13/30, 43.3% in EPT and 5/19, 26.3% in NET) and mutations of the MEN1 gene were present in 8/52 (15.3%) tumors (4/30 (13.3%) EPT and 4/22 (18.1%) NET). The somatic mutations were clustered in the 5' region of the coding sequence and most frequently encompassed missense mutations. All tumors with mutations exhibited a loss of the other allele and a wild-type sequence of the MEN1 gene in nontumorous DNA. In one additional patient with a NET of the lung and no clinical signs or history of MEN1, a 5178-9G-->A splice donor site mutation in intron 4 was identified in both the tumor and blood DNA, indicating the presence of a thus far unknown MEN1 syndrome. In most tumor groups the frequency of allelic deletions at 11q13 was 2 to 3 times higher than the frequency of identified MEN1 gene mutations. Some tumor types, including rare forms of EPT and NET of the duodenum and small intestine, exhibited mutations more frequently than other types. Furthermore, somatic mutations were not restricted to foregut tumors but were also detectable in a midgut tumor (15.2% versus 16.6%). Our data indicate that somatic MEN1 gene mutations contribute to a subset of sporadic EPT and NET, including midgut tumors. Because the frequency of mutations varies significantly among the investigated tumor subgroups and allelic deletions are 2 to 3 times more frequently observed, factors other than MEN1 gene inactivation, including other tumor-suppressor genes on 11q13, may also be involved in the tumorigenesis of these neoplasms.