Showing posts with label 4/16/10. Show all posts
Showing posts with label 4/16/10. Show all posts

Friday, April 16, 2010

Prepubertal periodontitis: A review of diagnostic criteria, pathogenesis, and differential diagnosis 4/16/10

Department of Pediatric Dentistry
Resident’s Name: Murphy Program: Lutheran Medical Center - Providence
Article title:Prepubertal periodontitis: A review of diagnostic criteria, pathogenesis, and differential diagnosis

Author(s): Watanabe, Keiko
Journal:
Year. Volume (number). Page #’s: 1990. 25. 31-48
Major topic: Prepubertal periodontitis(PP)
Minor topic(s):Clinical conditions presenting with signs/symptoms of PP
Main Purpose: Review the signs/symptoms of Localized PP (LPP), and generalized PP (GPP)
Overview of method of research: Varied case review, Review of literature(from 20 years ago)

Findings: Prepubertal periodontitis is essentially periodontitis of primary teeth, and may include gingival inflammation, early loss of primary teeth, and bone loss. PP MAY continue and appear in the adult dentition as periodontitis. PP is usually associated with a child who has some kind of underlying medical condition, including but not limited to neutropenia, hypophosphatasia, papillon lefevre synd, and acrodynia. However, PP can also occur in otherwise healthy children, although these kiddos do NOT suffer from bone or attachment loss. In 1983, page classified PP into two categories, LPP, and GPP. LPP is a localized form of PP, occurred in apparently otherwise healthy prepubescent children. GPP, the generalized form of PP occurs in children who had histories of delayed umbilical cord separation, delayed wound healing, persistent peripheral blood leukocytosis, cellulitis w/o pus, and various other serious infections. GPP has been identified as an oral manifestation of leukocyte adhesion deficiency(LAD).
The onset of both forms of PP is during or immediately following the eruption of primary teeth. LPP affects a various number of teeth, and the gingival inflammation is not as pronounced as expected. GPP affects all of the teeth, and presents with severely inflamed, erythmatous gingival.
There are many theories on why children get PP, ranging from a genetic disposition to numerous methodological factors. Possible etiologic factors include pathogenic bacteria, particularly A.A, bacteriodes intermedius, b. gingivalis, capnocytphagea,and e. corrodens. Sites with PP which had undergone bone loss showed evidence of infection with these culprits, especially AA.

Diseases associated with PP
Hypophosphatasia- Low levels or deficiency of alkaline phosphatase. Children who have HP present with premature loss of primary teeth(the most diagnostic factor), usually being the incisors, and possibly enlarged pulp chambers.

Papillon-Lefevre Syndrome(PLS)-Genetic autosomal dominant condition, child will present with hyperkeratosis of the palms and soles and periodontal destruction. PLS effects the majority of teeth in both the primary and permanent dentition. Symptoms include severe gingival inflammation and alveolar bone loss.

Neutropenia-Defined as a decrease in the number of PMN’s in the peripheral blood below certain values. Oral manifestations include severe gingival inflammation, ulcerations, and necrotic lesions anywhere in the oral cavity. Bone loss and early exfoliation are possible signs as well.

LAD-Autosomal recessive condition in which the expression of Mac-1. LFA-1, and p150,95 glycoprotein is severely depressed. Recurrent bacterial infections, impaired wound healing, severe gingival inflammation, gingival proliferation, cleft formation, and severe bone loss leading to early loss of primary teeth are clinical signs of LAD.

Chediak Higashi Syndrome(CHS)- Rare autosomal recessive disease in which leukocyte defects are associated with impared function of cytoplasmic microtubules, or microtubule assembly in PMN’s. Oral signs are severe inflammation, attachment and bone loss.

Leukemias-Group of conditions characterized by progressive uncontrolled proliferations of WBC’s. Oral signs include gingival bleeding, petechia, lymphadenopathy, gingival hyperplasia, hypertrophy, pallor, and alveolar bone resorption.

Acrodynia- Rare disease characterized by many clinical symptoms including gingival and mucosal hyperplasia, alveolar bone loss, early loss of primary teeth, loss of hair, and cramps.

Juvenile Diabetes- Decrease in insulin secretion or availability. Clinical oral signs include severe gingival inflammation and periodontitis and impaired wound healing.

HIV-Unusual gingivitis with diffuse erythema, gingival lesions similar to an atypical form of NUG, and rapid bone loss.

Treatment
LPP cases have been treated by either curettage followed by a standard child’s dose of penicillin for 5 days, and recare every 4 months.

For GPP, a consult with the physician is necessary to discuss the treatment options, which can range from curettage and AB therapy, to serial extraction.

In either case, it is advised that a CBC w/ diff, cell morphology, serum AP, and fasting glucose level is ordered.

Assessment of Article: Long, but helpful article. Lots of extra information on the different syndromes.

Thursday, April 15, 2010

Growth and Development Considerations in the Diagnosis of Gingivitis and Periodontitis in Children

Resident: Adam J. Bottrill
Date: 16APR10
Region: Providence
Article title:
Author(s): Enrique Bimstein and Lars Matsson
Journal: Pediatric Dentistry
Page #s: 186-191
Year: 21:3, 1999
Major topic: Periodontitis and gingivitis in children
Minor topic(s): NA
Type of Article: Topic Summary

Main Purpose: This topic summary is intended to point out certain areas of the clinical exam where the pediatric dentist should practice extra vigilance in order to differentiate between pathologic processes (periodontisis and gingivitis) and normal periodontal growth and development.

Overview of method of research: Summary of articles.

Key points in the article discussion:

I. Overview
The relative lack of information regarding periodontal pathosis in children, some pediatric dentists may be forced to rely on data that has been gathered from adult studies. It is becoming more obvious that this may provide inadequate data regarding this topic.

II. Conclusions:

A. Gingivitis:
-There is an age related tendancy to develop gingivitis (same amount of gingival plaque resulting in different degrees of gingivitis.

B. Bacterial composition of dental plaque:
-Different bacteria present in the gingival plaque of children vs. adults

C. Inflammatory cell response:
-Research supports the fact that age may actually have more of an influence then severity of the disease on serum AB levels.

D. Puberty:
-There is hormonal influence on the gingival inflammatory process concomitant to puberty.

E. Primary vs. permanent teeth:
-Junctional epithelium of primary teeth thicker than permanent teeth (less permiable).

F. Tooth eruption and exfoliation:
-It is possible that during eruption, the junctional epithelium may be compromised and more susceptible to bacterial infiltration.

G. Periodontitis:
-Localized prepubertal periodontitis has been studied mostly in syndromic patients or those with systemic disease. There are not many studies available for otherwise healthy children.

H. Apical migration of junctional epithelium:
-Apical migration is considered “normal” as there are many studies that support its existance through the growth and development of children.

I. Summary:
-Pediatric dentists should be aware of the age-dependant existence of periodontal changes in children. Considering these variables, we must be able to properly distinguish between periodontal pathosis and normal growth and development.

Assessment of article: Not bad Mr. Bimstein. Useful and informative. Organized well. NO shenanigans here.

Generalized Prepubertal Periodontitis

Resident: Roberts
Date: 4/16/10
Article title: Generalized prepubertal periodontitis
Author: Gurel, et al
Journal: Journal of Clinical Periodontology
Volume: 23, pages: 1104-1111
Year: 1996
Discussions
Generalized prepubertal peridontitis is a rare clinical entity characterized by acute inflammation and proliferation of the ginigiva with rapid destruction of the alveolar bone.
4 cases were presented in this article. All of which had a decrease in peripheral blood nertrophil chemotaxis. Peripheral blood lymphocyte subpopulations were analyzed by double – colored flow cytometetry using monoclonal antibodies for the receptors CD2, CD3, CD4, CD8, CD19, CD29, CD45RA, CD56, CD11bCD18. Lymphocytes bearing CD3 receptors showed a significant decrease compared to those of the controls. Natural Killer cells were lowered in 3 of the 4 cases. All of the patients showed a higher increase in CD11bCD18 expression. The evaluation of CD11bCD18 receptor in peripheral blood leukocytes may be of help explaining the role of neutrophils in the pathogenesis of the disease.
Assessment: An okay artcle, I wish there was more information on the disease and less of the actual biochemistry.