Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DEFECTIVES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,351 records · Page 75Linked to original sources

Egg-laying defective mutants of the nematode Caenorhabditis elegans.

We have isolated 145 fertile mutants of C. elegans that are defective in egg laying and have characterized 59 of them genetically, behaviorally and pharmacologically. These 59 mutants define 40 new genes called egl. for egg-laying abnormal. Most of the other mutants are defective in previously identified genes. The egl mutants differ with respect to the severity of their egg-laying defects and the presence of behavioral or morphological pleiotropies. We have defined four distinct categories of mutants based on their responses to the pharmacological agents serotonin and imipramine, which stimulate egg laying by wild-type hermaphrodites. These drugs test the functioning of the vulva, the vulval and uterine muscles and the hermaphrodite-specific neurons (HSNs), which innervate the vulval muscles. Mutants representing 14 egl genes fail to respond to serotonin and to imipramine and are likely to be defective in the functioning of the vulva or the vulval and uterine muscles. Four mutants (representing four different genes) lay eggs in response to serotonin but not to imipramine and appear to be egg-laying defective because of defects in the HSNs; three of these four were selected specifically for these drug responses. Mutants representing seven egl genes lay eggs in response to serotonin and to imipramine. One egl mutant responds to imipramine but not to serotonin. The remaining egl mutants show variable or intermediate responses to the drugs. Two of the HSN-defective mutants, egl-1 and her-1(n695), lack HSN cell bodies and are likely to be expressing the normally male-specific program of HSN cell death. Whereas egl-1 animals appear to be defective specifically in HSN development, her-1(n695) animals exhibit multiple morphological pleiotropies, displaying partial transformation of the sexual phenotype of many cells and tissues. At least two of the egl mutants appear to be defective in the processing of environmental signals that modulate egg laying and may define new components of the neural circuitry that control egg laying.

Animals↗

Mismatch repair defects in human carcinogenesis.

Mismatch repair defects are carcinogenic. This conclusion comes some 80 years after the original description of a type of familial colorectal cancer in which mismatch repair defects are involved, and from decades of dedicated basic science research into fundamental mechanisms cells use to repair their DNA. Mismatch repair (MMR) was described first in bacteria, later in yeast and finally in higher eukaryotes. In bacteria, one of its roles is the rapid repair of replicative errors thereby providing the genome with a 100-1000-fold level of protection against mutation. It also guards the genome by preventing recombination between non-homologous regions of DNA. The information gained from bacteria suddenly became relevant to human neoplasia in 1993 when the RER phenotype of microsatellite instability was discovered in human cancers and was rapidly shown to be due to defects in mismatch repair. Evidence supporting the role of MMR defects in carcinogenesis comes from a variety of independent sources including: (i) theoretical considerations of the requirement for a mutator phenotype as a step in multistage carcinogenesis; (ii) discovering that MMR defects cause a 'mutator phenotype' destabilizing endogenous expressed genes including those integral to carcinogenesis; (iii) finding MMR defects in the germline of HNPCC kindred members; (iv) finding that such defects behave as classic tumor suppressor genes in both familial and sporadic colorectal cancers; (v) discovering that MMR 'knockout' mice have an increased incidence of tumors; and (vi) discovering that genetic complementation of MMR defective cells stabilizes the MMR deficiency-associated microsatellite instability. Models of carcinogenesis now must integrate the concepts of a MMR defect induced mutator phenotype (Loeb) with the concepts of multistep colon carcinogenesis (Fearon and Vogelstein) and clonal heterogeneity/selection (Nowell).

Animals↗

The clinical correlates of articular cartilage defects in symptomatic knee osteoarthritis: a prospective study.

OBJECTIVES: To determine whether articular cartilage defects are associated with cartilage loss and joint replacement in subjects with symptomatic knee osteoarthritis (OA). METHODS: One hundred and seventeen subjects with symptomatic knee OA underwent magnetic resonance imaging of their dominant knee at baseline and 2 yr later. Cartilage defects were identified as prevalent (defect score > or =2) in each knee compartment. Occurrence of joint replacement by 4 yr was documented. RESULTS: Cartilage defects were present in 81% of medial, 64% of lateral tibiofemoral compartments and 55% of patellar cartilages. Annual patellar cartilage loss was highest in those with defects compared with no defects (5.5% vs 3.2%, P = 0.01). Tibial cartilage loss was not associated with defects in the medial (4.6% vs 5.8%, P = 0.42) or lateral (4.7% vs 6.5%, P = 0.21) tibial cartilages. Higher total cartilage defect scores (8-15) were associated with a 6.0-fold increased risk of joint replacement over 4 yr compared with those with lower scores (2-7) (95% confidence interval 1.6, 22.3), independently of potential confounders. CONCLUSIONS: Articular cartilage defects are associated with disease severity in knee OA and predict patellar cartilage loss and knee replacement.

Aged↗

Paternal age and the risk of birth defects in offspring.

Previous studies have shown that advanced paternal age is associated with an increase in new dominant mutations that may result in some rare congenital anomalies or syndromes in the offspring. Nevertheless, few epidemiologic studies have evaluated the effect of paternal age on the risk of more common birth defects. We examined data from the British Columbia Health Surveillance Registry, which included a total of 9,660 cases of birth defects (22 specific defect groups). We chose matched controls from the birth files of British Columbia (1952-1973). With the exception of an unusual change in direction in the 45-49 years age category, we found a general pattern of increasing relative risk estimates (adjusted for maternal age and other factors) with increasing paternal age for neural tube defects, congenital cataracts, reduction defects of the upper limb, and Down syndrome. For example, the adjusted relative risk estimates for neural tube defects in the offspring were 1.2 (for fathers age 30-34 years relative to 25-29 years); 1.3 (35-39); 1.6 (40-44); 0.6 (45-49); and 2.3 (men 50 years and older). Men under 20 years of age were also at increased risk for fathering children with birth defects such as neural tube defects, hypospadias, cystic kidney, and Down syndrome. We hypothesize that among certain commonly observed birth defects a subgroup of cases may be due to new, unrecognized dominant mutations.

Adult↗

Maternal fever, multivitamin use, and selected birth defects: evidence of interaction?

BACKGROUND: Multivitamin use has been associated with lower risks for some birth defects. We evaluated whether multivitamin use modified birth defect risks associated with febrile illness, a common and possibly teratogenic exposure. METHODS: From the population-based Atlanta Birth Defects Case-Control Study (1968-1980) we selected seven defects (neural tube defects, cleft lip and palate, cardiac outflow tract defects, ventricular septal defects, atrial septal defects, omphalocele, and limb deficiencies) because of their inverse relation with multivitamin supplement use documented in previous analyses. We defined four exposure categories from combinations of multivitamin use (periconceptional use compared with no use) and febrile illness (early pregnancy compared with no illness). The reference category was no multivitamin use and no illness. RESULTS: Febrile illness with no multivitamin use was associated with generally increased risk for the seven defects and the combined group (odds ratio = 2.1, 1.7, 1.5, 1.9, 2.9, 4.4, 3.3, and 2.3, respectively). With multivitamin use, however, the risk estimates associated with febrile illness were generally lower (odds ratio = 0.6, 1.1, 0.0, 1.5, 0.0, 0.8, 0.0, and 0.8, respectively). Some of the associated 95% confidence intervals included one. CONCLUSIONS: The pattern of findings suggests that multivitamin use might decrease the risk associated with febrile illness.

Case-Control Studies↗

Residence near power lines and the risk of birth defects.

BACKGROUND: There has been some concern that exposure to electromagnetic fields may cause birth defects. We studied risks of birth defects by residential exposure to 50-Hz magnetic fields from power lines. METHODS: We estimated the distance between residence and power lines for 161,844 Norwegian residences, and their corresponding magnetic fields in the period 1980 to 1997. Risks of 24 categories of birth defects were compared across exposure levels, adjusting for social and demographic variables. RESULTS: Among those living near power lines, the greatest reductions in risk were for cardiac defects (odds ratio = 0.5; 95% confidence interval = 0.3-0.9) and respiratory defects (0.4; 0.2-0.9). The largest increase in risk was for esophageal defects (2.5; 1.0-5.9). Other associations were weaker and had wide confidence intervals. CONCLUSIONS: There was little evidence that residence near power lines affected the risk of birth defects. The observed decreased risks of cardiac and respiratory defects and the increased risk of esophageal defects should be interpreted with caution given the number of endpoints, the imprecision in the calculations of the distance from the residence to the power line, and the limited information on pregnant women's change of residence.

Abnormalities, Radiation-Induced↗

Importance of the critical-size bone defect in testing bone-regenerating materials.

A substantial interest exists in developing substitute materials and human recombinant bone-inducing factors to enhance bone regeneration both in the craniofacial complex and in other parts of the skeleton. A persistent problem has been to find an animal model that allows for the comparison of different osteopromotive materials. The purpose of this investigation was 1) to determine whether a 5-mm calvarial defect in adult rats fulfilled the requirements of a critical-size bone defect and 2) to discuss the use of this animal model in assessing bone repair in the craniofacial region. Bilateral full-thickness calvarial defects were trephined in the calvarial bone of 56 5- to 6-month-old Wistar rats. Except for minor amounts of bone formation limited to the margins of the defect, none of the defects revealed any signs of spontaneous bone regeneration 6 and 12 months after surgery. The full-thickness 5-mm calvarial defects thus fulfill the criteria for a critical-size bone defect. This animal model allows for an experiment with a paired design, it avoids inclusion of the sagittal suture in the osseous defect, and it thereby minimizes morbidity by reducing the risk of damaging the midsagittal sinus. An adequate experimental model has been developed to evaluate the efficiency of osteopromotive materials in the healing of bone defects in the craniomaxillofacial region.

Animals↗

Tissue-engineered bone repair of sheep cranial defects with autologous bone marrow stromal cells.

Cranial bone defect remains a major challenge to craniofacial surgeons because of limited availability of autologous bone graft to repair the defects and the donor site defects secondary to tissue harvesting. In contrast, tissue-engineering technique can generate a large bone tissue using small amount of autologous cells and therefore avoid these problems. Bone Marrow Stromal Cells (MSCs) have the potential of multi-lineage (including osteogenic) differentiation. The objective of this study was to investigate the potential of using autologous MSCs to repair cranial bone defects by a tissue-engineering approach. Autologous MSCs were isolated from eight adult sheep respectively and were in vitro expanded and induced to become osteogenic cells. Bilateral full-thickness defects (20 mm in diameter) of parietal bones were created in animals and the bone defects were either repaired with the bone implants constituted with MSCs and calcium alginate at the experimental side (n = 8) or treated with calcium alginate only without MSCs (n = 4) or left unrepaired (n = 4) at the control side. New bone tissues were observed either grossly or histologically at the defects of experimental group as early as 6 weeks post-repairing, but not in control groups. The engineered bone tissue became more mature at 18 weeks post-repairing. Three-dimensional computerized tomography (CT) scan revealed an almost complete repair of the defect of experimental group at 18 weeks. This study may provide insight for future clinical repair of cranial defect.

Alginates↗

Hepatic scan defects following radiotherapy for lymphoma.

Twenty-one patients with lymphoma were evaluated for the presence of hepatic scan defects following radiotherapy to fields which included the left lobe of the liver. Two distinct patterns of hepatic scan defects were noted: (a) a radiation port defect (Type I), and (b) attenuation of the left lobe (Type II). Five of seven patients evaluated within six weeks after radiotherapy demonstrated Type I defects but all seven subsequently developed Type II defects. Seventeen of the 21 patients developed Type II defects which have persisted (follow-up, up to 66 months). These characteristic defects should not be confused with other causes of hepatic scan defects in evaluating patients with lymphoma. The defects occur in a high percentage of patients and may persist for long periods.

Diagnosis, Differential↗

Critical size defect in the goat's os ilium. A model to evaluate bone grafts and substitutes.

Bone defects and their treatment are a well known problem in orthopaedic surgery. A critical size defect is a suitable model to study bone replacement materials. This study describes a critical size defect in the goal and the evaluation of three bone fillers (particulate autograft, particulate allograft, and a polyethylene oxide/polybutylene terephthalate copolymer) in this defect. The goat allows for implantation of large implants and has a metabolic rate more comparable with that of humans than small animals. The critical size defect, located in the goat's iliac wing, is easily reproducible and allows qualitative and quantitative evaluation of bone grafts and bone graft substitutes. After 3 months of healing, the unfilled defects showed 13.5% bone in the defect, the autografted defects 36.3%, and the allografted 18.5%. The copolymer gave only 1.5% bone in the defect; this is in contrast to previous reports. The described model allows for the evaluation of bone graft substitutes before introduction into clinical practice.

Animals↗

Biomechanical study of pins in cementing of contained proximal tibia defect.

Defects from curettage for giant cell tumors of bone frequently have been reconstructed with bone cement with or without reinforcement pins. The biomechanical basis for the addition of reinforcement pins was examined using a model of a contained defect in the proximal tibia. Fifty-four cadaveric proximal tibia in matched pairs were divided into five test groups: intact tibia, medial metaphyseal contained defect, defect reconstructed with cement alone, defect reconstructed with cement and pins inserted within the medullary canal, and defect reconstructed with cement and pins inserted through the cortex. Specimens were tested to failure during one cycle of compressive loading. Defect specimens were significantly weaker and less stiff than intact specimens, establishing the validity of the model-contained defects. For the reconstructions, there was no statistically significant difference in load to failure, stiffness, energy to failure, or displacement for the polymethylmethacrylate treatment alone when compared with matched specimen receiving polymethylmethacrylate and pins treatment. Similarly, there was no statistical difference in biomechanical properties in comparing matched specimens treated with polymethylmethacrylate alone or polymethylmethacrylate/pins (cortex). For contained defects of the proximal tibia that are typical after curettage for giant cell tumor, there appears to be no biomechanical advantage to use of reinforcement pins in the cement.

Biomechanical Phenomena↗

Bone regeneration with resorbable polymeric membranes: treatment of diaphyseal bone defects in the rabbit radius with poly(L-lactide) membrane. A pilot study.

Tubular poly(L-lactide) membranes with a pore size of 5-15 microns and a molecular weight of 70,000 Daltons were implanted into 24 New Zealand skeletally mature rabbits to cover 10-mm mid-diaphyseal defects of the radius of the forelimb. An identical defect on the contralateral limb was not treated with the membrane and served as a control. The animals were killed at 1, 2, 4, 8, 12, 24, 36, and 64 weeks after implantation, and radiographic and microscopic studies were conducted. The canals of the polymeric tubes were initially filled with blood. At 2 weeks, there was direct woven bone formation within the polymeric tube in continuity with the fragment cortices and its medullary canal. The formation of woven bone across the defect progressed until reconstruction of the defect had occurred at 6-8 weeks. The bone continued to remodel throughout the observation period of 64 weeks. By 12 weeks, bone within the lumen of the implant consisted of cancellous bone and cortical bone lining the membrane walls. At 24, 36, and 64 weeks, the implants were filled with cancellous bone and cortical bone in direct apposition to the polymer membrane. For one implant, the newly formed woven bone had only incompletely filled the defect at 8 weeks. This resulted in a nonunion with a residual gap of 0.5 mm and the appearance of mature bone. There was extensive bone formation along the intraosseous membrane in both control and implanted defects, although the untreated defects were rapidly filled with overlying muscle and soft tissues. The osseous activity of the untreated defects appeared confined to the bone ends by the interposed muscle and fibrous soft-tissue margins. The untreated defects resulted in radial-ulnar synostosis along the intraosseous membrane with cortical bone caps at the bone ends. The poly(L-lactide) membrane remained intact throughout the 64-week period without evidence of significant degradation. The membranes were encapsulated in a thin fibrous tissue. There was no histological evidence of acute or chronic inflammation associated with the implants.

Animals↗

Reconstructive management of cranial base defects after tumor ablation.

Successful reconstruction after cranial base tumor ablation is paramount in preventing potentially life-threatening complications. The purpose of this study was to evaluate experiences of cranial base reconstruction and to identify reconstructive management principles that may assist in achieving successful cranial base reconstruction. All cranial base reconstructions performed by the Department of Plastic Surgery at the University of Texas M. D. Anderson Cancer Center between January of 1993 and September of 1999 were reviewed. Analyses were performed to assess the impact of location of defect, type of reconstruction, type of dural repair, and history of preoperative radiation and chemotherapy on rates of complications, and patient survival. The 77 patients who underwent cranial base reconstruction after tumor ablation during the study period had a mean age of 52 years (6 to 84 years). The mean follow-up period was 28.7 months (1 to 76 months). Squamous cell carcinoma, the most common histopathologic type, was present in 24 patients (31 percent), and 35 patients (45 percent) presented with recurrent disease. Location of defects involved region I (anterior) in 31 patients (40 percent), region II (anterior-lateral) in 18 (23 percent), region III (lateral-posterior) in six (8 percent), and more than one region in 22 (29 percent). Reconstructive methods included free flaps in 52 patients (68 percent), temporalis muscle flaps in 14 (18 percent), pericranial flaps in eight (10 percent), and other local flaps (two galeal, one scalp) in three (4 percent). Of the 52 free flaps, 18 (35 percent) were used in region I, 14 (27 percent) in region II, six (12 percent) in region III, and 14 (27 percent) in defects involving more than one region. Of the 14 temporalis muscle flaps, 13 (93 percent) were used for defects involving regions I or II and one (7 percent) was used for a defect involving region III. Of the 11 pericranial and other local flaps, nine (82 percent) were used in region I, one (9 percent) in region II, and one (9 percent) in a combination of regions II and III. Complications occurred in 21 patients (27 percent): three total flap losses (4 percent), three partial flap losses (4 percent), two cerebrospinal fluid leaks (3 percent), two cases of meningitis (3 percent), two abscesses (3 percent), five cases of delayed wound healing (6 percent), two hematomas (3 percent), one wound infection (1 percent), and one cerebrovascular accident (1 percent). Overall survival was 77 percent at 2 years and 58 percent at 4 years. The type of reconstruction, location of defect, type of dural repair, and history of preoperative radiation and chemotherapy had no significant association with the incidence of complications. Neither the type of reconstruction nor the location of defect showed a significant effect on patient survival. In this experience, local flaps, such as pericranial or temporalis muscle flaps, are good choices for reconstruction of smaller anterior or lateral cranial base defects. For defects that require larger amounts of soft tissue, free flaps are appropriate. With proper patient selection, successful cranial base reconstruction can be performed with either local or free flaps with a low incidence of complications.

Adolescent↗

Spontaneous bone regeneration in surgically induced bone defects in young rabbits.

Defects of the femoral shaft (15%, 20%, 25%, and 30% of the femoral length) with intact periosteum were made in young rabbits to investigate differences in union time. The mean union time was 7.3, 7.1, 7.4, and 7.0 weeks, respectively and there was no significant difference ( >0.05) between the groups. The mean healing indices were 6.7, 4.6, 3.9, and 3.1 weeks/cm, respectively and these were significantly different ( <0.05) between the 15% bone defect group and the other bone defect groups. These results suggested that union time was not affected by the amount of bone defect. Femoral lengthening of 20% was performed to compare the quality of callus with those of the femoral defect of 20%. The mean healing indices of defect and lengthening were 4.6 and 5.7, respectively and the difference was significant ( = 0.004). The callus stiffness of femoral defect was higher ( = 0.02) than that after femoral lengthening whereas the bone mineral density of the callus showed no significant difference ( = 0.37) between two groups. The method of filling bone defect with callus generated from the intact periosteum may be a new therapeutic option for the reconstruction of large bone defects in children when other treatments are not available.

Age Factors↗

New-onset conduction defects and their relationship with in-hospital major cardiac events in unstable angina pectoris.

BACKGROUND: The aim of this prospective cohort study was to describe the incidence and the risk factors for the development of intraventricular conduction defects and the relationship of these defects with in-hospital major cardiac events (MACE) in unstable angina pectoris. METHODS: Two-hundred-and-seventy consecutive patients presenting with Braunwald class IIIB angina without a conduction defect at admission were included in the study and followed up during the in-hospital period. RESULTS: Fifty-one patients who developed non-ST-elevation myocardial infarction during the first day were excluded from the study. Of the remaining 219 patients, 40 (18%) had a new permanent conduction defect (group 1) and 179 (82%) did not have a conduction defect (group 2) during the in-hospital period. The patients in group 1 were significantly older (mean age of 63.5 +/- 11 years compared with 59 +/- 10 years, P = 0.01) and a history of previous coronary artery bypass grafting (CABG) was more frequent in this group (12.5% compared with 1.6%, P = 0.004). By logistic regression analysis, age (P = 0.01, odds ratio (OR) = 1.473, 95% confidence interval (CI) = 1.108-2.612) and previous CABG (P = 0.005, OR = 3.995, 95% CI = 1.811-7.383) were also found to be risk factors for the development of a conduction defect. In-hospital total MACE, death and heart failure were more frequently observed in group 1 (P = 0.005, P = 0.02, P = 0.001, respectively). The incidences of recurrent refractory angina, acute myocardial infarction and urgent revascularization were not different between the groups. ST-segment depression at admission (P = 0.009, OR = 1.654, 95% CI = 1.228-2.675) and a new-onset conduction defect (P = 0.02, OR = 1.625, 95% CI = 1.244-2.754) were found to be predictors of the development of in-hospital MACE. CONCLUSIONS: In unstable angina pectoris, patients with a new-onset conduction defect are relatively older and have more frequently undergone previous CABG. Because in-hospital MACE, death and heart failure are more common in patients with a new conduction defect, they should be considered as high risk and treated more aggressively.

Aged↗

Articular cartilage adjacent to experimental defects is subject to atypical strains.

We tested the hypothesis that articular cartilage adjacent to experimental osteochondral defects is not subject to unusual strains under load. A 2.5-mm drill hole was made in the medial femoral condyle of 15 knees from 10 adult rabbits. Experimental joints were loaded with simulated quadriceps force, then frozen under load and preserved by freeze-substitution fixation. Deformation in the region of the defect was evaluated by scanning electron and light microscopy and compared with nondrilled and nonloaded control knees. To simulate blood clot, alginate was placed into some defects before loading. In loaded knees, articular cartilage at the edge of the drill hole was abnormally flattened and folded into the defect. Opposing tibial cartilage or meniscus intruded into the femoral defect beyond the cement line. Alginate did not prevent incursion of opposing cartilage. In this standard drill-hole model, the articular cartilage defect is occupied by the opposing surface when a joint is loaded. Any tissue growing or surgically implanted in the defect is subject to loading and displacement, therefore complicating attempts to characterize the healing or regenerative potential in similar drill-hole models. Deformation of cartilage at the defect edge suggests load concentration or increased compliance. Either phenomenon would contribute to subsequent degeneration of the cartilage adjacent to defects.

Animals↗

Microvascular reconstruction of the hypopharynx: defect classification, treatment algorithm, and functional outcome based on 165 consecutive cases.

The objectives of this study were three-fold: to develop a scheme for classification of hypopharyngeal defects, to establish a reconstructive algorithm based on this system, and to assess the functional outcome of such reconstruction. This study is a retrospective review of a 14-year experience with 165 consecutive microvascular reconstructions of the hypopharynx in 160 patients. The average patient age was 59 years (95 percent CI, 37 to 81). Thirty-four patients were operated on for recurrent disease; 71 had preoperative radiotherapy. Partial defects were reconstructed with radial forearm flaps (n = 52); circumferential defects were reconstructed with jejunum (n = 90); and extensive, noncircumferential longitudinal defects were reconstructed with rectus abdominis flaps (n = 23). The overall free flap success rate was 98 percent. Six flaps required reexploration, two of which were salvaged. The incidence of fistula was 7 percent and stricture, 4 percent. Preoperative radiotherapy was significantly associated with risk of recipient site complications (OR, 2.3; 95 percent CI, 1.0 to 5.0). Follow-up data were available on 95 percent of patients: 53 percent were able to tolerate an unrestricted diet, 23 percent a soft diet, 12 percent liquids only, and 12 percent were limited to tube feedings. The treatment algorithm for microvascular hypopharyngeal reconstruction is based on the type of defect with partial defects with radial forearm flaps, circumferential defects reconstructed with free jejunal flaps, and extensive, multilevel defects reconstructed with rectus abdominis myocutaneous flaps. Microvascular reconstruction of pharyngeal defects is highly successful with few postoperative complications. With appropriate flap selection, functional outcome can be optimized.

Adult↗

Reconstruction of concomitant lip and cheek through-and-through defects with combined free flap and an advancement flap from the remaining lip.

Massive facial defects involving the oral sphincter are challenging to the reconstructive surgeon. This study presents the authors' approach to simultaneous reconstruction of complex defects with an advancement flap from the remaining lip and free flaps. From January of 1997 to December of 2001, 22 patients were studied following ablative oral cancer surgery. Their ages ranged from 32 to 66 years. Nineteen patients had buccal cancer, two patients had tongue cancer, and one patient had lip cancer. In all cases, the disease was advanced squamous cell carcinoma. Nine patients underwent composite resection of tumor with segmental mandibulectomy, and seven patients underwent marginal mandibulectomy. Cheek defects ranged from 15 x 12 cm to 4 x 3 cm, and intraoral defects ranged from 14 x 8 cm to 5 x 4 cm in size. One third of the lower lip was excised in nine patients, both the upper and lower lips were excised in 10 patients, and only commissure defects were excised in three patients. An advancement flap from the remaining upper lip was used for reconstruction of the oral commissure and oral sphincter. Then, the composite through-and-through defect of the cheek was reconstructed with radial forearm flaps in 13 patients, fibula osteocutaneous flaps in five patients, double flaps in three patients, and an anterolateral thigh flap in one patient. The free flap survival rate was 96 percent, and only one flap failed. With regard to complications, there were two patients with cheek hematoma, six patients with orocutaneous fistula or neck infection, and one patient with osteomyelitis of the mandible. All but one patient had adequate oral competence. All patients had an adequate oral stoma and could eat a regular or soft diet; two patients could eat only a liquid diet. For moderate lip defects, immediate reconstruction of complex defects took place using an advancement flap from the remaining lip to obtain a normal and functional oral sphincter; the free flap can be used to reconstruct through-and-through defects. This simple procedure can provide patients with a useful oral stoma and acceptable cosmesis.

Adult↗