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Biomedical subjects

Charles A Powell

Publications and source records attributed to Charles A Powell.

At least 19 recordsLinked to original sources

Clinical predictors of metastatic disease to the brain from non-small cell lung carcinoma: primary tumor size, cell type, and lymph node metastases.

PURPOSE: To retrospectively assess possible clinical predictors of metastatic disease to the brain in patients with non-small cell lung carcinoma (NSCLC). MATERIALS AND METHODS: Institutional review board approval was obtained, informed consent was waived, and data and other information were obtained prior to implementation of HIPAA. A review was performed of 264 patients (mean age, 65 years; 158 men and 106 women) with NSCLC who had undergone imaging studies of the chest and head. Hierarchical logistic regression was used to determine the predicted probability of metastatic disease to the brain as a function of patient age and sex and of size, cell type, peripheral versus central location, and lymph node stage of the primary NSCLC. RESULTS: Ninety-five (36%) patients had evidence of metastatic disease to the brain. Mean diameter of the primary tumors was 4.0 cm +/- 2.2 (standard deviation). Cell types included adenocarcinoma (136 [52%] patients), undifferentiated (68 [26%] patients), and squamous (47 [18%] patients), for which metastatic disease to the brain occurred in 43%, 41%, and 13% (P = .003) of patients, respectively. The predicted probability of metastatic disease to the brain correlated positively with size of the primary tumor (P < .001), cell type (adenocarcinoma and undifferentiated vs squamous, P = .001), and lymph node stage (P < .017) but did not correlate with age, sex, or primary tumor location. For primary adenocarcinoma without lymph node spread, the predicted probabilities of metastatic disease to the brain from 2- and 6-cm primary tumors were .14 (95% confidence interval: .06, .27) and .72 (95% confidence interval: .48, .88), respectively (P < .02). CONCLUSION: The probability of metastatic disease to the brain from primary NSCLC is correlated with size of the primary tumor, cell type, and intrathoracic lymph node stage.

Adult↗

Expression profiling and lung cancer development.

Recent lung cancer research has been directed to using molecular approaches to facilitate early diagnosis, to identify clinically relevant biological factors associated with histologic heterogeneity, and to identify novel therapeutic agents. This research takes advantage of technical advances that allow rapid high throughput assays to interrogate the genome, proteome, and epigenome. In this review of gene expression profiling in lung carcinogenesis, we will focus upon recent advances in the understanding of malignant transformation of lung epithelial cells and of lung cancer differentiation and progression. These studies have provided important information about the genomic alterations of tobacco smoke-associated airway field carcinogenesis and about the developmental pathways that mediate lung tumor invasion and histologic differentiation in response to injury.

Adenocarcinoma↗

Expression of Aedes trypsin-modulating oostatic factor on the virion of TMV: A potential larvicide.

We report the engineering of the surface of the tobacco mosaic virus (TMV) virion with a mosquito decapeptide hormone, trypsin-modulating oostatic factor (TMOF). The TMV coat protein (CP) was fused to TMOF at the C terminus by using a read-through, leaky stop codon that facilitated expression of CP and chimeric CP-TMOF (20:1 ratio) that were coassembled into virus particles in infected Nicotiana tabacum. Plants that were infected with the hybrid TMV RNA accumulated TMOF to levels of 1.3% of total soluble protein. Infected tobacco leaf discs that were fed to Heliothis virescens fourth-instar larvae stunted their growth and inhibited trypsin and chymotrypsin activity in their midgut. Purified CP-TMOF virions fed to mosquito larvae stopped larval growth and caused death. Because TMV has a wide host range, expressing TMV-TMOF in plants can be used as a general method to protect them against agricultural insect pests and to control vector mosquitoes.

Aedes↗

Epigenetic inactivation of Betaig-h3 gene in human cancer cells.

Gene silencing by CpG island methylation in the promoter region is one of the mechanisms by which tumor suppressor genes are inactivated in human cancers. It has been shown previously that Betaig-h3 gene, which encodes an extracellular matrix protein involved in cell adhesion and tumorigenesis, is down-regulated or silenced in a variety of human cancer cell lines. To unravel the underlying molecular mechanism(s) for this phenomenon, DNA methylation patterns of Betaig-h3 CpG island were examined in normal, immortalized, and cancer cell lines derived from lung, prostate, mammary, and kidney. A good correlation was observed between promoter hypermethylation and lost expression of Betaig-h3 gene, which was supported by the data that demethylation of promoter by 5-aza-2'-deoxycytidine reactivated Betaig-h3 and restored its expression in Betaig-h3-silenced tumor cell lines. This result was further substantiated by a luciferase reporter assay, showing the restoration of promoter activities and increased response to transforming growth factor-beta treatment in Betaig-h3-negative 293T cells when transfected with unmethylated Betaig-h3 promoter. In contrast, activity of Betaig-h3 promoter was completely inactivated by in vitro methylation. Furthermore, CpG methylation of Betaig-h3 promoter was also shown in primary lung tumors that expressed decreased level of Betaig-h3 protein. These results suggest that promoter methylation plays a critical role in promoter silencing of the Betaig-h3 gene in human tumor cells.

Azacitidine↗

Combined endodontic-periodontic treatment of a palatal groove: a case report.

The palatal groove is a developmental anomaly that predisposes the tooth involved to a severe periodontal defect. When further complicated by pulp necrosis, these grooves often present a diagnostic and treatment planning challenge that requires an interdisciplinary treatment approach. This case report describes the successful collaborative management of a maxillary lateral incisor with an extensive palatal groove using a combination of nonsurgical endodontic therapy, odontoplasty, and periodontal regenerative techniques.

Adult↗

Genome sequence and molecular characterization of Homalodisca coagulata virus-1, a novel virus discovered in the glassy-winged sharpshooter (Hemiptera: Cicadellidae).

The complete nucleotide sequence of a novel single-stranded RNA virus infecting the glassy-winged sharpshooter, Homalodisca coagulata, has been determined. In silico analysis of H. coagulata virus-1 (HoCV-1) revealed a 9321-nt polyadenylated genome encoding two large open reading frames (ORF1 and ORF2) separated by a 182-nt intergenic region (IGR). The deduced amino acid sequence of the 5'-proximal ORF (ORF1, nt 420-5807) exhibited conserved core motifs characteristic of the helicases, cysteine proteases, and RNA-dependent RNA polymerases of other insect-infecting picorna-like viruses. A structural model created using Mfold exposed a series of stem loop (SL) structures immediately preceding the second ORF which are analogous to an internal ribosome entry site (IRES), suggesting that ORF2 begins with a noncognate GCA triplet rather than the canonical AUG. This 3' ORF2 (5990-8740) showed significant similarity to the structural proteins of members of the family Dicistroviridae, particularly those belonging to the genus Cripavirus. Evidence demonstrating relatedness of these viruses regarding genome organization, amino acid sequence similarity, and putative replication strategy substantiate inclusion of HoCV-1 into this taxonomic position.

Amino Acid Sequence↗

Palatal neurofibroma associated with localized periodontitis.

BACKGROUND: Neurofibromatosis type 1 (NF1) is the most common form of neurofibromatosis. While typically considered a dermatologic disorder, intraoral signs of neurofibromatosis occur quite commonly. This clinical entity can be confused with periodontitis because of the presence of periodontal pockets. In this report, we present the case of a palatal neurofibroma with radiographic involvement in a patient with NF1. METHODS: A 40-year-old female patient was referred from her general dentist to evaluate advanced periodontitis in the maxillary left quadrant. The patient's medical history was significant for a soft tissue lesion excised from her back 11 years previously and diagnosed as a neurofibroma. Subsequent medical examination at that time confirmed a systemic diagnosis of NF1. A comprehensive periodontal evaluation was performed, and panoramic and periapical radiographs were taken. Teeth were tested for vitality. An incisional biopsy was completed for histopathologic examination. RESULTS: The periodontal evaluation revealed the presence of 6 to 9 mm probing depths adjacent to teeth #14 and #15. Panoramic and periapical radiographs showed a circumscribed 0.8x0.9-cm unilocular radiolucency superimposed over the root of tooth #13 and extensive horizontal bone loss on the distal side of #15. Incisional biopsy confirmed the presence of a neurofibroma, and because of the extent of the lesion, the patient was referred to the Oral and Maxillofacial Surgery service for complete excision. CONCLUSIONS: Neurofibromas can cause extensive destruction of alveolar bone, mimicking periodontitis. Due to the potential systemic and genetic implications, the diagnosis of neurofibroma requires appropriate medical referral.

Adult↗

Clinical reliability of the "furcation arrow" as a diagnostic marker.

BACKGROUND: The radiographic entity known as the "furcation arrow" has long been used in practice even though little is known about its usefulness as a clinical indicator. The definitive study of the furcation arrow suggests that its presence on a radiograph reliably predicts furcation invasion, but this has not been confirmed in an in vivo investigation. The purpose of this study was to evaluate the furcation arrow in a clinical setting, testing the assertion that the furcation arrow image is an accurate predictor of furcation invasion. Specifically, we sought to determine the following. First, what is the prevalence of furcation arrow images in the radiographs of maxillary molars with periodontitis? Second, what is the interexaminer agreement on what constitutes a furcation arrow? Third, how does the presence or absence of a furcation arrow correlate with the true clinical status of the furcation? Fourth, what is the sensitivity and specificity of the furcation arrow as a diagnostic indicator? METHODS: Eighty-nine patients requiring surgical treatment of periodontitis in the maxillary molar regions were included in this study. Before surgery, one of five calibrated examiners viewed periapical and bitewing radiographs of the surgical site and recorded the presence or absence of a furcation arrow at each proximal furcation. Before administering anesthesia, the same examiner recorded a Hamp index value of each proximal furcation, with a second Hamp index taken after flap reflection and debridement. After surgery, each of the four remaining examiners independently reviewed the radiographs for furcation arrows. Descriptive statistical analysis was performed to correlate the appearance of the furcation arrow image to the actual degree of furcation invasion as determined by the intrasurgical Hamp index. RESULTS: A total of 164 maxillary molars were examined, providing 328 interproximal furcations; 111 (33.8%) furcations were determined at surgical debridement to have a furcation invasion of Hamp degree 1 or greater. Of the 111 furcation invasions, 43 (38.7%) were predicted by a furcation arrow image seen by at least three of the five examiners. When comparing the appearance of the radiographic image to the extent of furcation invasion, 20 of 64 (31.3%) Hamp 1 furcation invasions and 23 of 47 (48.9%) Hamp 2 and 3 furcation invasions were predicted by furcation arrows observed by at least three of five examiners. The multirater kappa statistic for interexaminer agreement on the presence or absence of the image was 0.489. The sensitivity of the furcation arrow image as a diagnostic marker was 38.7%, and the specificity was 92.2%; the positive predictive value of the image was 71.7%, and the negative predictive value was 74.6%. Of the 324 furcations used to compare clinical indices, the agreement of preanesthesia and postdebridement Hamp indices was 0% for degree 3, 83.7% for degree 2, and 98.4% for degree 1 furcation lesions. CONCLUSIONS: These data suggest that the furcation arrow has limited usefulness as a diagnostic marker of furcation invasion. The image is difficult to interpret and highly subjective and can correctly predict furcation invasions only approximately 70% of the time when present on the radiograph. In addition, when furcation invasions are truly present, the furcation arrow is seen in <40% of sites.

Furcation Defects↗

Lung adenocarcinoma global profiling identifies type II transforming growth factor-beta receptor as a repressor of invasiveness.

RATIONALE: Lung adenocarcinoma histology and clinical outcome are heterogeneous and associated with tumor invasiveness. OBJECTIVES: We hypothesized that invasiveness is associated with a distinct molecular signature and that genes differentially expressed in tumor or adjacent stroma will identify cell surface signal transduction and matrix remodeling pathways associated with the acquisition of invasiveness in lung adenocarcinoma. MAIN RESULTS: Microarray analysis of microdissected noninvasive bronchioloalveolar carcinoma (BAC) and invasive adenocarcinoma and adenocarcinoma-mixed type with BAC features identified transcriptional profiles of lung adenocarcinoma invasiveness. Among the signature set that was lower in adenocarcinoma-mixed compared with BAC was the type II transforming growth factor beta (TGF-beta) receptor, suggesting downregulation of TGFbetaRII is an early event in lung adenocarcinoma metastasis. Immunostaining in independently acquired specimens demonstrated a correlation between TbetaRII expression and length of tumor invasion. Repression of TGFbetaRII in lung cancer cells increased tumor cell invasiveness and activated p38 mitogen-activated protein kinases. Microarray analysis of invasive cells identified potential downstream mediators of TGFbetaRII with differential expression in lung adenocarcinomas. CONCLUSIONS: The repression of type II TGF-beta receptor may act as a significant determinant of lung adenocarcinoma invasiveness, an early step in tumor progression toward metastasis.

Adenocarcinoma↗

P16 loss and mitotic activity predict poor survival in patients with peritoneal malignant mesothelioma.

PURPOSE: Peritoneal malignant mesothelioma is an aggressive neoplasm for which intensive therapy improves survival in a subset of patients. We hypothesized that pathologic variables would stratify patients into favorable and unfavorable survival subgroups. EXPERIMENTAL DESIGN: Fifty-four patients with peritoneal malignant mesothelioma were evaluated for trimodal therapy from 1995 to 2003. Two pathologists evaluated pathologic variables independently, and p16 status was analyzed by immunohistochemistry. RESULTS: Patients not receiving trimodal therapy had a significantly increased risk of death [hazard ratio (HR), 9.6; 4.3-21.6; P < 0.0001]. Biphasic histology was also associated with increased risk of death (HR, 8.5; 3.4-21.8; P < 0.0001). In multivariate analysis adjusting for treatment modality and histologic type, high mitotic rate and p16 loss were associated with increased risk of death (HR, 3.074; 1.05-9.0; P < 0.04 and HR, 3.65; 1.3-10.2; P < 0.014, respectively). CONCLUSIONS: Biphasic histology, increased mitotic rate, and p16 loss were independently associated with poorer survival in peritoneal malignant mesothelioma. Among the trimodal treated patients, increased mitotic rate was associated with increased risk of death.

Adult↗

Utility of CD138 (syndecan-1) in distinguishing carcinomas from mesotheliomas.

CD138 (Syndecan-1) is a transmembrane heparan sulfate proteoglycan present on the surface of plasma cells and epithelial cells. CD138 is also expressed in some hematopoietic neoplasms and has recently been observed in carcinomas. We characterized CD138 expression in cell-block preparations of fluids/effusions, focusing on the distinction between carcinoma and mesothelioma. One hundred formalin-fixed, paraffin-embedded cell-block sections of fluids/effusions consisting of 58 metastatic carcinomas, 24 mesotheliomas, 11 reactive mesothelial cell proliferations, 3 lymphomas, 3 metastatic sarcomas, and 1 metastatic melanoma were stained with a monoclonal antibody against CD138. CD138 staining was observed in 32/58 (55%) metastatic carcinomas and 2/24 (8%) mesotheliomas; all reactive mesothelial cells, lymphomas, sarcomas, and melanoma were negative. CD138 is a highly specific marker in the differential diagnosis of carcinoma vs. mesothelioma. Distinct membranous staining without background staining of most inflammatory cells makes CD138 an ideal marker for cell-block preparations of fluids/effusions. It should be an integral component of the epithelial-mesothelial antibody panel.

Biomarkers, Tumor↗

CDX2 immunostaining as a gastrointestinal marker: expression in lung carcinomas is a potential pitfall.

Paraffin-embedded sections of various adenocarcinomas (13 colonic, 11 mucinous ovarian, 5 serous ovarian, 8 pancreatic, 6 ampullary, 12 gastric, 5 esophageal, 10 endometrial, 29 breast, and 55 lung) and 29 additional lung carcinomas (nonadenocarcinomas) were immunostained with antibodies to CDX2 protein, cytokeratin 7 (CK7), and cytokeratin 20 (CK20). The 84 lung carcinomas were also stained with antibody to thyroid transcription factor-1 (TTF-1). All colorectal and most ovarian mucinous carcinomas were strongly and diffusely immunoreactive for CDX2. Esophageal, gastric, and ampullary adenocarcinomas showed variable immunoreactivity for CDX2. All breast, nonmucinous ovarian, and most endometrial and pancreatic adenocarcinomas showed no immunoreactivity for CDX2. CK7 and CK20 expression was similar to previous reports. Ten of 84 primary lung carcinomas (12%) were immunoreactive for CDX2 expression. Of these, 5 (4 adenocarcinomas and 1 large cell carcinoma) were reactive for TTF-1. Gene expression profiling data--available for 32 of these 84 tumors--showed CDX2 gene expression in 7 of 8 (88%) CDX2 immunoreactive tumors whereas only 1 of 24 (4%) tumors negative for CDX2 immunoreactivity showed CDX2 gene expression. The authors conclude that CDX2 is a relatively specific marker for tumors with intestinal differentiation, with the caveat that its expression can be seen in primary large cell and adenocarcinomas of the lung and mucinous carcinomas of the ovary.

Adenocarcinoma↗

Differential transcriptional activity of plant-pathogenic begomoviruses in their whitefly vector (Bemisia tabaci, Gennadius: Hemiptera Aleyrodidae).

Plant-pathogenic begomoviruses have a complex association with their whitefly vector and aspects concerning virus genetic activity (genome replication and gene transcription) within the insect remain highly controversial. Virus transcript abundance was assessed by quantifying selected gene transcripts of Tomato mottle virus (ToMoV, a New World bipartite begomovirus) and Tomato yellow leaf curl virus (TYLCV, an Old World monopartite begomovirus) in whiteflies (Bemisia tabaci biotype B) after feeding on virus-infected tomato plants and after subsequent transfer to cotton, a plant that is immune to the selected begomoviruses. Real-time RT-PCR was performed using specific primers for three ToMoV genes (AV1, BC1 and BV1) and three TYLCV genes (V1, V2 and C3). The ToMoV gene transcripts rapidly became undetectable in whiteflies following transfer from tomato to cotton, probably because degradation was not accompanied by new synthesis. On the other hand, TYLCV transcripts increased after transfer of whiteflies to cotton, indicating active TYLCV transcription. Interestingly, the difference observed in ToMoV and TYLCV transcripts in the vector parallel observations on the different biological effects of these viruses on whiteflies, i.e. TYLCV, but not ToMoV, reduces whitefly fitness.

Animals↗

Post-surgical infections: prevalence associated with various periodontal surgical procedures.

BACKGROUND: Of the various adverse outcomes that may be encountered following periodontal surgery, the risk of infection stands at the forefront of concern to the surgeon, since infection can lead to morbidity and poor healing outcomes. This paper describes a large-scale retrospective study of multiple surgical modalities in a diverse periodontal practice undertaken to explore the prevalence of clinical infections post-surgically and the relationship between diverse treatment variables and infection rates. METHODS: A retrospective review of all available periodontal surgical records of patients treated in the Department of Periodontics at Wilford Hall Medical Center, San Antonio, Texas, was conducted. The sample comprised 395 patients and included 1,053 fully documented surgical procedures. Surgical techniques reviewed included osseous resective surgery, flap curettage, distal wedge procedures, gingivectomy, root resection, guided tissue regeneration, dental implant surgery, epithelialized free soft tissue autografts, subepithelial connective tissue autografts, coronally positioned flaps, sinus augmentations, and ridge preservation or augmentation procedures. Infection was defined as increasing and progressive swelling with the presence of suppuration. The impact of various treatment variables was examined including the use of bone grafts, membranes, soft tissue grafts, post-surgical chlorhexidine rinses, systemic antibiotics, and dressings. Results were analyzed using Fisher's exact test and Pearson's chi-square test. RESULTS: Of the 1,053 surgical procedures evaluated in this study, there were a total of 22 infections for an overall prevalence of 2.09%. Patients who received antibiotics as part of the surgical protocol (pre- and/ or post-surgically) developed eight infections in 281 procedures (2.85%) compared to 14 infections in 772 procedures (1.81%) where antibiotics were not used. Procedures in which chlorhexidine was used during post-surgical care had a lower infection rate (17 infections in 900 procedures, 1.89%) compared to procedures after which chlorhexidine was not used as part of post-surgical care (five infections in 153 procedures, 3.27%). The use of a post-surgical dressing demonstrated a slightly higher rate of infection (eight infections in 300 procedures, 2.67%) than non-use of a dressing (14 infections in 753 procedures, 1.86%). Despite these trends, no statistically significant relationship was found between post-surgical infection and any of the treatment variables examined, including the use of perioperative antibiotics. CONCLUSIONS: The results of this study confirm previous research demonstrating a low rate of postoperative infection following periodontal surgical procedures. Although perioperative antibiotics are commonly used when performing certain regenerative and implant surgical procedures, data from this and other studies suggest that there may be no benefit in using antibiotics for the sole purpose of preventing post-surgical infections. Further large-scale, controlled clinical studies are warranted to determine the role of perioperative antibiotics in the prevention of periodontal post-surgical infections.

Alveolar Ridge Augmentation↗

Expression of syndecan-1 and expression of epidermal growth factor receptor are associated with survival in patients with nonsmall cell lung carcinoma.

BACKGROUND: Recently, the authors identified molecular signatures and pathways associated with nonsmall cell lung carcinoma histology and lung development. They hypothesized that genetic classifiers of histology would provide insight into lung tumorigenesis and would be associated with clinical outcome when evaluated in a broader set of specimens. METHODS: Associations between patient survival and immunostaining for 11 representative histologic classifiers (epidermal growth factor receptor [EGFR], CDK4, syndecan-1, singed-like, TTF-1, keratin 5, HDAC2, docking protein 1, integrin alpha3, P63, and cyclin D1) were examined using a tissue microarray constructed from nonsmall cell lung carcinoma specimens. RESULTS: Sixty-three tumors were examined, including 43 adenocarcinomas, 11 large cell carcinomas, and 9 squamous cell carcinomas. Sixty-three percent of tumors were clinical Stage I lesions, and 37% were Stage II-III lesions. In a multivariate analysis that controlled for age, gender, and race, syndecan-1 expression was found to be associated with a significant reduction in the risk of death (hazard ratio, 0.31 [95% confidence interval, 0.18-0.87]; P < 0.05). Multivariate analysis also indicated that EGFR expression was associated with a significant reduced risk of death. CONCLUSIONS: The authors demonstrated that expression of either of the nonsmall cell lung carcinoma subtype classifiers syndecan-1 and EGFR was associated with a 30% reduction in the risk of death, with this reduction being independent of histology and other confounders. The results of the current study suggest that loss of expression of these histologic classifiers is associated with biologic aggressiveness in lung tumors and with poor outcome for patients with such tumors. If their significance can be validated prospectively, these biomarkers may be used to guide therapeutic planning for patients with nonsmall cell lung carcinoma.

Adenocarcinoma↗

Molecular signatures in biopsy specimens of lung cancer.

Gene expression profiles of resected tumors may predict treatment response and outcome. We hypothesized that profiles derived from lung tumor biopsies would discriminate tumor-specific gene signatures and provide predictive information about outcome. Lung carcinoma specimens were obtained from 23 patients undergoing computed tomography-guided transthoracic biopsy or endobronchial brushing for undiagnosed nodules. Excess tissue was processed for gene profiling. We built class prediction models for lung cancer histology and for cancer outcome. The histology model used an F test to identify 99 genes that were differentially expressed among lung cancer subtypes. The histology validation set class prediction accuracy rate was 86%. The outcome model used the maximum difference subset algorithm to identify 42 genes associated with high risk for cancer death. The outcome training set class prediction accuracy rate was 87%. In conclusion, gene expression profiles of biopsy specimens of lung cancers identify unique tumoral signatures that provide information about tissue morphology and prognosis. The use of specimens acquired from lung biopsy procedures to identify biomarkers of clinical outcome may have application in the management of patients with lung cancer. The procedures are safe and feasible; the efficacy and utility of this strategy will ultimately be determined by prospective clinical trials.

Adult↗

Osseous surgery for crown lengthening: a 6-month clinical study.

BACKGROUND: Despite the fact that surgical crown lengthening is a commonly performed treatment, little is known about the specific surgical endpoints of the procedure or the stability of the newly attained crown height over time. Recent clinical reports have ranged across a spectrum from significant tissue rebound to remarkable stability using similar surgical techniques. The purpose of this study was to assess the stability of surgical crown lengthening procedures performed by various surgeons using specific guidelines to determine surgical endpoints. Specifically, we sought to determine the following: 1) What is the immediate increase in clinical crown height following surgery? 2) How stable is the established crown length over a 6-month period? 3) How much supporting bone is removed to establish the new crown length? 4) How does the position of the flap margin relative to the alveolar bone at surgical closure relate to the stability of crown height? METHODS: Twenty-five patients requiring crown lengthening of 43 teeth were included in this study. Clinical indices recorded at eight sites on each molar and six sites on each premolar included plaque, bleeding on probing, probing depth, and relative attachment level from a customized probing stent. Surgical measurements at the same sites included the distance from stent to alveolar bone both before and after osseous surgery and the distance from flap margin to alveolar bone after suturing. Clinical measurements were repeated at 1, 3, and 6 months after surgery. Sites were divided into three groups. All sites on teeth targeted for crown lengthening were labeled treated sites (TT). Interproximal sites on neighboring teeth were labeled adjacent (AA) if they shared a proximal surface with a treated tooth and nonadjacent (AN) if they were on the opposite side, away from the treated tooth. RESULTS: Throughout the entire 6-month healing period, descriptive statistics revealed no significant time or group differences in plaque and bleeding scores. At treated sites, the mean gain of crown height at surgery was 2.27 +/- 1.1 mm. This was reduced to 1.91 +/- 1.08 mm at 1 month, 1.69 +/- 1.02 mm at 3 months, and 1.57 +/- 1.01 mm at 6 months. At adjacent sites, the gain of crown length was 2.18 +/- 0.98 mm, 1.61 +/- 0.98 mm, 1.43 +/- 0.96 mm, and 1.30 +/- 0.96 mm at surgery, 1, 3, and 6 months, respectively. At non-adjacent sites the crown height increased 1.06 +/- 1.07 mm, 1.00 +/- 0.93 mm, 0.84 +/- 1.00 mm, and 0.76 +/- 0.85 mm, respectively. These mean measurements were significantly different for each treatment group at each time interval and appeared not to have stabilized between 3 and 6 months. The mean osseous reduction at treated, adjacent, and non-adjacent sites was 1.13 +/- 0.90 mm, 0. 78 +/- 0.75 mm, and 0.065 +/- 0.69 mm, respectively. Frequency distribution of osseous reduction demonstrated that 23.6% of treated sites had 0 mm, 44.3% had 1 mm, 25.4% had 2 mm, 6.2% had 3 mm, and less than I % had > or = 4 mm of bone removed to establish crown height More bone removal was noted at premolar than at molar sites; however, this was not statistically significant. When tissue rebound following surgery was plotted against post-surgical flap position, it was noted that the closer the flap margin was sutured to the alveolar crest, the greater the tissue rebound during the post-surgical period. This rebound ranged from 1.33 +/- 1.02 mm when the flap was sutured < or = 1 mm from the alveolar crest, to -0.16 +/- 1.15 mm when the flap was sutured > or = 4 mm from the alveolar crest. CONCLUSIONS: These data suggest that there is a significant tissue rebound following crown-lengthening surgery that has not fully stabilized by 6 months. The amount of tissue rebound seems related to the position of the flap relative to the alveolar crest at suturing. These findings support the premise that clinicians should establish proper crown height during surgery without overreliance on flap placement at the osseous crest.

Alveolar Process↗