Histopathologic features of the initial and early stages of experimental gingivitis in man

Abstract

The pathologic alterations occurring in the gingival tissues of humans immediately following the beginning of plaque accumulation have not heen elucidated previously. Seven males, 22--31 years of age, free of clinical manifestations of dental and periodontal disease, and exhibiting a Plaque Index score of zero for the previous 28 days served as subjects. Plaque control measures were discontinued for 8 days and biopsies were taken from the buccal marginal gingiva of the first premolars on days 0, 2, 4, and 8. Paraffin- and Epon-embedded section, treated with a variety of histochemical stains were analyzed microscopically and cell counts were done on 1-micron Epon section. At 2 and 4 days following the beginning of plaque accumulation, the vessels subjacent to the juctional epithelium exhibited vasculitis and alterations in the perivascular collagen. There was a statistically significant increase in the number of neutrophils residing in the junctional epithelium. By the end of the 8-day period, the number of small mononuclear cells, mostly lymphocytes, in the connective tissues had increased by 3-fold and the area of collagen fiber alteration by 4-fold. In addition, the number of fibroblasts per unit area of connective tissue decreased significantly. Thus, within the period of 8 days following the beginning of plaque accumulation, an early lesion exhibiting many features characteristic of delayed hypersensitivity develops.

Salivary, blood and plasma nitrite concentrations in periodontal patients and healthy individuals before and after periodontal treatment

“…This inflammation may lead to destruction of connective tissue, periodontal ligament, and alveolar bone [1]. Disruption of the balance between proteolytic activity of matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) has been highly associated with the progression of periodontal diseases, periodontal pocket formation and bone mass loss [2].…”

Correlations between pentraxin 3 or cytokine levels in gingival crevicular fluid and clinical parameters of chronic periodontitis

“…The progression of periodontal disease is site-specific [1], and increased numbers of lymphocytes, neutrophils and macrophages are recognized in early lesions [2][3][4]. Gingival crevicular fluid (GCF) flow also increases during gingival inflammation [5,6].…”

Papel de los linfocitos T CD4+ en la destrucción ósea observada durante la periodontitis crónica

“…Mediante citometría de flujo se determinó que los pacientes con periodontitis crónica mostraron un infiltrado de linfocitos T CD4 + y CD8 + significativamente mayor que en individuos controles sanos. Estudios clásicos han establecido un predominio de infiltrado linfocitario en espécimenes gingivales humanos sometidos a lesión periodontal experimental a partir de una a dos semanas de interrumpida la higiene oral 44,45 . Seymour y colaboradores establecieron mediante inmunohistoquí-mica de muestras gingivales de estudiantes de odontología sometidos a lesiones periodontales experimentales que un predominio de linfocitos en el infiltrado inflamatorio se establecía al día 21 del período experimental 22 , observando que en todas las lesiones estudiadas alrededor del 70% correspondía al subtipo T 23 .…”

“…La presencia de células de naturaleza inflamatoria, como los polimorfonucleares neutrófilos, se consideran normales en tejidos gingivales clínicamen-te sanos, ya que participan en la homeostasis de los tejidos, infiltrando el tejido conectivo gingival desde los plexos capilares fenestrados subepiteliales y migrando al surco gingivodentario a través del epitelio de unión, en donde conforman la primera barrera defensiva del organismo ante la injuria bacteriana 20,46,47 . Por otro lado, signos histológicos de inflamación pueden aparecer en respuesta a acumulación de placa bacteriana clínicamente no visible, sin manifestar signos clínicos de inflamación 45,48 . Para evaluar el tipo celular infiltrante gingival responsable de la síntesis de RANKL en los tejidos periodon-Vernal R, Dutzan N, León R, Gamonal J.…”