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PubMed1995

Course of autosomal recessive polycystic kidney disease (ARPKD) in siblings: a clinical comparison of 20 sibships.

Forty-two children out of 20 sibships with autosomal recessive polycystic kidney disease were observed pro- and retrospectively over a mean period of 3.7 years in a long-term study on cystic kidney diseases in children. The intra- and interfamilial variability in terms of age at diagnosis, administration of antihypertensive therapy, liver affection, and renal function were evaluated. According to the 1971 subclassification of Blyth & Ockenden, defining different grades of severity, 12 patients were assigned to the perinatal, nine to the neonatal, 13 to the infantile, and eight to the juvenile subtype of autosomal recessive polycystic kidney disease. In 11 of the 20 families different subtypes were observed among affected siblings. In seven families, affected sibs belonged to adjacent subtypes, while major intrafamilial differences were observed in only four families. The defined subtypes, therefore, cannot be regarded as appropriate in distinguishing genetic groups of autosomal recessive polycystic kidney disease. With respect to the severity of autosomal recessive polycystic kidney disease, there is a wide spectrum of phenotypic manifestations, ranging from stillbirths to mildly affected of phenotypic manifestations, ranging from stillbirths to mildly affected adults, while intrafamilial variability of the clinical picture is generally small with multiple allelism as the most likely genetic explanation. Age at death, however, showed gross variation in eight sibships. Differences in the clinical course between several siblings cannot be explained by a sex influence in autosomal recessive polycystic kidney disease.

Adolescent↗

PubMed1984

Depth of alveolar bone dehiscences in relation to gingival recessions.

Dehiscence depths were measured in vivo during surgical treatment of 113 teeth with gingival recession in 27 subjects. The average dehiscence depth determined was 5.43 mm with an average recession depth of 2.67 mm. Statistical evidence of a correlation between recession depth and dehiscence depth (average distance between lowest point of recession and dehiscence = 2.8 mm) leaves 16 affected teeth (n = 113) with a distance of 4 mm or more (up to a maximum of 7.5 mm) between the gingival margin and the alveolar crest (facial) unaccounted for. The significance of these deviations from mean values in the etiology and prognosis of recessions is discussed.

Adult↗

PubMed1996

Fibrin glue application in conjunction with tetracycline root conditioning and coronally positioned flap procedure in the treatment of human gingival recession defects.

A split-mouth clinical study was designed to determine the effect of fibrin glue (FG) in addition to tetracycline HCI (TTC) root conditioning and the coronally positioned flap (CPF) procedure in the treatment of maxillary buccal recession defects. 11 patients presenting with a pair of Class I or II recession defects were selected. After initial therapy, defect-specific and full-mouth oral hygiene standards and gingival condition, recession depth, recession width, probing depth, attachment level, and width of keratinized gingiva were recorded. The surgical procedure included elevation of a full split thickness flap, root debridement and root conditioning with a 10 mg/ml TTC solution for 4 minutes. According to a randomization list, in each patient, 1 defect was treated with topical FG application, while the paired defect did not receive FG. The flap was adapted and sutured coronally to the cemento-enamel junction without tension. Healing was evaluated 6 months postsurgery. Significant recession depth reduction and attachment gain were observed for both treatments. Average root coverage amounted to 65% in FG treated defects and 55% in defects treated with TTC conditioning only. There were no clinical and statistical significant differences between the treatments for any parameter considered. This study suggests that FG may not meaningfully enhance the outcome of the CPF procedure with TTC root conditioning.

Administration, Topical↗

PubMed1998

Long-term stability of the mucogingival complex following guided tissue regeneration in gingival recession defects.

The purpose of the present study was to evaluate the stability of soft tissue conditions in gingival recession defects treated with guided tissue regeneration (GTR). The study population was selected among those patients who had been treated with GTR procedures for Miller's class I or II, deep (> or =3 mm), buccal gingival recession defects. Defects were included only when they had revealed recession depth reduction > or =2 mm and root coverage > or =60% at 6 months following GTR treatment. These defects were regarded as successfully treated and scheduled for further monitoring. 20 patients, 11 male and 9 female, aged 23 to 57 years (mean age: 33.2 years), each contributing 1 defect, were selected. 9 patients were smokers (> or =10 cigarette per day). Recession depth (RD), probing depth (PD), clinical attachment level (CAL), and width of keratinized gingiva (KG) were assessed immediately before surgery, at 6 months post-surgery (baseline examination), and at 4 years post-surgery (4-year examination). At baseline examination, RD reduction was 3.6+/-0.9 mm (mean root coverage: 80%). CAL gain amounted to 4.2+/-1.3 mm, 60% of the defects showing CAL gain > or =4 mm. KG increased from 1.9+/-1.2 mm at presurgery examination to 3.1+/-0.9 mm at baseline examination. At 4-year examination, no significant changes from baseline RD, CAL and KG recordings were observed. Differences in baseline-4 year changes between smokers and non-smokers were not statistically significant. The results of the present study demonstrate that clinical outcome achieved following GTR procedure in gingival recession defects can be maintained over periods up to 4 years.

Adult↗

PubMed1989

Visual and tactile observational error: comparative probing reliability with recession and cementoenamel junction measurements.

Probing error may arise from several sources, including visual observations and tactile detection of the cementoenamel junction (CEJ). This study examined two types of probe scale in relation to measurements of recession and CEJ from a flexible stent, and two types of probe design in addition, in relation to CEJ detection. 492 sites were studied in six patients with untreated periodontitis. Following stent construction, patients attended for measurement of recession and probing depth. This was repeated after 1 h, and then calculus was scaled in the vicinity of the CEJ. One week later, patients attended for CEJ measurements, which were similarly repeated. Measurements with an offset scale (between marks) were more reproducible in general, though no significant difference was detected between recession scores. The most reproducible detection of the CEJ was with a modified Cross calculus probe with an offset scale. A curious feature of the results was a bias affecting 9% of the recession measurements. It is possible that edematous enlargement of the gingiva occurred after the first measurement of probing depth, and was occasionally sufficient to alter the recession score.

Bias↗

PubMed1994

Characteristics of older adults experiencing periodontal attachment loss as gingival recession or probing depth.

While attachment loss currently is the best field examination indicator that periodontal disease has progressed, this measure is not disaggregated enough to differentiate between attachment loss that results in deeper pockets and attachment loss that results primarily in recession of the gingiva. If these two conditions have different etiologies, then efforts at predicting who will experience the condition from a single, general risk assessment model will be difficult. The purpose of this paper is to determine whether the characteristics of people who experience attachment loss primarily as increased probing depths are different from those people who experience attachment loss primarily as gingival recession. Baseline and 18-month follow-up periodontal measures were gathered on a representative sample of community-dwelling adults aged 65+. Based on measurement errors obtained one week apart on a reliability subsample, a threshold level of 3+mm was set to define attachment loss. Attachment loss was further characterized as resulting from mostly increased probing depth or from mostly increased gingival recession. In mesio-buccal sites, 58% of the people had attachment loss mostly due to increased probing depth with 42% having attachment loss mostly due to gingival recession. For buccal sites, the figures were 24% and 76% respectively. The logistic regression models for both sites indicated that people who had their attachment loss in the form of increased probing depths had different characteristics than people who had most of their attachment loss in the form of gingival recession.(ABSTRACT TRUNCATED AT 250 WORDS)

Black or African American↗

PubMed1995

A new X linked recessive deafness syndrome with blindness, dystonia, fractures, and mental deficiency is linked to Xq22.

X linked recessive deafness accounts for only 1.7% of all childhood deafness. Only a few of the at least 28 different X linked syndromes associated with hearing impairment have been characterised at the molecular level. In 1960, a large Norwegian family was reported with early onset progressive sensorineural deafness, which was indexed in McKusick as DFN-1, McKusick 304700. No associated symptoms were described at that time. This family has been restudied clinically. Extensive neurological, neurophysiological, neuroradiological, and biochemical, as well as molecular techniques, have been applied to characterise the X linked recessive syndrome. The family history and extensive characterisation of 16 affected males in five generations confirmed the X linked recessive inheritance and the postlingual progressive nature of the sensorineural deafness. Some obligate carrier females showed signs of minor neuropathy and mild hearing impairment. Restudy of the original DFN-1 family showed that the deafness is part of a progressive X linked recessive syndrome, which includes visual disability leading to cortical blindness, dystonia, fractures, and mental deficiency. Linkage analysis indicated that the gene was linked to locus DXS101 in Xq22 with a lod score of 5.37 (zero recombination). Based on lod-1 support interval of the multipoint analysis, the gene is located in a region spanning from 5 cM proximal to 3 cM distal to this locus. As the proteolipid protein gene (PLP) is within this region and mutations have been shown to be associated with non-classical PMD (Pelizaeus-Merzbacher disease), such as complex X linked hereditary spastic paraplegia, PLP may represent a candidate gene for this disorder. This family represents a new syndrome (Mohr-Tranebjaerg syndrome, MTS) and provides significant new information about a new X linked recessive sydromic type of deafness which was previously thought to be isolated deafness.

Adolescent↗

PubMed1997

Autosomal recessive diseases among Palestinian Arabs.

As a consequence of the high consanguinity rate among the Palestinian Arabs, many recessive disorders are present with a relatively high frequency. In a survey of 2000 different Palestinian Arab families who visited our genetic clinic, in 601 an autosomal recessive disease was diagnosed or strongly suspected. The distribution of these disorders was not uniform and some disorders, such as Krabbe disease, were found at high frequency in only a small part of the population. For some other disorders, a high prevalence was also reported among Palestinian Arabs living in other regions, for example, beta thalassaemia, Bardet-Biedl syndrome, Meckel syndrome, autosomal recessive congenital hydrocephalus, and recessive osteopetrosis. In addition, as another consequence of the high consanguinity rate, two different autosomal recessive diseases were diagnosed within the same sibship in 17 of the Palestinian Arab families.

Arabs↗

PubMed1999

Study on the gene and phenotypic characterisation of autosomal recessive demyelinating motor and sensory neuropathy (Charcot-Marie-Tooth disease) with a gene locus on chromosome 5q23-q33.

OBJECTIVES: To report the occurrence of the autosomal recessive form of demyelinating Charcot-Marie-Tooth disease (CMT) with a locus on chromosome 5q23-33 in six non-related European families, to refine gene mapping, and to define the disease phenotype. METHODS: In an Algerian patient with autosomal recessive demyelinating CMT mapped to chromosome 5q23-q33 the same unique nerve pathology was established as previously described in families with a special form of autosomal recessive demyelinating CMT. Subsequently, the DNA of patients with this phenotype was tested from five Dutch families and one Turkish family for the 5q23-q33 locus. RESULTS: These patients and the Algerian families showed a similar and highly typical combination of clinical and morphological features, suggesting a common genetic defect. A complete cosegregation for markers D5S413, D5S434, D5S636, and D5S410 was found in the families. Haplotype construction located the gene to a 7 cM region between D5S643 and D5S670. In the present Dutch families linkage disequilibrium could be shown for various risk alleles and haplotypes indicating that most of these families may have inherited the underlying genetic defect form a common distant ancestor. CONCLUSIONS: This study refines the gene localisation of autosomal recessive demyelinating CMT, mapping to chromosome 5q23-33 and defines the phenotype characterised by a precocious and rapidly progressive scoliosis in combination with a relatively mild neuropathy and a unique pathology. Morphological alterations in Schwann cells of the myelinated and unmyelinated type suggest the involvement of a protein present in both Schwann cell types or an extracellular matrix protein rather than a myelin protein. The combination of pathological features possibly discerns autosomal recessive demyelinating CMT with a gene locus on chromosome 5q23-33 from other demyelinating forms of CMT disease.

Adolescent↗

PubMed2006

Characterization of recessive severe type 1 and 3 von Willebrand Disease (VWD), asymptomatic heterozygous carriers versus bloodgroup O-related von Willebrand factor deficiency, and dominant type 1 VWD.

Recessive type 3 von Willebrand disease (VWD) is caused by homozygosity or double heterozygosity for two non-sense mutations (null alleles). Type 3 VWD is easy to diagnose by the combination of a strongly prolonged bleeding time (BT), absence of ristocetine-induced platelet aggregation (RIPA), absence of von Willebrand factor (VWF) protein, and prolonged activated partial thromboplastin time (aPTT) due to factor VIII:coagulant (FVIII:C) deficiency. VWD type 3 is associated with a pronounced tendency to mucocutaneous and musculoskeletal bleedings since early childhood. Carriers of one null allele are usually asymptomatic at VWF levels of 50% of normal. Recessive severe type 1 VWD is caused by homozygosity or double heterozygosity for a missense mutation. Recessive type 1 VWD differs from type 3 VWD by the presence of detectable von Willebrand factor: antigen VWF:Ag and FVIII:C levels between 0.09 and 0.40 U/mL. Patients with recessive type 1 VWD show an abnormal VWF multimeric pattern in plasma and/or platelets consistent with severe type 2 VWD. Carriers of a missense mutation may have mild bleeding and mild VWF deficiency and can be diagnosed by a double VWF peak on cross immunoelectrophoresis (CIE). There will be cases of mild and moderate recessive type 1 VWD due to double heterozygosity of two missense mutations, or with the combination of one missense mutation with a non-sense or bloodgroup O. Mild deficiency of VWF in the range of 0.20 to 0.60 U/mL, with normal ratios of von Willebrand factor: ristocetine cofactor/antigen VWF:RCo/Ag and VWF:collagen binding/antigen (VWF:CB/Ag), normal VWF multimers, and a completely normal response to desmopressin acetate (DDAVP) with VWF level rising from below to above 1.00 U/mL are very likely cases of so-called pseudo-VWF deficiency in individuals with normal VWF protein and gene. Autosomal dominant type 1 VWD variants are in fact type 2 variants caused by a heterozygous missense mutation in the VWF gene that produces a mutant VWF protein that has a dominant effect on normal VWF protein produced by the normal VWF allele with regard to the synthesis, processing, storage, secretion, and/or proteolysis of VWF in endothelial cells. A DDAVP challenge test clearly differentiates between dominant type 1 VWD phenotype and dominant type 2 M VWD.

ABO Blood-Group System↗

PubMed2006

Differences in the evolutionary history of disease genes affected by dominant or recessive mutations.

BACKGROUND: Global analyses of human disease genes by computational methods have yielded important advances in the understanding of human diseases. Generally these studies have treated the group of disease genes uniformly, thus ignoring the type of disease-causing mutations (dominant or recessive). In this report we present a comprehensive study of the evolutionary history of autosomal disease genes separated by mode of inheritance. RESULTS: We examine differences in protein and coding sequence conservation between dominant and recessive human disease genes. Our analysis shows that disease genes affected by dominant mutations are more conserved than those affected by recessive mutations. This could be a consequence of the fact that recessive mutations remain hidden from selection while heterozygous. Furthermore, we employ functional annotation analysis and investigations into disease severity to support this hypothesis. CONCLUSION: This study elucidates important differences between dominantly- and recessively-acting disease genes in terms of protein and DNA sequence conservation, paralogy and essentiality. We propose that the division of disease genes by mode of inheritance will enhance both understanding of the disease process and prediction of candidate disease genes in the future.

Animals↗

PubMed2003

Chloride channel ClCN7 mutations are responsible for severe recessive, dominant, and intermediate osteopetrosis.

UNLABELLED: Among 94 osteopetrotic patients presenting with a severe clinical picture and diagnosed early in life, 12 bore mutations in the ClCN7 gene, but only 7 of them had the expected two recessive mutations. The remaining five patients seem to be heterozygous for a ClCN7 mutation, and significant variations were observed in the clinical manifestations of their disease, even within the same family. INTRODUCTION: Human osteopetroses are a heterogeneous group of diseases that include both infantile severe, autosomal recessive (ARO) and adult autosomal dominant (ADO) forms. Two genes, Atp6a3 (TCIRG1) and ClCN7, have been shown to be associated with human ARO, the latter of which is also thought to be responsible for ADO-II. However, patients with an intermediate phenotype have been described: the genetic basis of these observances is unknown. MATERIALS AND METHODS: In this study, we report the clinical and molecular analysis of 94 patients in which a diagnosis of severe osteopetrosis was made within the first 2 years of age. Both TCIRG1 and CLCN7 genes were sequenced in all patients and the molecular findings were correlated to clinical parameters. RESULTS AND CONCLUSIONS: In 56 of 94 patients with a classical picture of ARO, TCIRG1-dependent recessive mutations were found. In contrast, ClCN7 mutations were found in 12 cases (13%) of severe osteopetrosis, but only 7 of them had two recessive mutations identified: in 6 of these 7 cases, central nervous system manifestations were noted, and these patients had a poor prognosis. The remaining five cases were heterozygous for a ClCN7 mutation, including two brothers from a large family with a history of ADO-II in which the presence of a second ClCN7 mutation was formally excluded. Despite an early and severe clinical presentation, these five patients all reached adulthood, suggesting that the degree of dominant interference with chloride channel function can vary widely. Our findings suggest that recessive ClCN7-dependent ARO may be associated with CNS involvement and have a very poor prognosis, whereas heterozygous ClCN7 mutations cause a wide range of phenotypes even in the same family, ranging from early severe to nearly asymptomatic forms. These findings have prognostic implications, might complicate prenatal diagnosis of human osteopetroses, and could be relevant to the management of these patients.

Adolescent↗

PubMed1999

Comparative clinical study of a bioabsorbable membrane and subepithelial connective tissue graft in the treatment of human gingival recession.

BACKGROUND: Connective tissue grafts and guided tissue regeneration (GTR) are the most current procedures in the treatment of gingival recession, but very few clinical comparative studies have been conducted. METHODS: The purpose of this study was to compare 2 types of treatment of gingival recession in the same patients. Fourteen pairs of Miller Class I defects were selected in 14 patients. In each pair, one recession was randomly assigned for treatment by GTR using a bioabsorbable membrane, and the other treated by subepithelial connective tissue graft (CTG). Height of recession (HR), clinical attachment level (CAL), probing sulcus depth (PSD), height of keratinized tissue (HKT), and distance from the cemento-enamel junction to the mucogingival junction (CEJ-MGJ) were recorded before surgery and 6 months postoperatively. RESULTS: The initial width and height of recession were, respectively, 3.73 mm (SD 0.56) and 3.85 mm (SD 1.15) for the CTG group, and 4.04 mm (SD 0.92) and 4.28 mm (SD 1.20) for the GTR group. The differences were not significant. CAL changes were not different. Both in the CTG group and in the GTR group, mean HR reduction was 2.89 mm (SD 1.18), representing a mean root coverage of 76% and 70.2%, respectively. The difference was not significant. HKT mean gain was significantly greater (P = 0.0001) with CTG (2.03 mm, SD 0.92) than with GTR (0.42 mm, SD 0.91). The GTR technique displaced the mucogingival junction significantly (P = 0.007) more coronally (2.35 mm, SD 1.44) than the CTG technique (0.78 mm, SD 1.23). CONCLUSIONS: Within the limits of this study, no difference could be found between subepithelial connective tissue graft and GTR with a bioabsorbable membrane with regard to root coverage, but the GTR technique did not increase the height of keratinized tissue and displaced the mucogingival junction more coronally at 6 months.

Absorption↗

PubMed2001

Comparison of 2 clinical techniques for treatment of gingival recession.

BACKGROUND: In early case studies, use of a collagen barrier as a guided tissue regeneration (GTR) material has shown particular promise in procedures aimed at root coverage. The similarities between collagen membrane and subepithelial connective tissue graft (SCTG) have made collagen membrane an attractive and a possible alternative material for root coverage. The purpose of this randomized clinical trial was to compare these 2 techniques, SCTG versus a GTR-based procedure (GTRC), for root coverage/recession treatment. METHODS: Sixteen patients with bilateral Miller's Class I or II (gingival recession > or = 3.0 mm) recession defects were treated either with SCTG or GTRC using a newly designed collagen membrane. Clinical parameters monitored included recession depth (RD), clinical attachment level (CAL), probing depth (PD), width of keratinized gingiva (KG), attached gingiva (AG), and recession width (RW), each measured at the mid-buccal area to the nearest 0.5 mm. Measurements were taken at baseline and 6 months. A standard mucogingival surgical procedure was performed. Data were reported as means +/- SD and were analyzed using the paired t test for univariate analysis and restricted/residual maximal likelihood (REML)-based mixed effect model for multivariate analysis. RESULTS: No statistically significant differences were observed in RD, CAL, KG, and AG between test and control groups at either time period. However, SCTG showed significantly more residual PD and more RW gain when compared to GTRC at 6 months. Both treatments resulted in a statistically significant (P < 0.05) reduction of recession defects (2.5 mm and 2.8 mm), gain of CAL (2.8 mm and 2.3 mm), reduction of RW (1.9 mm and 2.7 mm), and increase of KG (0.7 mm and 1.1 mm) and AG (0.7 mm and 0.5 mm) for GTRC and SCTG, respectively, when comparing 6-month data to baseline. Mean root coverage of 73% (collagen membrane) and 84% (subepithelial connective tissue graft) was achieved. CONCLUSIONS: The 2 techniques are clinically comparable. Use of a modified collagen membrane to attain root coverage may alleviate the need for donor site procurement of connective tissue.

Adult↗

PubMed2001

Root coverage of a palatal recession defect: a case report.

BACKGROUND: Obtaining predictable root coverage has become an important part of periodontal therapy. However, little has been reported concerning the treatment of palatal recession defects. This is a case report which demonstrates a technique to obtain root coverage of a palatal recession defect. METHODS: The technique involved elevating a partial-thickness palatal flap and placing a connective tissue graft beneath the flap and over the recession defect (subepithelial graft). The portion of the connective tissue graft placed over the recession defect was not covered by the flap. RESULTS: Clinically significant amounts of root coverage were obtained (84.6%), although the connective tissue graft was not covered by the flap. CONCLUSION: Root coverage of a palatal recession defect can be obtained with a subepithelial graft.

Adult↗

PubMed2002

Treatment of gingival recessions by combined periodontal regenerative technique, guided tissue regeneration, and subpedicle connective tissue graft. A comparative clinical study.

BACKGROUND: Many surgical techniques have been shown to be effective in correcting gingival recessions by covering the exposed root with soft tissue; however, the thickness of the gingival tissue over the root surface probably plays an important role in preventing the recurrence of tissue recession. The aim of the present study was to compare the results of a mucogingival bilaminar technique (BT), guided tissue regeneration (GTR), and a combined periodontal regenerative technique (CPRT) in achieving root coverage and increasing the gingival thickness 1 year after surgical treatment. METHODS: In 45 systemically healthy, non-smoking patients aged 33.6 +/- 4.3 years with no periodontal pockets >4 mm, a Miller's Class I or II gingival recession was treated for root coverage: 15 patients underwent BT (connective tissue with partial-thickness double pedicle graft), 15 GTR by a bioabsorbable membrane, and 15 CPRT by a collagen membrane and collagen-incorporated hydroxyapatite. Before and 1 year after surgical treatments, the following clinical parameters were recorded: gingival recession (GR), probing depth (PD), clinical attachment level (CAL), keratinized tissue width (KT), and gingival thickness (GT); the percentage of root coverage was also calculated and the data were statistically analyzed. RESULTS: All 3 techniques yielded significant improvements in terms of GR decrease, CAL and KT gain, and GT increase compared to baseline values. Mean root coverage was 90.0%, 81.01%, and 87.12% in BT, GTR, and CPRT groups, respectively. Complete root coverage was observed in 60%, 40%, and 53.3% of subjects from the BT, GTR, and CPRT groups, respectively. No significant differences were observed among the 3 techniques in GR or CAL improvements; however, BT produced a significantly (P<0.01) greater increase of KT, and BT and CPRT groups showed a significantly (P<0.01) greater increase of GT compared to the GTR group. CONCLUSIONS: BT, GTR, and CPRT successfully treated gingival recession defects, obtaining comparable percentages of root coverage, but BT and CPRT created a thick gingival tissue significantly greater than that achieved with GTR.

Absorbable Implants↗

PubMed2004

Laterally moved, coronally advanced flap: a modified surgical approach for isolated recession-type defects.

BACKGROUND: Various modifications of the laterally sliding flap have been proposed to reduce the risk of gingival recession at the donor tooth site, but the reported root coverage predictability was quite low. The goal of the present study was to evaluate the effectiveness with respect to root coverage of a modified surgical approach of the laterally moved flap procedure for the treatment of an isolated type of recession defect. METHODS: One hundred and twenty (120) isolated gingival recessions (Miller Class I or II) with specific features of the keratinized tissue lateral to the defects were treated with a new approach to the laterally moved flap. The main surgical modifications consisted of the coronal advancement of the laterally moved flap and the different thickness during flap elevation. Clinical evaluation was made 1 year after the surgery. RESULTS: At the 1-year examination, 97% of the root surface was covered with soft tissue and 96 defects (80%) showed complete root coverage. A statistical and clinically significant increase of keratinized tissue was observed. These favorable results were accomplished with no change in the position of gingival margin or in the height of gingival tissue at the donor tooth/site. CONCLUSIONS: The laterally moved, coronally advanced surgical technique was very effective in treating isolated gingival recessions. It combined the esthetic and root coverage advantages of the coronally advanced flap with the increase in gingival thickness and keratinized tissue associated with the laterally moved flap. The ideal gingival conditions must be present lateral to an isolated recession defect in order to render the proposed surgical technique an highly effective and predictable root coverage surgical procedure.

Chlorhexidine↗

PubMed2005

Treatment of gingival recession: comparison of two techniques of subepithelial connective tissue graft.

BACKGROUND: The increasing interest in esthetics and the subsequent need to solve related problems such as hypersensitivity and root caries have favored the development of many surgical procedures that permit the coverage of exposed roots. This clinical study was conducted to examine the coverage of gingival recession defects, where two different subepithelial connective tissue graft (SCTG) techniques (Langer and Langer and modified tunnel) were used. METHODS: Thirty one patients (21 females and 10 males), each contributing Miller Class I and II gingival recessions, were selected. Recession defects were randomly treated by using the Langer and Langer technique (17 patients) or the modified tunnel technique (14 patients). Vertical recession, probing depth (PD), and attachment level were assessed at baseline and 6 months postoperatively. RESULTS: Six months after the surgery, a significant reduction in recession depth was noticed in both groups. There was also a decrease of PD and attachment level for both groups, but not statistically significant. In comparison, at 6 months, statically significant differences were found between the tunnel and Langer and Langer techniques for root coverage and attachment gain. The percentage of root coverage was 96.4% and 75.5% in the tunnel and Langer and Langer groups, respectively. CONCLUSIONS: The present study suggests that the use of SCTG in combination with a tunnel procedure may result in an increased amount of root coverage and clinical attachment gain compared to the Langer and Langer technique. Further comparative studies are necessary to understand the periodontal healing generated by the tunnel procedure and Langer and Langer technique.

Adolescent↗