Parodontalna bolest (parodontopatija) je hronična inflamatorna bolest u čiju patogenezu su uključene različite ćelije urođenog i stečenog imuniteta, među kojima i makrofagi. Makrofagi su profesionalni fagociti čija je osnovna uloga ingestija i destrukcija mikroorganizama. Pored fagocitoze, ove ćelije su angažovane u produkciji proinflamatornih citokina i u prezentaciji antigena T-ćelijama, te se smatraju ključnim ćelijama urođenog imunskog odgovora. U našem istraživanju praćena je gustina i distribucija makrofaga u zdravoj i inflamiranoj gingive sa ciljem da se proceni njihov značaj u patogenezi parodontopatije. Materijal su činile gingivalne biopsije 96 pacijenata svrstanih u 4 grupe: zdrava gingiva, gingivitis, početna parodontopatija i uznapredovala parodontopatija. Za identifikaciju makrofaga korišćena je imunohistohemijska tehnika bojenja zasnovana na upotrebi monoklonskog antitela anti-CD68. Prema našem istraživanju gustina makrofaga je veća u gingivitisu i parodontopatiji u odnosu na zdravu gingivu. Između gingivitisa i parodontopatije nije nađena značajna razlika u gustini makrofaga. Grupisanje makrofaga u blizini delimično liziranih kolagenih vlakana u parodontopatiji ukazuje na njihovu kolagenolitičku aktivnost. Povećanje broja makrofaga u inflamiranoj gingivi može se dovesti u vezu i sa resorpcijom kosti jer se ove ćelije mogu diferencirati u osteoklaste.

Collagen is a major constituent of the gingival extracellular matrix, which crucially affects the histoarchitecture of the gingival tissue. Collagen type I dominates the gingival tissue, while type II, III and IV are present to a lesser extent. Changes in distribution and density occur in the inflamed gingiva. The aim of the study was to examine the organization and density of the collagen in healthy and inflamed gingiva. The material for the study consisted of the gingival biopsies performed in 96 patients aged from 13 to 70 years. The gingival specimens were classified into 4 groups: healthy gingiva, gingivitis, moderate periodontal disease and severe periodontal disease. The samples of the gingival tissues were stained by the method of Van Gieson’s Stain, while the VD of the collagen was measured bz the use of multipurpose testing system M42. In healthy gingival collagen are thick and receptive to color. In gingivitis collagen is mostly preserved structure, but reduced volume; in the periodontitis collagen bundles are reduced, short, thin, disorganized, often fragmented and less susceptibility to color. In healthy gingiva collagen fibers occupy 58.6 ± 5.1% of the volume of lamina propria; in gingivitis significantly lower (44.2 ± 6.2%); in moderate periodontitis 32.7 ± 8.5% and in the progressed periodontitis only 28.7 ± 9.7%. Based on our results, we concluded that in periodontal disease occurs collagenolysis. Quantitative evaluation of gingival collagen volume density may reflect the clinical severity of periodontal disease.

The nature of herpes simplex virus as infective agens, which can grow in number, only in live cells, and fact that many herpes virus infections of oral tissue have atypic and asymptomatic course, makes their diagnosis more difficult and complicate from infections caused by other microorganisms. The aim of this investigation were to established cytological findings oral lesions of primary and recurrent herpes infections.