Dental and Medical Problems
2012, vol. 49, nr 4, October-December, p. 567–575
Publication type: review
Language: English
License: Creative Commons Attribution 3.0 Unported (CC BY 3.0)
Localized Aggressive Periodontitis – Diagnostics, Epidemiology, Etiopathogenesis
Umiejscowione agresywne zapalenie przyzębia – diagnostyka, występowanie, etiopatogeneza
1 Department of Periodontology, Pomeranian University, Szczecin, Poland
2 University Dental Clinic, Pomeranian University, Szczecin, Poland
Abstract
Localized aggressive periodontitis (LAgP) is a very characteristic clinical entity. Numerous changes in the classification and naming of this periodontal disease over the last 35 years have not fundamentally changed its diagnostic criteria. Most of the research confirms the important role of Aggregatibacter actinomycetemcomitans in the etiopathogenesis of LAgP, especially the JP2 clone. Family history of the disease and racial differences suggest the influence of genetic factors. Research on the effects of the individual polymorphisms of genes involved in the regulation of the immune system does not give a clear answer on the relationship between polymorphisms of genes encoding various types of protein-modifying immune processes and the initiation and course of localized aggressive periodontitis. What is certain is that there is impaired chemotaxis and phagocytosis. The question remains whether these abnormalities are primary or are caused by the influence of an infectious agent. Nowadays, it is suspected that reduced production of defensins by the epithelial cells of the gingival sulcus plays a crucial role in the formation of LAgP. The aim of this study was to gather information on the diagnosis, prevalence and etiology of localized aggressive periodontitis based on the state of the art.
Streszczenie
Umiejscowione agresywne zapalenie przyzębia (LAgP) jest bardzo charakterystyczną jednostką kliniczną. Liczne przekształcenia klasyfikacji i nazewnictwa chorób przyzębia w okresie ostatnich 35 lat nie zmieniły zasadniczo kryteriów diagnostycznych dla tej jednostki chorobowej. Większość badań potwierdza istotną rolę Aggregatibacter actinomycetemcomitans w etiopatogezie LAgP, zwłaszcza jego klonu JP2. Rodzinne występowanie choroby i różnice rasowe przemawiają za wpływem czynników genetycznych. Badania nad wpływem polimorfizmu pojedynczych genów związanych z regulacją czynności układu immunologicznego nie dają jednoznacznej odpowiedzi na temat związku polimorfizmu genów kodujących poszczególne rodzaje białek modyfikujących procesy immunologiczne z powstawaniem i przebiegiem umiejscowionego agresywnego zapalenia przyzębia. Zjawiskami pewnymi są zaburzenia chemotaksji i fagocytozy. Przedmiotem dyskusji pozostaje fakt, czy zaburzenia te mają charakter pierwotny, czy są wywołane wpływem czynnika infekcyjnego. Pewną rolę w powstawaniu LAgP przypisuje się obecnie zmniejszonemu wydzielaniu defensyw, wytwarzanych przez komórki nabłonka kieszonki dziąsłowej. Celem pracy było zebranie informacji na temat diagnostyki, częstości występowania i etiopatogenezy umiejscowionego agresywnego zapalenia przyzębia na podstawie współczesnego stanu wiedzy.
Key words
localized aggressive periodontitis, diagnosis, prevalence, etiology
Słowa kluczowe
agresywne umiejscowione zapalenie przyzębia, diagnostyka, występowanie, etiopatogeneza
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