Медицина/ 8. Морфология

Ph.D Shnayder

Odessa State Medical University, Odessa, Ukraine

Periodontum Tissue regenration after the modelling of periodontitis

The course of chronic periodontitis consists of consequent exacerbation and remission periods. Severe disease is assiciated with prolonged exacerbations with heavier periodontum tissue damage, while the duration of remission periods decreases. Researcher are focused on determination of exacerbation causes after remission and development of pathogenesis-based strategies of exacerbation prevention. Various exogenous negative factors are being studied (ecological factors, anthropogenous factors, etc). Organism’s resistance and reactivity disorders and their role in the process of remission conversion to exacerbation are considered to be points of concern also.

Previous studies provided the morphometric characteristics of periodontum tissue damage at various stages of the disease; however, the processes of periodontum regeneration during the remission period are not yet fully studied. No systematized data on periodontum tissue regeneration capacity are available; therefore, the development of outcomes prediction methods and treatment efficacy control methods becomes impossible.

Study objective: evaluation of periodontum tissue regeneration after completion of periodontitis modelling. Adult Wistar male rats were used for modelling. The study was conducted according to the principles of European Convent on protection of vertebrates used for research and scientific purposes. Model of decreased mastication was used for reconstruction of chronic generalized periodontitis. Rats were slaughtered at Day 30 of modelling and at Days 7, 14, 21 and 30 after the completion of reconstruction. The fragment of maxilla was removed for preparation of histological specimen, using the standard methods. Staining – hematoxillin-eosin and Van Gisone; light microsopy was used during the analysis.

In order to form the control group, the tissue of periodontum at Day 30 of modelling was characterized. All structural elements of periodontum were involved in the inflammation at that time. The gingival epithelium was flattened, with large areas of keratinized plaques desquamation. Nuclei of spiked cells without any signs of functioning. The margin between epithelium and connective tissue wasnot clear. The gingival connective tissue was characterised by edema and structural desorganization with collagen fibres degrading. Edema-related changes of fibroblasts and fibrocytes. Incrased number of tissue basophilic cells. Widened blood vessels with manifested hyperemia and multiple leukocytes (both granular and agranular) in lumen were found. The size of gingival pouches was decreased; the structure of dental-gingival connections was disordered. Collagen fibres of periodontum: disorganisation and degrading. Blood vessels: marked dilation, wall integrity breached with perivascular hemorrhages. Lysis of bone tissue and cementum of teeth radices. Region of radix apex: destruction of periodontum. Areas of periodontum close to dental-gingival connection: infiltration with leukocytes.

Day 7 after the completion of modelling: no significant regeneration-related chages of periodontum were observed. Rate of destruction was found to be comparable with changes at Day 30 of periodontitis modelling. Changes were limited to lesser number of hemorrhages in periodontum. Day 14 after completion of modelling: increased functional activity of nuclei in basal and spiked layers of gingival epithelium. Increased number of mitosis was found in epithelium cells. Single areas of hemorrhage were found in periodontum. The regeneration of dental – gingival connection was found.

Day 21 after modeling completion: areas of periodontium collagen fibers were still found in periodontium around the radices of molars. Areas close to dental-gingival connection: local changes of periodontium destruction were still found; however, the number and areas of infiltrates decreased and their cell components changed. In particular, mostly plasma cells were found. Complete regeneration of dental-gingival epithelium connection was not demonstrated.

Day 30 after modeling completion: structure of collagen fibers of periodontium not restored. Most significant changes were found in regions close to tooth radix and the dental-gingival epithelial connection. Gingival connective tissue: areas of fibrosis with overlying epithelium containing more cells with decreased functional activity were found. Regeneration of dental-gingival connection was found in all areas examined; however, the histo-topographic changes of periodontium (e.g., relative denudation of molars) would not return to level found in intact controls.

Therefore, periodontitis modeling based on mastication loading decrease is associated with degeneration of periodontium tissues. The signs of inflammation occur at Day 30 of the modeling. Lack of complete regeneration after modeling can probably promote recurrent disease. Probably, the destruction of collagen fibers architectonics resulting in disordered distribution of loading on periodontium that causes mechanical destruction of the latter. These conditions promote further disorganization of collagen fibers of periodontium associated with destruction of alveolar process of the jaw. All these factors increase the mobility of teeth that was demonstrated by our previous studies. Therefore, the pathological vicious circle is formed that promotes the progression of disease. Incomplete regeneration of the dental-gingival barrier decreases the resistance rate of periodontium tissues to traumas, oral flora and inflammation. These factors promote the recurrence of the disease and increase its progress rate.

Conclusions. Modeling of periodontitis based on mastication loading decrease is associated with prevalence of dystrophic changes in periodontium. Sequence of structures affected by the pathological process during the modeling of periodontitis: connective tissue of gingival mucosa, gingival epithelium, periodontium close to dental-gingival connection, bone tissue of alveolar process of maxilla. No complete regeneration of periodontium tissue occurs after modeling; the regeneration of periodontium and gingival mucosa remains incomplete. The changes of periodontum’s collagen fibers architectonics and the remaining degenerative changes of gingival mucosa promote the recurrence of periodontitis.