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PubMed2005

Accuracy of quantitative magnetic resonance imaging in the detection of ex vivo focal cartilage defects.

BACKGROUND: No established, non-invasive diagnostic procedure for quantifying focal cartilage defects is currently available. OBJECTIVE: To test the accuracy of quantitative magnetic resonance imaging (qMRI) for reliable determination of cartilage defect size in various compartments of the human knee. METHODS: 24 tibial and patellar cartilage plates were harvested during knee arthroplasty. 74 cylindrical defects with diameters of 3, 5, and 8 mm were created with a punch. In 15 specimens (51 defects), the cartilage cylinders (inside the punch) were removed (approach 1), while in 9 specimens (23 defects) the surrounding tissue was removed mechanically and the cartilage cylinder was left in place (approach 2). All plates were imaged with a T(1) weighted water excitation gradient echo sequence at a resolution of 1.5 mm x 0.31 mm x 0.31 mm. The defect size was computed from the image data after interactive segmentation and compared with the known dimensions of the cylinders. RESULTS: Although there was a significant overestimation of the defect size by qMRI in 3 mm defects (mean (SD) +1.3 (0.58) mm = +/-42%; p<0.001), the overestimation was only +1.0 (0.57) mm (+/-21%; p<0.05) in 5 mm defects and +0.1 (0.39) mm (+/-4%; p = 0.31) in 8 mm defects (approach 1). Values were similar for approaches 1 and 2 and for patellar and tibial cartilage plates. CONCLUSIONS: These findings show that qMRI allows accurate quantification of focal cartilage defects. It may therefore represent a valuable tool in the diagnosis of traumatic cartilage lesions, osteochondrosis dissecans, and osteochondral fractures, and in monitoring their responsiveness to surgical or other treatments.

Cartilage, Articular↗
PubMed2002

A mathematical model of rat collecting duct. III. Paradigms for distal acidification defects.

The present clinical taxonomy of distal renal tubular acidoses includes "gradient," "secretory," and "voltage" defects. These categories refer to presumed collecting duct defects in which the epithelium may be abnormally permeable and unable to sustain an ion gradient, in which luminal proton ATPases are defective, or in which electrogenic Na+ reabsorption is impaired and luminal electronegativity is reduced. Classification of affected individuals is based on urinary pH and ion concentrations during spontaneous acidosis and during SO(4)(2-) infusion, as well as urinary PCO2 during HCO(3)(-) loading. A model of rat CD has been developed that has been used to examine determinants of urinary acidification (Weinstein AM. Am J Physiol Renal Physiol 283: F1252-F1266, 2002) and the interplay of HCO(3)(-) and PO(4)(3-) loads to generate a disequlibrium pH and equilibrium PCO2. In this paper, pure forms of gradient, voltage, and secretory defects are simulated, with attention to variability in the locus of the defect in the cortical (CCD), outer medullary (OMCD), or inner medullary collecting duct (IMCD). The objective of these calculations is to discover whether the intuitive description of these defects is sustained quantitatively. The most important positive finding is that the locus of the transport defect along the CD plays a critical role in the apparent severity of the lesion, with more proximal defects being less severe and more easily correctable. In particular, model calculations suggest that for gradient or secretory defects to be clinically detectable they need to involve the OMCD and/or IMCD. Additionally, the calculations reveal a possible mechanism for CD K+ wasting, which does not involve failure of H+ - K+-ATPase but derives from a paracellular anion leak and thereby a more electronegative lumen. The most important negative finding is the lack of support for the category of renal tubular acidosis associated with a voltage defect. Although CD lesions that present with both K+ and H+ secretory defects suggest mediation by transepithelial electrical potential difference (PD), both PD changes and proton pump PD sensitivity appear too small to account for the observed abnormalities.

Acids↗
PubMed1990

Characterization of rat calvarial nonunion defects.

This study examined the healing of nonunions by describing the histology and ultrastructural appearance of craniotomy defects as a model. Bone defects (3, 4 and 8 mm) were created in the calvaria of adult rats. Central and peripheral specimens of 8-mm defects were retrieved at 1, 3, 7, 10, 14, 21, 28 and 42 days and examined using both light and transmission electron microscopy. Specimens from the 3- and 4-mm defects were retrieved at 28 days and examined using light microscopy. In all sizes of defects, bony repair was consistently localized to the dural side of the defect. The 3- and 4 mm defects demonstrated the greatest degree of osseous bridging and evidence of normal osseous repair throughout the defect. The 8-mm defects repaired in general with the formation of nonunions which contained a small amount of bone at the periphery and fibrous connective tissue. Bone formation was evident at 10 days in the peripheral regions of the 8-mm defects and exhibited bony peninsulas with normal primary calcification fronts. Matrix vesicles containing hydroxyapatite-like crystals were present. In contrast, the central regions of the 8-mm defects were characterized by several islands of cartilage-like cells which stained metachromatically with toluidine blue. Transmission electron microscopy of this region at 14 days demonstrated a dense, collagenous extracellular matrix with matrix vesicles infiltrating the collagen bundles. There was no evidence of crystal formation in the matrix vesicles nor of calcification in the collagenous matrix. At 21 days, both the central and peripheral regions of the 8-mm calvarial nonunions were characterized by dense fibrous connective tissue repair and inactive fibroblasts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Feasibility of identifying families for genetic studies of birth defects using the National Health Interview Survey.

BACKGROUND: The purpose of this study was to determine whether the National Health Interview Survey is a useful source to identify informative families for genetic studies of birth defects. METHODS: The 1994/1995 National Health Interview Survey (NHIS) was used to identify households where individuals with two or more birth defects reside. Four groups of households were identified: 1) single non-familial (one individual with one birth defect); 2) single familial (more than one individual with one birth defect); 3) multiple non-familial (one individual with more than one birth defect), and 4) multiple familial (more than one individual with more than one birth defect). The March 2000 U.S. Census on households was used to estimate the total number of households in which there are individuals with birth defects. RESULTS: Of a total of 28,094 households and surveyed about birth defects and impairments, 1,083 single non-familial, 55 multiple non-familial, 54 single familial, and 8 multiple familial households were identified. Based on the 2000 U.S. census, it is estimated that there are 4,472,385 households where at least one person has one birth defect in the United States and in 234,846 of them there are at least two affected individuals. Western states had the highest prevalence rates. CONCLUSIONS: Population-based methods, such as the NHIS, are modestly useful to identify the number and the regions where candidate families for genetic studies of birth defects reside. Clinic based studies and birth defects surveillance systems that collect family history offer better probability of ascertainment.

Age Distribution↗
PubMed2002

Birth defects, season of conception, and sex of children born to pesticide applicators living in the Red River Valley of Minnesota, USA.

We previously demonstrated that the frequency of birth defects among children of residents of the Red River Valley (RRV), Minnesota, USA, was significantly higher than in other major agricultural regions of the state during the years 1989-1991, with children born to male pesticide applicators having the highest risk. The present, smaller cross-sectional study of 695 families and 1,532 children, conducted during 1997-1998, provides a more detailed examination of reproductive health outcomes in farm families ascertained from parent-reported birth defects. In the present study, in the first year of life, the birth defect rate was 31.3 births per 1,000, with 83% of the total reported birth defects confirmed by medical records. Inclusion of children identified with birth or developmental disorders within the first 3 years of life and later led to a rate of 47.0 per 1,000 (72 children from 1,532 live births). Conceptions in spring resulted in significantly more children with birth defects than found in any other season (7.6 vs. 3.7%). Twelve families had more than one child with a birth defect (n = 28 children). Forty-two percent of the children from families with recurrent birth defects were conceived in spring, a significantly higher rate than that for any other season. Three families in the kinships defined contributed a first-degree relative other than a sibling with the same or similar birth defect, consistent with a Mendelian inheritance pattern. The remaining nine families did not follow a Mendelian inheritance pattern. The sex ratio of children with birth defects born to applicator families shows a male predominance (1.75 to 1) across specific pesticide class use and exposure categories exclusive of fungicides. In the fungicide exposure category, normal female births significantly exceed male births (1.25 to 1). Similarly, the proportion of male to female children with birth defects is significantly lower (0.57 to 1; p = 0.02). Adverse neurologic and neurobehavioral developmental effects clustered among the children born to applicators of the fumigant phosphine (odds ratio [OR] = 2.48; confidence interval [CI], 1.2-5.1). Use of the herbicide glyphosate yielded an OR of 3.6 (CI, 1.3-9.6) in the neurobehavioral category. Finally, these studies point out that (a) herbicides applied in the spring may be a factor in the birth defects observed and (b) fungicides can be a significant factor in the determination of sex of the children of the families of the RRV. Thus, two distinct classes of pesticides seem to have adverse effects on different reproductive outcomes. Biologically based confirmatory studies are needed.

Adult↗
PubMed2004

In vitro differentiation of CD14 cells from osteopetrotic subjects: contrasting phenotypes with TCIRG1, CLCN7, and attachment defects.

UNLABELLED: We studied osteoclastic differentiation from normal and osteopetrotic human CD14 cells in vitro. Defects in acid transport, organic matrix removal, and cell fusion with deficient attachment were found. Analysis of genotypes showed that TCIRG1 anomalies correlated with acid transport defects, but surprisingly, organic matrix removal failure correlated with CLCN7 defects; an attachment defect had normal TCIRG1 and CLCN7. INTRODUCTION: Osteopetrotic subjects usually have normal macrophage activity, and despite identification of genetic defects associated with osteopetrosis, the specific developmental and biochemical defects in most cases are unclear. Indeed, patients with identical genotypes often have different clinical courses. We classified defects in osteoclast differentiation in vitro using four osteopetrotic subjects without immune or platelet defects, three of them severe infantile cases, compared with normals. MATERIALS AND METHODS: Osteoclast differentiation used isolated CD14 cells; results were correlated with independent analysis of two key genes, CLCN7 and TCIRG1. CD14 cell attachment and cell surface markers and extent of differentiation in RANKL and colony-stimulating factor (CSF)-1 were studied using acid secretion, bone pitting, enzyme, and attachment proteins assays. RESULTS AND CONCLUSIONS: CD14 cells from all subjects had similar lysosomal and nonspecific esterase activity. With the exception of cells from one osteopetrotic subject, CD14 cells from osteopetrotic and control monocytes attached similarly to bone or tissue culture substrate. Cells from one osteopetrotic subject, with normal CLCN7 and TCIRG1, did not attach to bone, did not multinucleate, and formed no podosomes or actin rings in RANKL and CSF-1. Attachment defects are described in osteopetrosis, most commonly mild osteopetrosis with Glantzman's thrombasthenia. However, this case, with abnormal integrin alphavbeta3 aggregates and no osteoclasts, seems to be unique. Two subjects were compound heterozygotes for TCIRG1 defects; both had CD14 cells that attached to bone but did not acidify attachments; cell fusion and attachment occurred, however, in RANKL and CSF-1. This is consistent with TCIRG1, essential for H+-ATPase assembly at the ruffled border. A compound heterozygote for CLCN7 defects had CD14 cells that fused in vitro, attached to bone, and secreted acid, TRACP, and cathepsin K. However, lacunae were shallow and retained demineralized matrix. This suggests that CLCN7 may not limit H+-ATPase activity as hypothesized, but may be involved in control of organic matrix degradation or removal.

Acid Phosphatase↗
PubMed2006

Hospitalizations of newborns with folate-sensitive birth defects before and after fortification of foods with folic acid.

CONTEXT: The prevalence of neural tube defects is reduced in populations of women who receive folic acid supplementation. Since 1998, grain products in the United States have been fortified with folic acid. Fortification may have additional benefits by reducing the national prevalence of newborn hospitalizations for other folate-sensitive birth defects. OBJECTIVE: Our purpose with this work was to compare rates of hospitalizations of newborns with folate-sensitive birth defects before and after implementation of fortification of grains. METHOD: National hospital discharge data from the Healthcare Cost and Utilization Project were used to compute rates of newborn hospitalizations for selected birth defects per 10,000 live births in the United States. Newborn hospitalization rates involving congenital anomalies recognizable at birth were analyzed for 5 years before fortification of grains and 5 years after fortification. Additional analyses compared changes in newborn hospitalization rates for birth defects by race/ethnicity, income, insurance status, and region of the country. RESULTS: Newborn hospitalization rates for spina bifida decreased 21% from 1993-1997 to 1998-2002. Newborn hospitalization rates also decreased for anencephaly (20%) and limb-reduction defects (4%). Decline in hospitalizations for spina bifida occurred more often among Hispanic newborns (33%) than among white (13%) or black (21%) newborns. Decline in limb-reduction defects was seen primarily among blacks (11%). Findings using hospitalization data were similar to recent reports using birth defect surveillance systems with the exception of findings for orofacial clefts and conotruncal heart defects. No reductions were noted in newborn hospitalizations for these anomalies. CONCLUSIONS: Results from this ecological study fail to demonstrate substantial declines in newborn hospitalizations beyond those anticipated from a reduction in neural tube defects. The society-wide impact of the fortification program on birth defects and other health conditions should continue to be monitored.

Congenital Abnormalities↗
PubMed1990

The apical location of calculus within the intrabony defect.

Although several studies have concluded that calculus removal becomes more difficult as pocket depth increases, few have examined the clinical location of calculus within the intrabony defect. This study evaluated the relationship between apical calculus position and the depth and morphology of the intrabony defect. As part of an on-going study of new attachment procedures in humans, 260 intrabony defects were surgically entered in 39 patients. Using magnifying loops and fiber optics in all defects, the most apical level of calculus was grooved to serve as both a clinical and histologic reference point. Clinical measurements made prior to root debridement included the alveolar crest to base of calculus, and the base of calculus to base of defect. The type of defect was classified by the number of remaining osseous walls. Calculus has not been found apical to the groove in any histologic section. The mean distance measured clinically between the base of the calculus and the base of the defect was found to increase with the depth of the defect. This relationship did not vary with either tooth type or number of remaining osseous walls in the defect. Data analysis of this group of patients (N = 39) showed a positive correlation (r = .83) between increasing depth of intrabony defect and the distance of the most apical calculus from the defect base.

Alveolar Process↗
PubMed1997

Guided tissue regeneration therapy of 203 consecutively treated intrabony defects using a bioabsorbable matrix barrier. Clinical and radiographic findings.

THE AIM OF THIS RETROSPECTIVE three-center study was to evaluate guided tissue regeneration (GTR) therapy in a clinical periodontal setting. The material consisted of 203 consecutively treated intrabony defects > or = 4 mm in 143 patients using a bioabsorbable matrix barrier. Each center followed the same protocol for presurgical, intrasurgical, and follow up examinations. Initial therapy, surgical, and follow-up treatments followed the routine of each center. Treatment was evaluated after 1 year by clinical assessments for probing depth (PD) reduction and clinical attachment level (CAL) gain and by bone fill from computer digitized radiographs. Initial intrabony defect depth averaged 6.3 +/- 1.0 mm clinically and 5.7 +/- 1.8 mm radiographically. Mean PD was reduced from 9.0 +/- 1.0 mm to 3.3 +/- 1.0 mm. Mean CAL gain amounted to 4.8 +/- 1.5 mm corresponding to 79 +/- 13% of the initial intrabony defect depth; 78% of the defects exhibited CAL gain > or = 4 mm. Bone fill averaged 3.2 +2- 1.8 mm. Together with a crestal resorption of 1.1 +/- 1.4 mm this resulted in a defect resolution of 4.3 +/- 1.9 mm or 72%. Forty-seven percent (47%) of the variability in CAL gain could be explained by defect depth, defect width, early barrier exposure, and presence of plaque in the treated area. CAL gain and bone fill were positively correlated to the intrabony defect depth; i.e., the deeper the defect the more the CAL gain and bone fill. Sites with barrier exposure during the first 2 weeks of healing showed significantly less CAL gain than sites at which exposure occurred at a later stage or not at all. Presence of plaque in the treated area had a significant negative impact on both CAL gain and bone fill. It was concluded that GTR-treatment of intrabony defects > or = 4 mm in a periodontal specialist practice will result in clinical attachment level gain and bone fill comparable to what has been demonstrated in case studies and controlled clinical trials. The predictability to obtain CAL gain > or = 4 mm in defects > or = 4 mm was 78%.

Alveolar Bone Loss↗
PubMed2000

Multi-center clinical comparison of combination anorganic bovine-derived hydroxyapatite matrix (ABM)/cell binding peptide (P-15) and ABM in human periodontal osseous defects. 6-month results.

BACKGROUND: Intraosseous periodontal defects present a particular treatment problem. New bone replacement grafts offer promise for improved results. METHODS: The role of a synthetic cell-binding peptide (P-15), combined with anorganic [corrected] bovine-derived hydroxyapatite bone matrix (ABM), was compared to ABM alone in human periodontal osseous defects in a controlled, monitored, multi-center trial. Following appropriate initial preparation procedures, flap surgery with defect and root debridement was performed. Two osseous defects per patient were treated randomly with each procedure after surgical preparation. Appropriate periodontal maintenance schedules were followed, and at 6 to 7 months, re-entry flap surgery was performed for documentation and finalization of treatment. RESULTS: T test and Mann-Whitney U analyses of patient mean values from 33 patients revealed that the combination ABM/P-15 grafts demonstrated significantly better mean defect fill of 2.9 +/- 1.2 mm (72.9%) versus a mean defect fill of 2.2 +/- 1.4 mm (50.67%) for defects treated with ABM (P<0.05). Other hard tissue findings showed similar clinically superior results with the use of ABM/P-15. Relative defect fill results showed 81% positive (50% to 100% defect fill) responses with ABM/P-15 and 67% positive responses with ABM. There were 3.5 times as many optimal results (> or = 90% defect fill) with ABM/P-15 and twice as many failures (minimal response) with ABM. Soft tissue findings showed no significant differences between treatments. CONCLUSIONS: These results suggest that the use of the P-15 synthetic cell-binding peptide combined with ABM yields better clinical results than the ABM alone in intrabony periodontal defects.

Adult↗
PubMed2000

Treatment of intraosseous defects with bioabsorbable barriers alone or in combination with decalcified freeze-dried bone allograft: a randomized clinical trial.

BACKGROUND: This study clinically compares the outcomes obtained from the use of a bioabsorbable barrier device in combination with demineralized freeze-dried bone allograft (DFDBA) to the results obtained from the barrier device used alone in the treatment of human intraosseous defects. METHODS: The study consisted of 30 patients with one intraosseous periodontal defect each. The trial included defects with loss of attachment of > or = 6 mm, with a radiographically detectable defect of at least 4 mm and with at least 2 remaining osseous walls. After the hygienic phase, at baseline, probing depth (PD), clinical attachment level (CAL), and recession (REC) were measured. During open flap debridement, the defects were randomly assigned to receive either a polylactic acid (PLA) barrier in combination with DFDBA (test) or a PLA barrier alone (control). Additionally, baseline osseous intrasurgical measurements of the periodontal defect were obtained to evaluate the amount of bone regeneration. PD, CAL, and REC were remeasured at 6 and 12 months postsurgery and osseous measurements repeated at 12 months during a re-entry procedure. RESULTS: Two-sample t-test comparisons of mean PD, CAL, and REC measurements (mm) between test (PLA+DFDBA) and control (PLA alone) groups at baseline, PLA+DFDBA: PD = 7.3, CAL = 8.1, REC = -0.7; PLA-alone: PD = 7.9, CAL = 8.4, REC = -0.5, were not statistically different (P>0.05). The following mean changes (delta) at 6 months for the test and the control groups were: decreased PD = 3.6 and 4.0 mm; gain CAL = 2.7 and 3.1 mm; and increased REC = -0.8 and -0.8 mm, respectively. At 12 months the changes for the test and control groups were: decreased PD = 3.3 and 4.1 mm; gain CAL = 2.3 and 3.2 mm; and increased REC = -0.8 and -1.0 mm, respectively. Two-sample t-test comparisons between PD, CAL, and REC changes yielded no significant differences between treatments (P > 0.05), except for the change in CAL at 12 months in favor of the control group, P = 0.008. Comparisons of osseous measurements resulted in no significant differences between groups at baseline and at 12 months (P > 0.05). The intrabony defect filled on the average 3.72 mm for the test and 4.85 mm for the control group. The experimental defects showed a 4.73 mm defect depth reduction, while the control defects reduced 5.35 mm. Re-entry measurements of osseous crest resorption were 1.1 mm for the test and 0.61 mm for the control. CONCLUSIONS: In the intraosseous defects treated in this study, the addition of DFDBA to the GTR procedure did not significantly enhance the clinical results obtained with the GTR procedure alone.

Absorbable Implants↗
PubMed2003

Repair of articular cartilage defects with osteogenic protein-1 (BMP-7) in dogs.

BACKGROUND: Articular cartilage injury has a poor prognosis for repair. Mesenchymal cells, when exposed to osteogenic proteins and other cytokines, can differentiate into cells that behave phenotypically as chondrocytes. In this study, we examined the ability of recombinant human osteogenic protein-1 (rhOP-1 or rhBMP-7) to elicit the repair of osteochondral defects in dogs. METHODS: Bilateral osteochondral defects that were 5 mm in diameter by 6 mm deep were surgically created in the medial femoral condyles of sixty-five adult dogs. rhOP-1-treated (100 mg of a 3.5-mg rhOP-1/g bovine bone-derived Type-I collagen device) and control defects (untreated or treated with 100 mg bovine bone-derived collagen implants) were evaluated grossly and histologically at six, twelve, sixteen, twenty-six, and fifty-two weeks postoperatively. The influence of protected initial weight-bearing and surgical placement of periosteal flaps was also evaluated. RESULTS: Gross and histologic grading of the defect repair indicated improvement in the rhOP-1-treated defects compared with that in the controls. Grossly, the repair tissue in the rhOP-1-treated defects was continuous with the adjacent intact cartilage and appeared translucent. By comparison, the repair tissue in the control defects was discontinuous and opaque or inhomogeneous in nature. Histologically, maturing cartilage similar in appearance to the intact articular cartilage was present in the rhOP-1-treated defects. Cartilage at the defect interface was minimally degraded. The control defects were filled primarily with fibrous tissue and fibrocartilage. Significant differences based upon treatment type were observed at twelve weeks, sixteen weeks, and for all time-periods combined (p = 0.0385, p = 0.0070, and p = 0.0026, respectively). CONCLUSION: rhOP-1 (rhBMP-7) induced hyaline cartilage-like repair of full-thickness osteochondral defects in a dog model. Differences in cartilage repair were maintained at fifty-two weeks postoperatively with no significant degradation of the rhOP-1-induced repair tissue.

Animals↗
PubMed2003

Allogeneic mesenchymal stem cells regenerate bone in a critical-sized canine segmental defect.

BACKGROUND: Mesenchymal stem cells from adult bone marrow are multipotent cells capable of forming bone, cartilage, and other connective tissues. In a previous study, we demonstrated that autologous mesenchymal stem cells could repair a critical-sized bone defect in the dog. The objective of this study was to determine whether the use of allogeneic mesenchymal stem cells could heal a critical-sized bone defect in the femoral diaphysis in dogs without the use of immunosuppressive therapy. METHODS: A critical-sized segmental bone defect, 21 mm in length, was created in the mid-portion of the femoral diaphysis of twelve adult dogs that weighed between 22 and 25 kg. Each defect was treated with allogeneic mesenchymal stem cells loaded onto a hollow ceramic cylinder consisting of hydroxyapatite-tricalcium phosphate. A complete mismatch between donor stem cells and recipient dogs was identified by dog leukocyte antigen typing prior to implantation. The healing response was evaluated histologically and radiographically at four, eight, and sixteen weeks after implantation. The radiographic and histological results at sixteen weeks were compared with the historical data for the control defects, which included defects that had been treated with a cylinder loaded with autologous mesenchymal stem cells, defects treated with a cylinder without mesenchymal stem cells, and defects that had been left untreated (empty). The systemic immune response was evaluated by the analysis of recipient serum for production of antibodies against allogeneic cells. RESULTS: For defects treated with allogeneic mesenchymal stem cell implants, no adverse host response could be detected at any time-point. Histologically, no lymphocytic infiltration occurred and no antibodies against allogeneic cells were detected. Histologically, by eight weeks, a callus spanned the length of the defect, and lamellar bone filled the pores of the implant at the host bone-implant interface. Fluorescently labeled allogeneic cells were also detected. At sixteen weeks, new bone had formed throughout the implant. These results were consistent with those seen in implants loaded with autologous cells. Implants loaded with allogeneic or autologous stem cells had significantly greater amounts of bone within the available pore space than did cell-free implants at sixteen weeks (p < 0.05). CONCLUSIONS: The results of this study demonstrated that allogeneic mesenchymal stem cells loaded on hydroxyapatite-tricalcium phosphate implants enhanced the repair of a critical-sized segmental defect in the canine femur without the use of immunosuppressive therapy. No adverse immune response was detected in this model.

Animals↗
PubMed2006

Recombinant human osteogenic protein-1 induces bone formation in a chronically infected, internally stabilized segmental defect in the rat femur.

BACKGROUND: Recombinant human osteogenic protein-1 (rhOP-1), combined with a collagen carrier, has been shown to induce new-bone formation in a variety of animal models. The purpose of the present investigation was to test the hypotheses that rhOP-1 would accelerate bone formation in an internally stabilized, chronically infected, critical-size defect in the rat femur and that this effect would be enhanced by the administration of systemic antibiotic. METHODS: A 6-mm segmental defect was created surgically, stabilized with a polyacetyl plate and six Kirschner wires, and contaminated with 10(4) colony-forming units of Staphylococcus aureus in one femur in each of 168 Sprague-Dawley rats. After two weeks, these infected defects were débrided surgically and were assigned to one of six treatment groups. The defects in the thirty animals in the first group received lyophilized collagen carrier mixed with 200 microg of rhOP-1 dissolved in buffer, the defects in the thirty animals in the second group received carrier with 20 microg of rhOP-1 in buffer, and the defects in the twenty-four control animals in the third group received carrier mixed with buffer without rhOP-1. The last three groups were treated identically to the first three groups, except that the animals also received the antibiotic ceftriaxone for twenty-eight days after débridement. The animals were killed at two, four, eight, or twelve weeks after débridement. Newly mineralized callus within the defect, and adjacent to and bridging the outside of the defect, was assessed with use of quantitative high-resolution radiography, microcomputed tomography, torsional failure testing, and histological analysis of undecalcified sections. RESULTS: Bacterial cultures confirmed the presence of a chronic infection during the study period in all animals. At the later time-points, significantly more newly mineralized callus was present within and adjacent to the débrided defects that had been treated with 200 microg of rhOP-1, whereas minimal amounts of callus were present within and adjacent to the defects that had been treated without rhOP-1 and with 20 microg of rhOP-1. At eight and twelve weeks after débridement, there was significantly more newly mineralized callus in the group that had been treated with 200 microg of rhOP-1 with antibiotic than in the group that had been treated with 200 microg of rhOP-1 without antibiotic (p < 0.05). At twelve weeks, the values for torque, energy to failure, and linear stiffness for femora that had been treated with 200 microg of rhOP-1 with antibiotic were not significantly different from the values for intact, contralateral control femora, whereas the values for femora that had been treated with 200 microg of rhOP-1 without antibiotic remained significantly lower than those for the intact, contralateral controls (p < 0.05). CONCLUSIONS: Recombinant human osteogenic protein-1 maintained its osteoinductive capability in the presence of chronic infection, and this property was enhanced by antibiotic therapy. No substantial callus formed in the infected defects without a sufficiently high dose of rhOP-1. CLINICAL RELEVANCE: The treatment of an infection at the site of a fracture often necessitates removal of internal fixation. However, internal fixation is needed for fracture stability. This study presents an intervention that may accelerate fracture-healing in the presence of infection and colonized hardware, thereby permitting earlier removal of the hardware and more timely and effective treatment of the infection.

Animals↗
PubMed1999

Consanguinity and recurrence risk of birth defects: a population-based study.

Recurrence risks give insight into the causes of birth defects and are useful in genetic counseling. There are few population-based studies of recurrence of birth defects for subsequent sibs with consanguineous parents. The aim of this study was to estimate and compare the recurrence risk of birth defects for offspring of first cousins and nonconsanguineous parents. The study population consisted of all single births with a previous sib born in Norway between 1967 and 1995. Altogether 660,398 children had nonconsanguineous parents, and 3,583 had parents who were first cousins. For nonconsanguineous parents the risk of a birth defect for the subsequent sib was 15 per 1,000 births (95% confidence interval: 14.5-15.1) if the previous child did not have a birth defect and 33 (95% confidence interval: 30-37) if the previous child had a birth defect. For parents who were first cousins the risk of a birth defect for the subsequent sib was 36 per 1,000 (95% confidence interval: 30-42) if the previous child did not have a birth defect and 68 (95% confidence interval: 33-122) if the previous child had a birth defect. The risk of recurrence of birth defects is higher for subsequent sibs with first-cousin parents than for those with nonconsanguineous parents. This difference indicates the degree to which the increased homozygosity among offspring of consanguineous parents influences the risk of recurrence of birth defects.

Age Factors↗
PubMed1999

An anisocoria produces a small relative afferent pupillary defect in the eye with the smaller pupil.

OBJECTIVES: To determine whether an anisocoria can produce a relative afferent pupillary defect of clinical importance. MATERIAL AND METHODS: Anisocoria and relative afferent pupillary defect were measured with infrared videography in three clinical experiments: 1) every few minutes in eight normal subjects who remained in darkness as one pupil was dilating from mydriatic drops; 2) every 2 hours, for 8 hours in six normal subjects who remained in room light after one pupil was dilated with mydriatic drops; and 3) before and after dilation of one pupil in 24 patients with known afferent defects from optic nerve disease and who remained in room light. RESULTS: In the presence of an anisocoria, the relative afferent pupillary defect was almost always in the eye with the smaller pupil. The results of the three experiments were: 1) In darkness, the induced pupillary defect was found to be related to the ratio of the areas of the two pupils (R = 0.942), and 0.14 log unit of pupillary defect was produced in the eye with the smaller pupil for every millimeter of anisocoria. 2) In room light, the induced pupillary defect was in the eye with the smaller pupil but was less than in Experiment 1 and persisted throughout the 8 hours. This was presumably because the eye with the larger pupil had become more light adapted in the clinic light than the eye with the smaller pupil. 3) In room light, inducing an anisocoria in patients with preexisting afferent pupillary defect tended to shift the pupillary defect toward the eye with the smaller pupil (R = 0.68). CONCLUSIONS: Clinically, approximately 0.1 log unit of relative afferent pupillary defect is produced in the eye with the smaller pupil for every millimeter of anisocoria. Therefore, the anisocoria must be larger than 2 mm in diameter difference to induce a clinically significant relative afferent pupillary defect.

Anisocoria↗
PubMed2003

[Unawareness for homonymous visual field defect].

BACKGROUND: There was no report which dealt with the relationship between emotional state, degree of defective visual search, severity of hemianopic dyslexia, the episode when the patient became aware of the defect, and unawareness of visual loss in homonymous hemifield. OBJECTIVE: To investigate the relationship between degree of awareness and those factors that might be responsible for the unawareness, including the aspects listed above. METHODS: Four patients with visual field defects caused by a brain lesion after a stroke was investigated. Self rating of emotional state, search performance for an object among many placed on a table, and for text reading, as well as visual field, visual positive phenomena, and hemispatial neglect were evaluated. Degree of unawareness for field loss was evaluated by modified version of the method of Bisiach et al. (1985). In addition, the episodes when the patient became aware of the defect were asked. RESULT: In accordance with the previous studies, we found no relationship between the degree of awareness of field defect and anatomic lesions, co-existence of hemispatial neglect, or the degree of awareness of hemiplegia. However, the patient with neglect was unaware of their troubles in vision at all, whereas the patients without neglect were aware of the troubles but misinterpreted them as problems of the eyes including acuity. In accordance with previous studies, co-existence of visual hallucinations or illusions seemed to be associated with awareness of visual field defect. No relationship was found between the degree of awareness of field defect and emotional state, degree of field loss, degree of defective visual search, or severity of hemianopic dyslexia. Their responses to the inquiry about the degree of awareness of field defect were not consistent. Thus, the awareness of the field defect seemed to be difficult to be kept firmly in their mind. On the other hand, the patients could remember the episode when they became aware of the defect for the first time, being able to specify time, place, and situation. CONCLUSION: Levine (1990) suggested that the sensory loss in this sort of patients was never phenomenally immediate but instead must be discovered by observation and inference. Non-specificity of the lesion, qualitative difference in awareness between the patient with and without hemispatial neglect, association of positive visual phenomena and awareness, fluctuation of awareness, and dependence of awareness on personal experiences found in our patients, can be explained with this 'discovery' hypothesis.

Aged↗
PubMed2003

[Analysis of congenital defects contributing to perinatal mortality in the Czech Republic].

OBJECTIVE: Analysis of the proportion of selected types of congenital defects in stillbirth, frequent neonatal and perinatal death rate in the Czech Republic in the years 1994-2002. DESIGN: A retrospective demographic-epidemiological analysis. SETTING: Institute for the Care of Mother and Child, Prague. MATERIALS AND METHODS: The study analyzed individual anonymous data from the Institute of Medical Information and Statistics of the Czech Republic in the period of 1994-2002 (preliminary data only for 2002) from the National Registry of Congental Defects. Fourteen types of defects were selected from the data set. The proportion of children with a certain selected congenital defect which died during the perinatal period were calculated in comparison with the total number of subjects diagnosed for this congential defect in the Czech Republic over the period of observation. RESULTS: A total of 4,436 children died during the perinatal period in the Czech Republic over the period of 1994-2002, while 879 of them suffered from one or more congenital defects. The congenital defects represent more than 10% of stillbirth in this period, 32.5% of deceased individuals in early neonatal death rate and almost 20% in perinatal death rate. In 25% of these cases the prenatal diagnosis was positive, whereas prenatal diagnosis was negative or not indicated (a negative screening) in 48% of cases, and in 27% the data were not filled out. More than 45% of children deceased with a congenital defect in the perinatal period had two or more congenital defects. CONCLUSIONS: Analysis of these results from the registry of congenital defects in the Czech Republic contributed to the information on prenatal deaths in the period of 1994-2002. The proportion of congenital defects in perinatal death rate makes up almost 20%, but it also significantly participates in late newborn and post-newborn mortality and morbidity.

Congenital Abnormalities↗