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Biomedical subjects

J M Dersot

Publications and source records attributed to J M Dersot.

7 recordsLinked to original sources
PubMed1991

[Posterior bite collapse. 2. Therapeutic proposals].

In the treatment of posterior bite collapse, the orthodontic phase consists of three steps: uprighting of molar teeth, leveling of the mandibular arch and closure of anterior diastemas. During and after orthodontic therapy, the maintenance of periodontal health is important. For patients in which there is a reduced periodontium, splinting should be accomplished after the teeth are moved into their desired position.

Diastema↗
PubMed1989

[Posterior bite collapse. 1. Etiology and diagnosis].

The posterior Bite Collapse is a sequelae of advanced break down. The presence of periodontal inflammation and loss of osseous support can induce teeth migration in a direction partially imposed by occlusal forces. Posterior Bite Collapse often causes mesial drifting of the posterior teeth and flaring of the anterior segments. It may be aggravated by early loss of teeth that are not replaced, by malocclusion or by a neuro muscular disorder.

Bicuspid↗
PubMed1989

Periodontal and femoral bone status in periodontitis-affected hamsters receiving a high dose indomethacin treatment.

The aim of this study was to test the effect of a high dose (6 mg/kg/d) of indomethacin, a PG-synthesis inhibitor, on hamster periodontitis and to verify a possible systemic skeletal action. Thirty animals were separated into three groups: control, untreated periodontitis-affected, and indomethacin treated groups. Compared to affected untreated animals, indomethacin reduced the number of osteoclasts (p less than 0.001) to the control level, and accordingly the extent of resorption (p less than 0.01). A partial decrease in reversal (p less than 0.05) was also obtained; the persistence of aborted reversal lacunae was the scar of the pretreatment period. The extent of formation was markedly increased by indomethacin (p less than 0.01). Bacterial plaque accumulation was not modified but PMNLs investing plaque were dramatically decreased (p less than 0.02). Indomethacin had no influence on the femoral periosteal remodeling, nor on metaphyseal and epiphyseal trabecular density, nor on growth plate thickness. These results confirm the positive effect of indomethacin on hamster periodontitis and emphasize the role of PGs on periodontitic bone disturbances, particularly on the uncoupling of the remodeling sequence. The reduction in PMNL migration is an important feature, which possibly participates in the improvement of the bone status. The lack of femoral changes indicates that a mid-term treatment with indomethacin has no detrimental action on ordered skeletal growth and bone mass.

Alveolar Process↗