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Dextran‐lnduced Inflammation and Its Effect on Keratinized Gingival Epithelium in Monkeys
Author(s) -
Nasjleti Carlos E.,
Caffesse Raul G.,
Kowalski Charles J.
Publication year - 1984
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1984.55.9.531
Subject(s) - gingival inflammation , inflammation , dextran , epithelium , medicine , mucosal inflammation , dentistry , pathology , chemistry , immunology , gingivitis , biochemistry
T he cell population present during dextran‐induced inflammation and its effect upon induced keratinization of the sulcular epithelium was investigated in two young adult male Rhesus monkeys. Keratinization of the sulcus epithelium was induced by a combined regimen of scaling, an intravenous injection of achromycin and daily rubber cup prophylaxes. After keratinization was confirmed by means of biopsies, inflammation was induced either by injecting 200 μ l of a 5% dextran saline solution or by applying the solution topically on the marginal gingiva for 2 weeks. Clinical grade dextran, molecular weight 70,000, was used. Physiologic saline solution, either injected or topical, was also used. At the same time, the daily prophylaxes were continued. After the 2 weeks, gingival biopsies were taken from each tooth treated with the different regimens. One‐half of each biopsy was routinely processed and stained with hematoxylin and eosin or Rhodamine B, while the other half was processed for and stained with alcoholic and aqueous PAS to detect dextran in tissues. Histologic evaluation was carried out in three areas: a crestal zone, a cervical zone and an oral gingival zone. An Inflammatory Index (II) was determined and the width and length of keratin were measured. Dextran, either topical or injected, produced mainly a chronic inflammatory response characterized by lymphocytes (30–35%), monocytes‐macrophages(5–10%), plasma cells (10%), polymorphonuclear leukocytes (PMNs) (15%) and unidentified cells (35%). Conversely, the physiologic saline‐induced inflammation showed PMNs (75%), lymphocytes (5%) and unidentified cells (20%). The II for injected areas was significantly higher than for those topically treated or for nontreated controls. However, the increased II did not affect the degree of keratinization achieved. The results indicate that chronic inflammation may not necessarily affect tissue keratinization if thorough removal of bacterial plaque is well maintained.