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Biomedical subjects

R Rotundo

Publications and source records attributed to R Rotundo.

10 recordsLinked to original sources
PubMed2002

Viral etiology of gingival recession. A case report.

Herpes simplex virus-type I (HSV-1) is responsible for both primary and recurrent infections of the oral mucosa. The aim of this case report is to show how HSV-1 may cause periodontal damage such as gingival recession. A 26-year-old male patient presented in a private office for the treatment of gingival recessions. He reported that the recessions had appeared suddenly with marginal inflammation of the gingiva and vesicle formation; within a few hours, the gingival tissue had been completely destroyed. The lesions were accompanied by pain, fever, and regional lymphadenopathy. Two weeks later, the patient returned complaining of a recurrence accompanied by pain and lymphadenopathy. The following day, the patient's condition had worsened and the depth of the recession had increased. A biopsy was taken for histological examination. A free epithelial-connective tissue graft was performed. Histological and direct immunofluorescence examinations confirmed the herpetic origin of the lesion. Eight months after surgery, a new herpetic lesion was detected in correspondence to the gingival margin of the first lower right premolar; therefore, acyclovir was prescribed. After 1 week, the antiviral therapy was completely successful; the gingival lesion disappeared, and no recession of the soft tissue margin was observed. Based on these clinical features, diagnosis of gingival recession induced by HSV-1 must be carried out at an early stage to establish a successful therapy.

Acyclovir↗
PubMed2001

Oral Acanthosis nigricans as a marker of internal malignancy. A case report.

BACKGROUND: Acanthosis nigricans (AN) is a rare mucocutaneous condition that can involve the oral tissues. There are 2 clinical forms of AN: benign and malignant. Benign AN is related to systemic diseases such as diabetes and obesity or can be induced by drugs such as systemic corticosteroids, nicotinic acid, estrogens, insulin, and fusidic acid. Malignant AN appears in association with tumors such as lung, ovarian, breast, and gastric carcinoma. METHODS: A rare case of malignant AN that initially manifested in the oral cavity of a 73-year-old patient is reported. RESULTS: A bladder and lung carcinoma were detected following the diagnosis of AN. CONCLUSIONS: The diagnostic importance of oral AN is emphasized because, in our patient, its recognition led to the detection of 2 occult malignant tumors.

Acanthosis Nigricans↗
PubMed2001

Retrospective evaluation of the influence of the interleukin-1 genotype on radiographic bone levels in treated periodontal patients over 10 years.

BACKGROUND: A difference in genetic susceptibility to plaque accumulation has been advocated to explain different responses to periodontal therapy. The purpose of this study is to assess the role of the interleukin-1 (IL-1) polymorphism on the rate of bone and tooth loss in non-smoking periodontally treated patients during maintenance. METHODS: Sixty consecutive non-smoking patients (mean age 46.8 +/- 5.0) with moderate to severe periodontitis, treated and maintained for over 10 years were selected. At baseline (T0), radiographic evaluation (cemento-enamel junction [CEJ]-root apex, CEJ-bottom of defect mesial and distal, CEJ-bone crest mesial and distal, crown-root ratio) was performed. All patients received scaling and root planing; 36 patients then underwent surgical therapy. Subsequently, all patients were enrolled in a periodontal maintenance program with recall visits every 3.4 +/- 1.0 months for at least 10 years. At the latest recall visit (T2) the same radiographic measurements evaluated at baseline were taken and a DNA sample for IL-1 genetic susceptibility testing was collected and sent for analysis. RESULTS: Twenty-three of the 60 patients (38.3%) were IL-1 genotype positive. A total of 52 teeth (3.3%) out of 1,566 were lost due to periodontitis between T0 and T2; 28 of 957 (2.9%) in the IL-1 genotype negative group and 24 of 609 (3.9%) in IL-1 genotype positive group. The mean variation in bone defect level (DeltaBD) averaged -0.04 mm in IL-1 genotype negative patients and 0.01 mm in IL-1 genotype positive patients. The mean variation in bone crest level (DeltaBC) averaged -0.24 mm in IL-1 genotype negative patients and -0.28 mm in IL-1 genotype positive patients. However, a few patients showed significant differences in response to therapy based on initial bone levels and genotype. IL-1 negative patients who showed minimal initial bone loss responded to the therapy better than the IL-1 positive patients. IL-1 positive patients with severe initial bone loss showed a better response to the therapy than IL-1 negative patients. CONCLUSIONS: On average, there were no significant differences related to IL-1 genotype in tooth loss after 10 years in a non-smoking, well-maintained periodontal population. On an individual patient basis, the IL-1 genotype, in combination with the initial bone level, seems useful at the beginning of therapy for predicting bone level variation.

Adult↗
PubMed1999

Coronally advanced flap procedure for root coverage. Treatment of root surface: root planning versus polishing.

This clinical study was designed to determine if mechanical instrumentation (root planing) of the exposed root is useful in treating gingival recession caused by traumatic toothbrushing following a coronally advanced flap (CAF). Ten patients with high levels of oral hygiene (full-mouth plaque score <20%), from 25 to 57 years of age, were selected for the study. Each patient showed 2 bilateral Class I or II maxillary recessions. A total of 20 recessions were treated. The difference in the recessions was < or =1 mm. In each patient, one recession was randomly assigned to the test group and the contralateral one to the control group. In the test group, the exposed root surface was polished at slow speed with a rubber cup and prophylaxis paste for 60 seconds. In the control group, the exposed root surface was planed with a sharp curet. In both test and control groups, a trapezoidal full- and partial-thickness flap was elevated, coronally displaced, and sutured to cover the treated root surface. Before treatment, the mean recession depth in the test group (polishing) was 3.1+/-1.1 mm; and in the control group (root planing), 2.9+/-1.0 mm. Three months after the described procedures, the test group (polishing) showed a mean recession reduction of 2.6+/-0.6 mm; mean percent root coverage was 89+/-14%. In the control group (root planing), the mean recession reduction was 2.3+/-0.7 mm and mean percent root coverage was 83+/-16%. The difference of recession reduction between the test and control group was not statistically significant (P = 0.1405), even though the test group showed slightly better clinical results in terms of root coverage. This prospective clinical, controlled, randomized study shows that mechanical instrumentation (root planing) of the exposed root surfaces is not necessary when shallow recessions caused by traumatic toothbrushing are treated using a coronally advanced flap (CAF) in patients with high levels of oral hygiene.

Adult↗
PubMed1993

The properties and function of gamma-glutamyl hydrolase and poly-gamma-glutamate.

gamma-Glutamyl hydrolase is a ubiquitous enzyme that has the capacity to cleave gamma-glutamyl bonds of cellular folyl- and antifolylpoly-gamma-glutamates. This study has revealed that the enzyme is secreted by primary cultures of rat hepatocytes and by H35 hepatoma cells. It was found that more than 99% of the total enzyme from H35 cells accumulated in the medium after 48 hr incubation with the serum-free medium. The cells were shown to remain intact during the secretion period since lactate dehydrogenase, dihydrofolate reductase and lysosomal hydrolases other than gamma-glutamyl hydrolase were retained within the cell. When PteGlu5 (folylGlu4) is used as a substrate the initial product is PteGlu (folate), and there is no appearance of intermediate chain length pteroyl polyglutamates. Therefore, the secreted and cellular gamma-glutamyl hydrolase from hepatoma cells appears to be an endopeptidase. Polyclonal antibodies to the poly-gamma-glutamate substrates of the enzyme were prepared and characterized. The antibodies recognize the structural differences between alpha- and gamma-glutamyl linkages but appear equally active with PteGlu5 and its analogs such as 4-NH2-10-CH3PteGlu5 and pABAGlu5. The affinity of the antibodies is related to the gamma-glutamyl structure since L-glutamic acid, folate or p-aminobenzoic acid are inactive with the antibodies. Furthermore, poly-gamma-glutamate has lower affinity for the antibodies than the poly-gamma-glutamate derivatives of PteGlu, 4-NH2-10-CH3PteGlu or pABA.

Animals↗
PubMed1989

The characteristics and consequences of folate depletion in hepatoma cells in vitro by inhibition of dihydrofolate reductase.

Growth of rat hepatoma cells in subtoxic concentrations of the DHFR inhibitor metoprine caused a marked time and concentration dependent reduction in cellular folates. As much as 75% total cellular folates can be lost without impairing growth. Increasing the concentration of metoprine into a range that causes inhibition of growth results in no further reduction in cellular folates. This effect is presumably mediated through inhibition of DHFR and several mechanisms are discussed which may account for these results. Cells grown in medium in which the concentration of folate is changed from 4 microM to 20 nM had intracellular folate levels that were reduced 85%. This is nearly the same reduction caused by treating cells grown in normal medium (4 microM folate) with continuous, subtoxic levels of metoprine. The reduction in cellular folates caused by growth in nM folic acid caused enhanced growth inhibitory activity of several antifolates. On a concentration basis metoprine was 12-fold more active under these conditions, PDDF was 37-fold more active and DDATHF was 44-fold more active. The reason for the enhanced sensitivity to PDDF and DDATHF may also be analogous to the reason for their synergism with the low concentration of metoprine and trimetrexate (12).

Animals↗
PubMedDate not supplied

[Diabetes mellitus as a risk factor for periodontitis].

Diabetes mellitus is an important disease of the endocrine system. Many studies have associated this disease to the pathogenesis and the severity of periodontal disease. The aim of this article is to illustrate the relation between diabetes mellitus and periodontal disease. Many studies show an important association between diabetes and the pathogenesis of periodontal disease. Vascular changes caused by hyperglycemia are associated to the development of periodontal pathogens species. Moreover diabetics show an exacerbate host response with hyperproduction of inflammatory mediators and polymorphonuclear dysfunction. Diabetics with good metabolic control and patients with good oral hygiene show a reduced risk of periodontitis. In conclusion, diabetes mellitus (IDDM and NIDDM) is an important risk factor for periodontitis. Odds Ratio is 3. Diabetes mellitus determines changes in bacterial population and production of inflammatory mediators, and reduces the efficacy of the host response. Good controlled diabetes do not cause a major risk of periodontitis and improve the results of the periodontal therapy. Moreover periodontal therapy may reduce the request of insulin in diabetics. It is reasonable a two-ways relation between diabetes and periodontal disease.

Diabetes Complications↗
PubMedDate not supplied

[Periodontic-endodontic lesions: diagnostic and therapeutic indications].

The presence of connections between periodontium and endodontium can lead to the diffusion of an infection from one apparatus to another. The involvement of both periodontium and endodontium is defined as Combined Periodontic-Endodontic lesions. This definition is not based on the initial etiology of the lesion and either the endodontic or periodontal lesion may be the cause or the result of the other or both may develop independently. The lesions must be correctly diagnosed for the best therapeutic approach. The diagnosis is based on clinical symptoms and radiographic analysis; clinical signs must show the presence of periodontal probing and pulpal necrosis. Radiographic examination can confirm the involvement of both periodontium and endodontium only if the lesion is present on the mesial and distal part of the diseased tooth; in the case of a palatal/lingual or vestibular lesion such evidence will not be detectable. The therapeutic approach is always based on an initial endodontic treatment followed, if needed, by the proper periodontal treatment.

Dental Pulp Diseases↗