Clinical and inflammatory effects of galvano-ceramic and metal-ceramic crowns on periodontal tissues.

Prosthetic crowns made by galvano-forming are considered to be highly biocompatible and aesthetic restorations. Therefore, they represent an alternative crown-system to conventional metal-ceramic crowns in replacing lost tooth structure. However, there are few data available on clinical and biochemical effects of galvano-ceramic crowns on periodontal tissues. The purpose of this controlled study was to test the impact of galvano-ceramic crowns and metal-ceramic crowns on clinical and inflammatory responses of periodontal tissues. A prospective, blinded randomized clinical trial was conducted. Galvano-ceramic crowns and metal-ceramic crowns were placed in 52 periodontally healthy patients in split-mouth design. Clinical parameters (gingival index, plaque index, probing depths and recessions) were recorded from six sites per tooth. Initial tissue alteration was accessed analysing the gingival crevicular fluid flow rate and IgG concentration in gingival crevicular fluid. After 24 months, 34 patients could be re-evaluated. All crowns were in adequate function and obvious clinical inflammation was rarely observed. After 24 months of follow-up, gingival tissues adjacent to galvano-ceramic crowns showed significantly less signs of clinical and inflammatory responses according to plaque index (P = 0.004), gingival index (P < 0.001), gingival crevicular fluid flow rate (P = 0.012) and IgG (P = 0.002). Data were also analyzed for buccal and oral sites separately. Gingival tissues adjacent to metal-ceramic crowns showed significantly increased clinical and inflammatory values for plaque index (P = 0.005), gingival index (P = 0.008), gingival crevicular fluid flow rate (P = 0.006), IgG (P = 0.007) at oral sites compared to galvano-ceramic crowns. Our data suggest a stabilizing effect of galvano-ceramic crowns on periodontal tissues over time.

Levels of parotid and submandibular/sublingual salivary immunoglobulin A in response to experimental gingivitis in humans.

Salivary secretory IgA (s-IgA) is considered to act as an important first line of defense mechanism in the oral cavity. It has therefore been suggested that an increased antigenic load would induce an increase in salivary IgA production. This study investigated the pure glandular levels of salivary IgA in parotid and submandibular/sublingual (SM/SL) saliva during plaque accumulation leading to experimental gingivitis. Starting from regular oral hygiene, 14 healthy, nonsmoking men refrained from all oral hygiene measures for 12 days. On days -2, 0, 3, 6, and 12 a plaque index, a bleeding index, and unstimulated and stimulated saliva from the parotid and the SM/SL glands were measured. Salivary IgA was quantified using a sandwich ELISA. All subjects developed gingivitis as measured by a bleeding index. Compared to baseline the salivary flow rate was increased on day 12. Regarding the secretion rate of IgA there was a statistically significant increase in stimulated parotid saliva but not SM/SL saliva compared to baseline after 6 and 12 days without oral hygiene. No significant changes were observed for the concentration of IgA during the trial. Thus, in healthy subjects with regular oral hygiene the development of plaque induced gingivitis is associated with increased salivary gland output and increased total IgA output levels in stimulated parotid saliva but not in SM/SL saliva.

Salivary IgA subclasses and bacteria-reactive IgA in patients with aggressive periodontitis.

The local salivary immunoglobulin A (IgA) response in patients with aggressive periodontitis to oral microorganisms and its role for the pathogenesis has not been determined. This study investigated the hypothesis that aggressive periodontitis patients have impaired oral secretory immunity. Our test group was made-up of 19 aggressive periodontitis patients and 19 age- and gender-matched periodontally healthy controls. Total IgA, IgA subclass 1, IgA subclass 2 and IgA reactive to Actinobacillus actinomycetemcomitans Y4, Treponema denticola ATCC 35404 and Candida albicans DSM 3454 were determined by enzyme-linked immunosorbent assay in whole unstimulated and stimulated saliva. A statistically significantly lower concentration and secretion rate of total salivary IgA (P < 0.01) and IgA1 (P < 0.001) was found in the aggressive periodontitis group in resting and stimulated saliva. A decrease of IgA2 (P < 0.05) was seen in resting saliva. Although only minor differences were detected in the concentration and secretion of bacteria-reactive IgA in both groups, the proportion of bacteria-reactive IgA from the total IgA was significantly higher (P < 0.01) in the aggressive periodontitis group in all three microorganisms tested. Our results indicate an inhibition of total secretory IgA. In particular an IgA subclass 1-specific decrease in aggressive periodontitis was noted, while the bacteria-reactive humoral immune system in saliva was activated. The role of the decrease of IgA1 immunoglobulins in aggressive periodontitis with respect to susceptibility for periodontal diseases has to be elucidated.

Total IgA and Porphyromonas gingivalis-reactive IgA in the saliva of patients with generalised early-onset periodontitis.

Generalised early-onset periodontitis (GEOP) is characterized by acute inflammatory bursts, resulting in rapid destruction of the periodontal apparatus in young adults. An impaired host defense seems to play an important role as etiological factor of periodontitis, especially in the development of GEOP. As the gram-negative Porphyromonas gingivalis has been identified as one of the causative anaerobic bacteria, the humoral immune response to this micro-organism is of particular interest in patients with GEOP. To evaluate the local immune status, we measured total and P. gingivalis-reactive salivary IgA in GEOP patients and in age- and gender-matched periodontally normal controls. We found a significantly lower concentration and secretion rate of total salivary IgA in the GEOP group. Although no differences were detected in the concentration or secretion of P. gingivalis-reactive IgA between groups, the specific fraction of P. gingivalis-reactive IgA of the total IgA was significantly higher in the GEOP group. These findings indicate an inhibition of total secretory IgA in GEOP, while the P. gingivalis-reactive humoral immune system in saliva is, however, activated. P. gingivalis seems to selectively activate IgA lymphocyte clones and induces a switch in the fraction of specific IgA.

[Treatment of a patient with advanced periodontitis]. / Behandlung eines Patienten mit weit fortgeschrittener Parodontitis.

This case report presents the planning and clinical treatment of a patient with advanced periodontitis and insufficient prosthetic reconstruction. After initial therapy with extraction of the unrestorable teeth, periodontal surgery was performed partly by means of the implantation of hydroxyapatite into bony defects. The prosthodontic treatment consisted of a fixed/removable prosthesis in the maxilla, together with a shortened teeth arch in the mandible. This clinical treatment, combined with regular recalls, has ensured the patient a functional and esthetic reconstruction for a period of 4 years.

[Role of antibodies in periodontal disease]. / Rôle des anticorps dans les parodontopathies.

Bacteria and their products play a key role in the etiology of periodontitis. They activate the host immunologic system which produces specific immunoglobulins (Ig). Mainly IgA, IgG and IgM are found in the oral environment, in the saliva IgA are present as secretory IgA. In case of periodontitis, the tissular destruction could be practically explained by spontaneous hypersensibility reactions which may contribute to deteriorate the periodontal tissues. Considering the complexity of the factors involved in periodontal inflammation (i.e. bacterial variety, difference of properties, patient's individuality, difference of analysis methods), the question of the exact role played by the antibodies still remains open.