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Leukocyte adhesion deficiency (LAD) is a rare inherited primary immunodeficiency disorder characterized by the presence of a defect of phagocytic function resulting from a lack of leukocyte cell surface expression of β₂ integrin molecules (CD11 and CD18) that are essential for leukocyte adhesion to endothelial cells and chemotaxis. A small number of patients with LAD-1 have a milder defect, with residual expression of CD18. These patients tend to survive beyond infancy; they manifest progressive severe periodontitis, leading to partial or total premature loss of the primary and permanent dentitions. Close cooperation with pediatricians and immunologists is often the key to successful management of pediatric patients with LAD. The purpose of this report was to present the case of a 5-year-old boy with moderate leukocyte adhesion deficiency-1 and severe periodontitis, cellulitis and illustrate the need for periodic oral checkups to avoid the progression of oral diseases and prevent premature tooth loss.

The purpose of this paper was to report 3 cases of localized aggressive periodontal bone destruction related to improper use of orthodontic elastic bands to close diastemas in permanent anterior teeth and to compare the results to previous studies. Some common signs and symptoms of this particular destruction were observed with these patients that had been previously reported when the comparisons of these cases were made. The patients usually experienced a painful sensation, and an isolated pyogenic-like granuloma appeared at the interdental area. Radiographs revealed localized periodontal destruction, with tooth extrusion and clinical crown divergence and radiographic root convergence; the two involved teeth moved simultaneously during mobility testing. Surgical intervention and treatment of the cases was described. The prognosis is usually decided by the severity of the condition, and many factors may influence the healing of treated cases.

The purpose of this case report is to detail an initial periodontal manifestation of Crohn's disease in a 6-year-old boy. The first clinical diagnosis, localized aggressive periodontitis, was based on the microbiological isolation of Actinobacillus actinomycetemcomitans from subgingival sites. On examination, gingival lesions, together with bleeding on probing, edema, and erythema, were observed. Although an increased probing depth was detected, no radiographically visible alveolar bone loss was observed. According to these findings, periodontitis as a manifestation of a systemic disease was assumed. Furthermore, fissural ulcerations of the lips were noted. The patient also reported a swelling of the upper lip in the morning. Oral hygiene procedures, scaling, root planning, and the application of metronidazole and amoxicillin were not successful. Metabolic and several immunological tests, however, showed normal values. Two months after the first periodontal signs, the child suffered from severe malnutrition, accompanied by diarrhaea and abdominal pain. Active colitis with multiple granulomas was detected histopathologically from biopsies. Crohn's disease was then diagnosed by the internist. If in doubt, medical examinations in every case of childhood periodontitis are recommended to determine whether the findings speak for initial symptoms of a systemic disorder (eg, Crohn's disease).