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PubMed1975

Congenital respiratory tract defects in lambs.

One hundred and forty-seven newborn lambs with congenital defects of the respiratory tract were examined during a 3-year investigation into the causes of perinatal lamb mortality. Respiratory defects were found in 3.3% of the 4,417 lambs examined and in one-third (36.6%) of the 401 congenitally malformed lambs. All the defects were secondary to other more extensive malformations. The upper respiratory tract was involved 3 times more than the lower tract. Males were involved more than females (4:3). The upper tract defects were harelip, cleft palate, atelorrhinia, arrhinia, proboscis, fused nostrils and choanal atresia. One of the facial clefts was a rare median harelip associated with cleft palate and fused nostrils. The lower tract defects were pulmonary agenesis, hypoplasia and duplication. The 2 most common defects were choanal atresia and secondary pulmonary hypoplasia. It was concluded that primary defects of the respiratory tract of sheep are rare and that secondary defects are relatively common.

Abnormalities, Multiple↗
PubMed1982

Functional characterization of cleavage-defective mutants of encephalomyocarditis virus.

We characterized seven temperature-sensitive capsid cleavage (cleavage-defective) mutants of encephalomyocarditis virus. Our experimental approach was to monitor in vitro proteolysis reactions of either wild-type or cleavage-defective mutant capsid precursors mixed with cell-free translation products (containing the viral protease) of either wild-type or mutant viral RNA. The cell-free translation reactions and in vitro proteolysis reactions were done at 38 degrees C, because at this temperature cleavage of the capsid precursors was restricted in reactions containing cleavage-defective mutant viral RNA as the message, relative to those reactions containing wild-type viral RNA as the message. Wild-type or cleavage-defective mutant capsid precursors were prepared by adding cycloheximide to cell-free translation reactions primed with wild-type or mutant viral RNA, respectively, 12 min after the initiation of translation. In vitro proteolysis of wild-type capsid precursors with cell-free translation products of either wild-type or cleavage-defective mutant viral RNA led to similar products at 38 degrees C, indicating that the cleavage-defective mutant viral protease was not temperature sensitive. As a corollary to this, at 38 degrees C cleavage-defective mutant capsid precursors were not cleaved as completely as were wild-type capsid precursors by products of cell-free translation of wild-type viral RNA. The results from these in vitro proteolysis experiments indicate that all seven of the cleavage-defective mutants have capsid precursors with a temperature-sensitive configuration.

Capsid↗
PubMed2003

Comparison of localised nerve fibre layer defects in normal tension glaucoma and primary open angle glaucoma.

AIM: To compare the pattern of localised nerve fibre layer (NFL) defects in normal tension glaucoma (NTG) and primary open angle glaucoma (POAG). METHODS: 50 NTG eyes and 36 POAG eyes, all with localised NFL defects, were enrolled. On retinal NFL photography, the proximity of the defect to the centre of the fovea (angle alpha) and the sum of the angular width of the defects (angle beta) were determined. Angle alpha was the angle made by a line from the centre of the fovea to the disc centre and a line from the disc centre to the disc margin, where the nearest border of the defect met. The patterns of localised NFL defects in NTG and POAG were compared with angles alpha and beta. Independent t test was used for statistical analysis. RESULTS: Angle alpha in NTG (35.1 (SD 20.0) degrees ) was significantly smaller than that of POAG (45.9 (21.9) degrees ) (p=0.02), while angle beta in NTG (49.0 (31.9) degrees ) was significantly larger than that of POAG (33.1 (23.9) degrees ) (p=0.01). CONCLUSIONS: The pattern of NFL defects in NTG was different from that in POAG. Localised NFL defects in NTG were closer to the fovea and wider in width than those in POAG.

Adult↗
PubMed1995

Diagnosis of congenital pericardial defects, including a pathognomic sign for dangerous apical ventricular herniation, on magnetic resonance imaging.

OBJECTIVE: To establish criteria for the accurate diagnosis of different forms of left sided pericardial defects on magnetic resonance imaging. Early detection of a partial apical defect is essential as it is potentially fatal. DESIGN: Examination of four children with congenital pericardial defects by magnetic resonance imaging, the results being compared with the features on conventional chest radiography and echocardiography and with published data. RESULTS: Magnetic resonance imaging improved the ability to diagnose and distinguish between complete and partial left sided pericardial defects. A deep myocardial crease was visualised in a patient with apical pericardial defect, indicating the risk of a life threatening ventricular strangulation. A prominent left atrial appendage was, in contrast to many reports, not a reliable sign for partial left sided pericardial defect. CONCLUSIONS: The various forms of congenital left sided pericardial defects cannot reliably be diagnosed in plain chest radiographs or on echocardiography. Their diagnosis and the distinction between partial and complete defects, however, is of clinical importance and can be accomplished more confidently by magnetic resonance imaging.

Adolescent↗
PubMed1988

Congenital defects and work in pregnancy.

The risk of congenital defect was examined in 47,913 pregnancies of women employed for 15 hours a week or more at time of conception. The rate of defects of all types per 1000 births in this series was 25.0; 1.8 from defects classified as chromosomal (group A), 10.8 as developmental (group B), and 12.5 as musculoskeletal (group C). Some evidence of an excess in the risk ratio (p less than 0.05) was found in the services sector and in four occupations--agriculture and horticulture (2.61), telephone and postal clerks (1.74), a miscellaneous group of service jobs (1.68), and receptionists and information clerks (1.47); excesses of lower statistical significance (p less than 0.1) were found in those engaged in plastics and rubber manufacture (2.02) and in child minders (1.84). There were two cases of tracheo-oesophageal fistula--a rare defect--among eight defects (1.32 expected) in agriculture and horticulture. Overall, the distribution of risk ratios in the 60 occupations examined was not significantly heterogeneous. Analysis of chemical exposure profiles for each occupational group showed no evidence of any increased risk, perhaps due to lack of sensitivity and discrimination in this method of exposure estimation. In 152 pregnancies of doctors and nurses who had administered antineoplastic drugs in the first month eight defects, miscellaneous in type, were observed compared with 4.05 expected (p = 0.05). Special study of musculoskeletal defects and work demands showed some evidence of an association with a long working week (greater than or equal to 46 hours) but no other ergonomic factor. With these few exceptions the survey failed to identify appreciable risk of congenital defect related to occupation.

Anesthetics↗
PubMed2001

Relation between trihalomethane compounds and birth defects.

OBJECTIVES: To evaluate the risk of birth defects relative to exposure to specific trihalomethanes in public water supplies. METHODS: A retrospective cohort study was conducted based on data from a population based perinatal database in Nova Scotia, Canada and from the results of routine water monitoring tests. The cohort consisted of women who had a singleton birth in Nova Scotia between 1988 and 1995 and who lived in an area with a municipal water supply. The birth defects analyzed included neural tube defects, cardiovascular defects, cleft defects, and chromosomal abnormalities. Two of the four trihalomethane compounds occur in large enough concentrations to be analyzed (chloroform and bromodichloromethane (BDCM)). RESULTS: Exposure to BDCM at concentrations of 20 microg/l or over was associated with an increased risk of neural tube defects (adjusted relative risk (RR) 2.5, 95% confidence interval (95% CI) 1.2 to 5.1) whereas exposure to chloroform was not. Exposure to BDCM of 20 microg/l and over was associated with decreased risks of cardiovascular anomalies (RR 0.3, 95% CI 0.2 to 0.7). There was a suggestion of an increased risk of chromosomal abnormalities associated with exposure to chloroform, and no evidence of any association between either trihalomethane compound and cleft defects. CONCLUSIONS: In this cohort, differences were found in the RR associated with exposure to chloroform and BDCM for each of the congenital anomalies under study. These findings point to the importance of examining specific byproduct compounds relative to risk for these birth outcomes and in particular implicate BDCM and other correlated disinfection byproducts in the aetiology of neural tube defects.

Abnormalities, Drug-Induced↗
PubMed2006

Annihilation of nematic point defects: pre-collision and post-collision evolution.

The annihilation of the nematic hedgehog and anti-hedgehog within an infinite cylinder of radius R is studied. The semi-microscopic lattice-type model and Brownian molecular dynamics are used. We distinguish among the i) early pre-collision, ii) late pre-collision, iii) early post-collision, and iv) late post-collision stages. In the pre-collision stage our results agree qualitatively with the existing experimental observations and also continuum-type simulations. The core of each defect exhibits a ring-like structure, where the ring axis is set perpendicular to the cylinder symmetry axis. For xi(0)d/(2R) > 1 the interaction between defects is negligible, where xi(0)d describes the initial separation of defects. Consequently, the defects annihilate within the simulation time window for xi(0)d/(2R) < 1. For close enough defects their separation scales as xi(d) [see text] (t(c)- t)(0.4+/-0.1), where t(c) stands for the collision time. In elastically anisotropic medium the hedgehog is faster than the anti-hedgehog. In the early pre-collision stage the defects can be treated as point-like particles, possessing inherent core structure, that interact via the nematic director field. In the late pre-collision stage the cores reflect the interaction between defects. After the collision a charge-less ring structure is first formed. In the early post-collision stage the ring adopts an essentially untwisted circular structure of the radius xi(r). In the late post-collision stage we observe two qualitatively different scenarios. For mu = xi(r)/R < mu(c) approximately 0.25 the ring collapses leading to the escaped radial equilibrium structure. For mu > mu(c) the chargeless ring triggers the nucleation growth into the planar polar structure with line defects.

Anisotropy↗
PubMed1995

Inherited hearing defects in mice.

Mouse mutants with hearing impairment are useful for elucidating the pathological processes underlying auditory system defects, as well as for understanding the normal process of auditory development and sensory transduction. Deaf mouse mutants are also valuable for identifying the responsible genes by positional cloning, and are used to expedite the search for genes involved in human deafness. The distribution of candidate genes for deafness across the mouse genome is presented, together with a summary of the key features of the mutants involved. Genetic defects affecting hearing can be grouped into broad categories according to their pathological features. These categories include middle ear defects, morphogenetic inner ear defects, central auditory system defects, peripheral neural defects, neuroepithelial defects, cochleo-saccular defects, and late onset hearing loss. The biological features and molecular basis of each type of hearing impairment are described. Finally, the effects of mutations in orthologous genes involved in the auditory system in humans and mice are compared.

Animals↗
PubMed2006

Congenital combined defects of factor VII: a critical review.

Factor VII deficiency is the least rare among uncommon congenital coagulation disorders. The majority of cases are isolated deficiencies. In some cases, FVII deficiency has been found to be associated with the deficiency in another coagulation factor or with non-coagulation-related abnormalities or defects. The evaluation of all published studies on the subject has shown that the FVII defect has been reported in association with FV, FVIII, FIX, FX, FXI and protein C defects. Furthermore, FVII deficiency has been described in association with bilirubin metabolism disorders, mental retardation, microcephaly, epicanthus, cleft palate and persistence of ductus arteriosus. The most interesting association appears to be that with FX. This has been shown to be due to a deletion in part of the long arm of chromosome 13. This arm contains genes coding for both FVII and FX. Interestingly, this combined coagulation defect has been found to be associated with carotid body tumors and several other malformations. Combined defects in blood coagulation often create diagnostic difficulties since results cannot be explained if a single factor deficiency is assumed. For example the combined FVII and FX defect yields a rather peculiar laboratory picture (prolonged prothrombin time and partial thromboplastin time, but normal thrombin time) that could suggest FII or FV or FX single deficiency and not FVII deficiency, indicating the need for specific factor assays whenever data are confusing. Finally, the elevated incidence of mental and skeletal malformations present in these combined defects indicates the need for a careful evaluation of all these patients lest some aspects of the defect are missed.

Adolescent↗
PubMed1979

Pathologic basis of thallium-201 scintigraphic defects in patients with fatal myocardial injury.

Using a quantitative, computer-aided circumferential profile technique, we have shown that thallium-201 scintigrams with large defects can identify a group of patients with a high mortality after acute myocardial infarction. To determine whether high-risk thallium scintigrams predict poor survival because of a critical loss of myocardium, we correlated infarct size in 24 autopsied patients with the extent of thallium defect in three views. Of 13 patients with large defects (computer score greater than or equal to 7.0) eight (62%) had greater than 25% loss of left ventricular (LV) myocardium, but five (38%) had smaller infarcts (4--24% of LV myocardium), suggesting that part of the scintigraphic defect was related to ischemia without necrosis. Eight of the nine patients with loss greater than or equal to 25% LV myocardium had large defects. In 10 of 11 patients with small defects (computer score less than 7.0), infarcts involved less than 20% of LV myocardium. Although scintigrams with large defects predicted a critical loss of myocardium in over 60% of our patients, they included an important second group, in which the scintigraphic defect appeared to reflect a small infarct and a large surrounding area of reversibly ischemic myocardium.

Adult↗
PubMed2005

Location of the glenoid defect in shoulders with recurrent anterior dislocation.

BACKGROUND: In patients with recurrent anterior dislocations of the shoulder, it is well known that the glenoid rim is often deficient (8%-95%). However, little is known regarding the precise location of the bony defect of the glenoid. HYPOTHESIS: The bony defect is anterior rather than anteroinferior to the glenoid. STUDY DESIGN: Cohort study (symptom prevalence); Level of evidence, 2. METHODS: The authors studied 3-dimensional images of the glenoid reconstructed from computed tomography to determine the location of the glenoid defect in 123 shoulders of 123 patients with recurrent anterior dislocations of the shoulder. They measured the location, extent, and orientation of the defect based on the clock face of the glenoid. RESULTS: The defects were located between 12:08 and 6:32, with the range between 2:30 and 4:20 being the most frequent. The extent of the glenoid defect was 106.7 degrees +/- 27.1 degrees (mean +/- standard deviation). The mean orientation of the defect was pointing toward 3:01 on the clock face of the glenoid, at a mean angle of 90.5 degrees +/- 10.4 degrees from the 12-o'clock direction. CONCLUSION: The glenoid defect is located almost anterior to the glenoid.

Adolescent↗
PubMed2005

Biochemical and biomechanical properties of lesion and adjacent articular cartilage after chondral defect repair in an equine model.

BACKGROUND: Chondral defects may lead to degradative changes in the surrounding cartilage, predisposing patients to developing osteoarthritis. PURPOSE: To quantify changes in the biomechanical and biochemical properties of the articular cartilage adjacent to chondral defects after experimental defect repair. STUDY DESIGN: Controlled laboratory study. METHODS: Specimens were harvested from tissue within (lesion), immediately adjacent to, and at a distance from (remote area) a full-thickness cartilage defect 8 months after cartilage repair with genetically modified chondrocytes expressing insulin-like growth factor-I or unmodified, control chondrocytes. Biomechanical properties, including instantaneous Young's and equilibrium aggregate moduli, were determined by confined compression testing. Biochemical properties, such as water and proteoglycan content, were also measured. RESULTS: The instantaneous Young's modulus, equilibrium modulus, and proteoglycan content increased, whereas water content decreased with increasing distance from the repaired lesion. The instantaneous Young's and equilibrium moduli of the adjacent articular cartilage were 80% and 50% that of remote area samples, respectively, whereas water content increased 0.9% and proteoglycan content was decreased by 35%. No significant changes in biomechanical and biochemical properties were found either in the lesion tissue or in adjacent cartilage with genetic modification of the chondrocytes. CONCLUSION: Articular cartilage adjacent to repaired chondral defects showed significant remodeling 8 months after chondral defect repair, regardless of whether genetically modified or unmodified cells were implanted. CLINICAL RELEVANCE: Changes in the biochemical and biomechanical properties of articular cartilage adjacent to repaired chondral defects may represent remodeling as part of an adaptive process or degeneration secondary to an altered distribution of joint forces. Quantification of these changes could provide important parameters for assessing progress after operative chondral defect repair.

Animals↗
PubMed1995

Identification of three distinct peroxisomal protein import defects in patients with peroxisome biogenesis disorders.

Zellweger syndrome, neonatal adrenoleukodystrophy, infantile Refsum's disease, and classical rhizomelic chondrodysplasia punctata are lethal genetic disorders caused by defects in peroxisome biogenesis. We report here a characterization of the peroxisomal matrix protein import capabilities of fibroblasts from 62 of these peroxisome biogenesis disorder patients representing all ten known complementation groups. Using an immunofluorescence microscopy assay, we identified three distinct peroxisomal protein import defects among these patients. Type-1 cells have a specific inability to import proteins containing the PTS1 peroxisomal targeting signal, type-2 cells have a specific defect in import of proteins containing the PTS2 signal, and type-3 cells exhibit a loss of, or reduction in, the import of both PTS1 and PTS2 proteins. Considering that the common cellular phenotype of Zellweger syndrome, neonatal adrenoleukodystrophy and infantile Refsum's disease has been proposed to be a complete defect in peroxisomal matrix protein import, the observation that 85% (40/47) of the type-3 cell lines imported a low but detectable amount of both PTS1 and PTS2 proteins was surprising. Furthermore, different cell lines with the type-3 defect exhibited a broad spectrum of different phenotypes; some showed a complete absence of matrix protein import while others contained 50-100 matrix protein-containing peroxisomes per cell. We also noted certain relationships between the import phenotypes and clinical diagnoses: both type-1 cell lines were from neonatal adrenoleukodystrophy patients, all 13 type-2 cell lines were from classical rhizomelic chondrodysplasia punctata patients, and the type-3 import defect was found in the vast majority of Zellweger syndrome (22/22), neonatal adrenoleukodytrophy (17/19), and infantile Refsum's disease (7/7) patients. Our finding that all type-1 cell lines were from the second complementation group (CG2), all 13 type-2 cell lines were from CG11, and that cells from the eight remaining complementation groups only exhibit the type-3 defect indicates that mutations in particular genes give rise to the different types of peroxisomal protein import defects. This hypothesis is further supported by correlations between certain complementation groups and particular type-3 subphenotypes: all patient cell lines belonging to CG3 and CG10 showed a complete absence of peroxisomal matrix protein import while those from CG6, CG7, and CG8 imported some peroxisomal matrix proteins. However, the fact that cell lines from within particular complementation groups (CG1, CG4) could have different matrix protein import characteristics suggests that allelic heterogeneity also plays an important role in generating different import phenotypes in certain patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenoleukodystrophy↗
PubMed2006

Comparison of simulated periodontal bone defect depth measured in digital radiographs in dedicated and non-dedicated software systems.

OBJECTIVES: To compare simulated periodontal bone defect depth measured in digital radiographs with dedicated and non-dedicated software systems and to compare the depth measurements from each program with the measurements in dry mandibles. METHODS: Forty periodontal bone defects were created at the proximal area of the first premolar in dry pig mandibles. Measurements of the defects were performed with a periodontal probe in the dry mandible. Periapical digital radiographs of the defects were recorded using the Schick sensor in a standardized exposure setting. All images were read using a Schick dedicated software system (CDR DICOM for Windows v.3.5), and three commonly available non-dedicated software systems (Vix Win 2000 v.1.2; Adobe Photoshop 7.0 and Image Tool 3.0). The defects were measured three times in each image and a consensus was reached among three examiners using the four software systems. The difference between the radiographic measurements was analysed using analysis of variance (ANOVA) and by comparing the measurements from each software system with the dry mandibles measurements using Student's t-test. RESULTS: The mean values of the bone defects measured in the radiographs were 5.07 mm, 5.06 mm, 5.01 mm and 5.11 mm for CDR Digital Image and Communication in Medicine (DICOM) for Windows, Vix Win, Adobe Photoshop, and Image Tool, respectively, and 6.67 mm for the dry mandible. The means of the measurements performed in the four software systems were not significantly different, ANOVA (P = 0.958). A significant underestimation of defect depth was obtained when we compared the mean depths from each software system with the dry mandible measurements (t-test; P approximately equal to 0.000). CONCLUSIONS: The periodontal bone defect measurements in dedicated and in three non-dedicated software systems were not significantly different, but they all underestimated the measurements when compared with the measurements obtained in the dry mandibles.

Alveolar Bone Loss↗
PubMed2004

Regeneration of cartilage tissue by autologous chondrocytes transplantation for cartilage defects in a experimental bovine model.

To evaluate the effects of chondrocytes transplantation on the regeneration of cartilage by intraarticular injection or injection into blood clots at cartilage defects, eight full-thickness cartilage defects were created surgically on the articular surface of each femoral trochlea of two calves. Autologous chondrocytes were isolated individually from the cartilage pieces collected at the creation of defects. And isolated cells were cultured in monolayers for proliferation. Cells were injected into synovial fluid (Group 2, n=11) or into the blood clots at the cartilage defects (Group 3, n=5) of the left femoropatellar joint on weeks 2 and 3, respectively after the operation. The defects (Group 1, n=16) of right femoropatellar joint were left untreated in the control group. After 14 weeks, repaired tissues were evaluated based on gross and histological examinations. In Group 3, more repaired tissues and a better interface between the repaired tissue and host cartilage were observed compared with the results for Groups 1 and 2. Moreover, cartilaginous tissue were observed more in defects of Group 3 than in defects of other groups. In conclusion, the present study suggests that the injection of cells into the blood clot at a cartilage defect might be applicable for the regeneration of damaged cartilage.

Animals↗
PubMed2006

Automated defect detection system using wavelet packet frame and Gaussian mixture model.

This paper proposes an approach for automated defect detection in homogeneous textiles using texture analysis. The texture features are extracted by the wavelet packet frame decomposition followed by the Karhunen-Loève transform. The texture feature vector for each pixel is used as an input to a Gaussian mixture model that determines whether or not each pixel is defective. The parameters of the Gaussian mixture model are estimated with nondefective textile images in supervised defect detection. An approach for unsupervised defect detection is also presented that can identify the heterogeneous subblocks on the basis of the Kullback-Leibler divergence between two Gaussian mixtures. The proposed method was evaluated on 25 different homogeneous textile image pairs, one of each pair with a defect and the other with no defect, and was compared with existing methods using texture analysis. The experimental results yielded visually good segmentation and an excellent detection rate with a low false alarm rate for both supervised and unsupervised defect detection. This confirms the validity of the proposed approach for automated defect detection and localization.

Journal Article↗
PubMed2004

ECG score predicts those with the greatest percentage of perfusion defects due to acute pulmonary thromboembolic disease.

BACKGROUND: More aggressive management may be warranted for patients with acute pulmonary embolism (PE) and the greatest pulmonary vascular obstruction. We hypothesized that a scoring system based on the ECG might identify such patients. METHODS: Consecutive patients investigated for PE at Christchurch Hospital between 1997 and 2002 with high-probability ventilation/perfusion (V/Q) scan findings were studied. The ECG obtained closest to and within 48 h of the scan was scored by two independent observers, and the mean ECG score was calculated. V/Q scan findings were categorized into those with < 30%, 30 to 50%, and > 50% perfusion defect by two independent observers experienced in V/Q interpretation. A consensus score was taken when disagreement occurred. RESULTS: Two hundred twenty-nine patients were included in the study. The interobserver agreement for ECG score was 0.96 (Cronbach alpha) and V/Q score was 0.55 (kappa). The ECG predicted those with the greatest amount of perfusion defects. Mean ECG score was 2.6 (SD 2.8) in patients with < 30% perfusion defect, 3.2 (SD 2.9) in patients with 30 to 50% perfusion defect, and 5.3 (SD 3.7) in patients with > 50% perfusion defect. The area under the receiver operating characteristic curve for ECG score and those with > 50% perfusion defect was 0.71 (SE 0.04). An ECG score of > or = 3 predicted those with > 50% perfusion defect with a sensitivity of 70% (95% confidence interval [CI], 59 to 81%), and a specificity of 59% (95% CI, 51 to 67%). CONCLUSION: An ECG score, simple to derive, predicts those with the greatest percentage of perfusion defect. Using the ECG for management warrants prospective evaluation.

Acute Disease↗
PubMed2005

Bioactive glass efficacy in the periodontal healing of intrabony defects in monkeys.

The purpose of this study was the histomorphologic analysis of the efficacy of bioactive glass particles with a narrow size range (Biogran) in the periodontal healing of 2-wall intrabony defects in monkeys. The 2-wall defects were made in the mesial area of the left and right second premolars of four monkeys, filled with gutta-percha and, after 15 days, they were debrided and either naturally filled with coagulum (control) or implanted with bioactive glass (test). In the control sites, the junctional epithelium migrated up to the base of the defect. The presence of newly formed cementum was more significant in the test defects. Both control and test sites showed newly formed bone at the base of the defect. The test defects presented foci of newly formed bone around and within the glass particles localized in the middle third, distant from the defect walls. Histologic analysis showed that the 300- to 355-microm bioactive glass particles aided new periodontal insertion. In conclusion, the tested bioactive glass had better healing potential than debridement only. The graft material showed a promising inhibition of apical migration of the junctional epithelium and greater cementum deposition on the radicular surface of the intrabony defects. The replacement of bioactive glass particles by new bone occurred due not only to an osteoconductive property, but also to an osteostimulatory capacity. Future investigations should evaluate this potential comparatively or together with other grafting materials, regenerative techniques and biological modifiers, as well as assess the longitudinal stability of the new attachment.

Alveolar Bone Loss↗