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At least 1,135 records · Page 63Linked to original sources
PubMed1986

Treatment of localized gingival recessions with coronally displaced flaps and citric acid. An experimental study in the dog.

The present study was designed to examine the effect of citric acid conditioning on the result of healing following treatment of localized gingival recessions with coronally displaced flaps. In 3 beagle dogs, localized gingival recessions were surgically created at the buccal surfaces of canines, premolars and molars. All experimental sites were allowed to accumulate plaque for a period of 6 months. Following preparation of notches in the buccal root surfaces at the level of the gingival margin, buccal and lingual mucoperiosteal flaps were raised. The exposed portion of the root surfaces was scaled and the cementum layer was removed. Another notch was prepared in the root surfaces at the level of the crest of the alveolar bone. Half the number of the roots were treated by topical application of citric acid while the remaining roots were used as non-acid treated controls. The flaps were sutured in a coronally displaced position. After 3 months of healing, the dogs were sacrificed and the jaws removed and placed in fixative. After decalcification, histological sections of the experimental roots and their periodontal tissues were produced. The 2 notches described above were used as reference points in the histological examination. The histological analysis disclosed that new attachment had formed on all test and control roots and extended in some specimens of both groups to a position coronal to the presurgical level of the gingival margin. The amount of new attachment was similar in the 2 categories of roots, demonstrating that citric acid conditioning did not produce additional new attachment.

Animals↗
PubMed1987

Lack of association between width of attached gingiva and development of soft tissue recession. A 5-year longitudinal study.

The purpose of this study was to longitudinally monitor changes in the position of the soft tissue margin at 26 buccal sites surgically deprived of all gingival tissue. A baseline examination carried out 6 months after treatment revealed that the sites to be monitored were lacking or had only a minimal zone (less than 1 mm) of regenerated attached gingiva. 12 control sites with an "adequate" width of attached gingiva (greater than 1 mm) were also examined. Assessments of oral hygiene and gingival conditions, probing pocket depths, probing attachment levels, position of the soft tissue margin, and gingival width were carried out at baseline and after 5 years. The results revealed that in the test sites, a slight increase of the width of the gingiva occurred during the observation period. 7 out of the 26 areas showed a coronal regrowth of the soft tissue margin, while 2 sites showed a further apical displacement of the soft tissue margin. In the control areas, 3 sites developed recession accompanied by a reduction in the width of the gingiva. Hence, it appears that in patients maintaining a proper plaque control, the lack of an "adequate" zone of attached gingiva does not result in an increased incidence of soft tissue recessions.

Dental Plaque Index↗
PubMed1997

Gingival recession. Reappraisal of an enigmatic condition and a new index for monitoring.

Gingival recession (GR) is an intriguing condition. This brief communication, after proposing a definition for GR, considers the possible relevance of anatomical, physiological, pathological and traumatic factors in its etiology. It is probable that no one factor in isolation leads to the development of GR. Because of the possible influence of several factors, not necessarily acting synchronously, the occurrence of GR at a given site may be difficult to explain fully, and any subsequent changes may be hard to predict. The importance of the CEJ (or other fixed point) in assessment of GR severity is discussed. A new two-figure Index of Recession (IR) (e.g., F2-4asterisk) is also described, in which the 1st digit relates to the proportional evaluation of the horizontal extent of GR at the level of CEJ, and the 2nd digit is the vertical extent of GR from CEJ in millimetres; the asterisk denotes involvement of the MGJ. The prefixed F (or L) denotes whether GR is facial (or lingual) to the involved root.

Gingiva↗
PubMed1998

Healing patterns in recession defects treated with ePTFE membranes and with free connective tissue grafts. A histologic and histometric study in the beagle dog.

This study focussed on the biologic success of 2 different procedures for root coverage. In the maxillary canines of 7 beagle dogs, buccal recessions were created and treated on one side with an ePTFE membrane (GTR-group) and on the contralateral side with a free connective tissue graft from the palate (CT-group). 2 areas served as negative controls. After 4 months of healing, histologic sections were processed and histologically analyzed. The evaluated parameters were coverage height, bone, cementum and connective tissue attachment regeneration, length of the epithelium, resorption, and ankylosis. Histologically, both GTR-group and CT-group produced more new bone, new cementum and new connective tissue attachment than the two control teeth. When histologically evaluated, the amount of new bone was more pronounced in the GTR-group than in the CT-group, however, no statistical differences in any of the evaluated parameters could be detected between the 2 procedures tested. Frequency and distribution of resorption and ankylosis were similar in the GTR-group and in the CT-group. Within the limits of this study, no differences in terms of the biologic rehabilitation between those recessions treated with ePTFE membranes and those treated with a free connective tissue graft could be found.

Animals↗
PubMed1993

Hereditary gingival fibromatosis with a recessive mode of inheritance. Case reports.

Hereditary gingival fibromatosis is characterized by varying degrees of attached gingival hyperplasia and may in rare cases present as a feature of a generalized syndrome. It is usually inherited as an autosomal dominant condition though recessive forms are described. The dental and genetic features of an affected brother and sister with a probably unique autosomal recessive hereditary fibromatosis syndrome are presented.

Adolescent↗
PubMed2001

Triallelic inheritance in Bardet-Biedl syndrome, a Mendelian recessive disorder.

Bardet-Biedl syndrome (BBS) is a genetically heterogeneous disorder characterized by multiple clinical features that include pigmentary retinal dystrophy, polydactyly, obesity, developmental delay, and renal defects. BBS is considered an autosomal recessive disorder, and recent positional cloning efforts have identified two BBS genes (BBS2 and BBS6). We screened our cohort of 163 BBS families for mutations in both BBS2 and BBS6 and report the presence of three mutant alleles in affected individuals in four pedigrees. In addition, we detected unaffected individuals in two pedigrees who carry two BBS2 mutations but not a BBS6 mutation. We therefore propose that BBS may not be a single-gene recessive disease but a complex trait requiring three mutant alleles to manifest the phenotype. This triallelic model of disease transmission may be important in the study of both Mendelian and multifactorial disorders.

Alleles↗
PubMed1992

The skeletal muscle chloride channel in dominant and recessive human myotonia.

Autosomal recessive generalized myotonia (Becker's disease) (GM) and autosomal dominant myotonia congenita (Thomsen's disease) (MC) are characterized by skeletal muscle stiffness that is a result of muscle membrane hyperexcitability. For both diseases, alterations in muscle chloride or sodium currents or both have been observed. A complementary DNA for a human skeletal muscle chloride channel (CLC-1) was cloned, physically localized on chromosome 7, and linked to the T cell receptor beta (TCRB) locus. Tight linkage of these two loci to GM and MC was found in German families. An unusual restriction site in the CLC-1 locus in two GM families identified a mutation associated with that disease, a phenylalanine-to-cysteine substitution in putative transmembrane domain D8. This suggests that different mutations in CLC-1 may cause dominant or recessive myotonia.

Amino Acid Sequence↗
PubMed1987

Three recessive loci required for insulin-dependent diabetes in nonobese diabetic mice.

A polygenic basis for susceptibility to insulin-dependent diabetes in nonobese diabetic (NOD) mice has been established by outcross to a related inbred strain, nonobese normal (NON). Analysis of first and second backcross progeny has shown that at least three recessive genes are required for development of overt diabetes. One, Idd-1s, is tightly linked to the H-2K locus on chromosome 17; another, Idd-2s, is localized proximal to the Thy-1/Alp-1 cluster on chromosome 9. Segregation of a third, Idd-3s, could be shown in a second backcross. Neither Idd-1s nor Idd-2s could individually be identified as the locus controlling insulitis; leukocytic infiltrates in pancreas were common in most asymptomatic BC1 mice. Both F1 and BC1 mice exhibited the unusually high percentage of splenic T lymphocytes characteristic of NOD, suggesting dominant inheritance of this trait. The polygenic control of diabetogenesis in NOD mice, in which a recessive gene linked to the major histocompatibility complex is but one of several controlling loci, suggests that similar polygenic interactions underlie this type of diabetes in humans.

Animals↗
PubMed1978

Evidence that spo0A mutations are recessive in spo0A-/spo0A+ merodiploid strains of Bacillus subtilis.

The spo0A locus contains two types of closely linked mutations that block sporulation at stage 0: spo0A mutations (the most pleiotropic of the stage 0 markers) and spo0C mutations. It was previously thought that spo0A mutations were dominant in merodiploids of Bacillus subtilis, whereas spo0C mutations were recessive. We have shown that spo0A mutations were recessive when spo0A-/spo0A+ merodiploids were made in the genetic backgrounds of strains that were resistant to antibiotic produced by the wild-type strain. Reinvestigation of cultures of spo0A-/spo0A+ merodiploids constructed in the antibiotic-sensitive spo0A strain showed that they contained the spo0A allele at a low frequency, and they produced very few haploid Spo- segregants. These facts indicated that the cultures contained mostly homogenotic (spo0A+/spo0A+) cells. The reason for the poor survival of the spo0A-/spo0A+ merodiploids in the genetic background of the antibiotic-sensitive strain was not clear, but several possible explanations were given. It may have been related to the diploid state of other genes in the same merodiploid cells. The previous indication that spo0A mutations were dominant seems to have been based on the properties of a rare class of Spo- segregants that were probably selected in the presence of antibiotic.

Anti-Bacterial Agents↗
PubMed1989

Suppression of a -1 frameshift mutation by a recessive tRNA suppressor which causes doublet decoding.

sufS was found to suppress the only known suppressible-1 frameshift mutation, trpE91, at a site identified as GGA and mapped within the single gene of the only tRNA that can decode GGA in Escherichia coli. It mapped to the same gene in Salmonella typhimurium. sufS alleles were recessive, and dominant alleles could not be isolated. This is in contrast to all other tRNA structural gene mutations identified thus far that cause frameshift suppression. The recessiveness implies that all sufS alleles are poor competitors against their wild-type tRNA(Gly2) counterparts. The base G immediately 5' of the GGA suppression site influenced the level but was not critical for suppression by sufS601. From this result, it is inferred that sufS601 causes frameshifting by doublet decoding.

Alleles↗
PubMed2000

Resistance to Friend murine leukemia virus infection conferred by the Fv-4 gene is recessive but appears dominant from the effect of the immune system.

Fv-4 is a mouse gene that dominantly confers resistance to infection with Friend murine leukemia virus (F-MuLV) (S. Suzuki, Jpn. J. Exp. Med. 45:473-478, 1975). However, the resistance caused by Fv-4 is recessive in nude mice, which suggests that immunological effects play important roles in this resistance in vivo (K. Higo, Y. Kubo, Y. Iwatani, T. Ono, M. Maeda, H. Hiai, T. Masuda, K. Kuribayashi, F. Zhang, T. Lamin, A. Adachi, and A. Ishimoto, J. Virol. 71:750-754, 1997). To determine the immunological effect on the resistance in vivo, we infected immunologically immature newborn mice homozygous (Fv-4(r/r)) and heterozygous (Fv-4(r/-)) for Fv-4. Although the Fv-4(r/r) mice showed complete resistance to F-MuLV whether infected neonatally or as adolescents, the Fv-4(r/-) mice showed high sensitivity to viral proliferation and disease induction when infected as newborns but complete resistance when infected as adolescent mice. To confirm the immunological effect on the resistance in adolescent mice with the Fv-4(r/r) and Fv-4(r/-) genotypes, we examined the effect of an immunosuppressant drug, FK506, on the resistance. The mice with the Fv-4(r/r) genotype treated with FK506 still showed resistance, but the mice with the Fv-4(r/-) genotype became highly sensitive to F-MuLV infection. Flow cytometric analysis to detect the Fv-4 gene product showed that the Fv-4 gene product was expressed on the cells from newborn and adolescent mice. The Fv-4 gene product was also detected on the cells from the FK506-treated mice as well as on those from untreated mice. However, a quantitative difference in the gene product between the cells with the Fv-4(r/r) and Fv-4(r/-) genotypes was detected by indirect staining for flow cytometry. These results show that the resistance to F-MuLV infection conferred by the Fv-4 gene is originally recessive, but it looks dominant in adolescent mice mainly because of the effect of the immune system.

Animals↗
PubMed2001

Recessive resistance in Pisum sativum and potyvirus pathotype resolved in a gene-for-cistron correspondence between host and virus.

Pea seed-borne mosaic potyvirus (PSbMV) isolates are divided into pathotypes P-1, P-2, and P-4 according to their infection profile on a panel of Pisum sativum lines. P. sativum PI 269818 is resistant to P-1 and P-2 isolates and is susceptible to P-4 isolates. Resistance to P-1 is inherited as a single recessive gene, denoted sbm-1, and the pathogenicity determinant has previously been mapped to the virus-coded protein VPg. In the cultivar Bonneville, a second recessive gene, sbm-2, confers specific resistance to P-2. By exchanging cistrons between a P-2 and a P-4 isolate, the P3-6k1 cistron was identified as the PSbMV host-specific pathogenicity determinant on Bonneville. Exchange of P3-6k1 did not affect infection on PI 269818, and infection of Bonneville was not altered by substitution of the VPg cistron, indicating that P3-6k1 and VPg are independent determinants of pathotype-specific infectivity. On PI 269818 the pathogenicity determinant of both P-1 and P-2 mapped to the N terminus of VPg. This suggests that VPg from the P-1 and P-2 isolates are functionally similar on this host and that resistance to P-1 and P-2 in PI 269818 may operate by the same mechanism. Identification of VPg-sbm-1 and P3-6k1-sbm-2 as independent pairs of genetic interactors between PSbMV and P. sativum provides a simple explanation of the three known pathotypes of PSbMV. Furthermore, analysis of beta-glucuronidase-tagged P-2 virus indicated that sbm-2 resistance affected an early step in infection, implying that the P3-6k1 region plays a critical role in potyvirus replication or cell-to-cell movement.

Genes↗
PubMed1982

Chemical carcinogens transform BHK cells by inducing a recessive mutation.

Treatment of BHK cells with mutagenic carcinogens induced neoplastic transformation in a single step. This transformation displayed the characteristics expected for a recessive mutation. Increasing doses of carcinogens induced transformants with kinetics similar to the kinetics with which they induced 6-thioguanine-resistant or ouabain-resistant mutants in the same population of cells. Transformants with temperature-restricted phenotypes were easily induced by carcinogens which cause mutations by base changes, but when ICR frameshift mutagens were used, the proportion of temperature-limited transformants was inversely related to the frequency with which a particular mutagen induced frameshift mutations. In hybrids between pseudodiploid isogenic strains of normal and transformed BHK cells, transformation was expressed as a dominant trait when the transformed parent was induced by a papovavirus, but was suppressed as a recessive trait when the transformed parent arose spontaneously or was chemically induced. Segregation of transformation was observed upon growth of suppressed normal hybrids, and the transformed phenotype which was reexpressed was in most cases characteristics of the original transformed parent.

4-Nitroquinoline-1-oxide↗
PubMed1986

Genetic analysis of families of patients with Behçet's syndrome: data incompatible with autosomal recessive inheritance.

Data on families with Behçet's syndrome were analysed to test a hypothesis of autosomal recessive inheritance. Fifteen families from the UK and nine from Turkey were included. There were 27 individuals with Behçet's syndrome according to the Japanese criteria and 119 unaffected individuals. There were no affected parents in the families. The 'goodness of fit' test of Elandt-Johnson was applied to the distribution of affected individuals in these families, and the data were found to be incompatible with autosomal recessive inheritance. HLA associations were also examined in patients and relatives, and this led to re-examination of previously published data on HLA associations with Behçet's syndrome.

Behcet Syndrome↗
PubMed1981

Primary vitreoretinal dysplasia transmitted as an autosomal recessive disorder.

A sibship of a brother and sister with congenital bilateral pseudoglioma is described. The most prominent abnormality was a greyish-white vascularised mass in the retrolental spaces, which was noted as early as the first weeks of life. Corneal opacities, posterior synechiae, and complicated cataracts developed within 1 to 2 years age. The sibship showed normal chromosomes and had no systemic disorders, including mental and hearing impairment. The parents and other relatives were normal. Autosomal recessive disease, rather than Norrie's disease, was the most probable explanation for the dysplasia of the vitreous and retina in the sibship. This is probably the third report of familial occurrence with autosomal recessively inherited vitreoretinal dysplasia without systemic anomalies. The importance of the disease in genetic counselling is discussed.

Blindness↗
PubMed1999

Phenotype of autosomal recessive congenital microphthalmia mapping to chromosome 14q32.

BACKGROUND: Congenital microphthalmia (OMIM: 309700) may occur in isolation or in association with a variety of systemic malformations. Isolated microphthalmia may be inherited as an autosomal dominant, an autosomal recessive, or an X linked trait. METHODS: Based on a whole genome linkage analysis, in a six generation consanguineous family with autosomal recessive inheritance, the first locus for isolated microphthalmia was mapped to chromosome 14q32. Eight members of this family underwent clinical examination to determine the nature of the microphthalmia phenotype associated with this locus. RESULTS: All affected individuals in this family suffered from bilateral microphthalmia in association with anterior segment abnormalities, and the best visual acuity achieved was "perception of light". Corneal changes included partial or complete congenital sclerocornea, and the later development of corneal vascularisation and anterior staphyloma. Intraocular pressure, as measured by Schiotz tonometry, was greatly elevated in many cases. CONCLUSIONS: This combination of ocular defects suggests an embryological disorder involving tissues derived from both the neuroectoderm and neural crest. Other families with defects in the microphthalmia gene located on 14q32 may have a similar ocular phenotype aiding their identification.

Adolescent↗
PubMed1988

Autosomal recessive distal myopathy.

Five patients with an autosomally recessively transmitted distal myopathy were investigated. Of these, three belonged to a single sibship. Studies included electromyography, histological examination of muscle tissue, histochemical, electron microscopical, and biochemical analyses. One of the cases resembled the Nonaka form while the others were regarded as expressions of the commoner variety of recessive distal dystrophy.

Adult↗
PubMed1977

Probable autosomal recessive Marfan syndrome.

A probable autosomal recessive mode of inheritance is described in a family with two affected sisters. The sisters showed the typical picture of Marfan syndrome and were of normal intelligence. Both parents and all four grandparents were personally examined and found to be normal. Homocystinuria was ruled out on repeated examinations. This family suggests genetic heterogeneity in Marfan syndrome and that in some rare families the mode of inheritance may be autosomal recessive.

Child↗