Cigarette smoking leads to lowered elastase and neutrophil levels in the oral cavity. The oral neutrophil elastase assay, therefore, cannot be used to measure the periodontal status of smokers.

The study was designed to find out whether oral elastase activity could be used as a simple biochemical indicator of periodontal health. Both stimulated whole saliva and water rinse samples were collected from subjects with different degrees of adult periodontitis, gingivitis or healthy periodontium. In both sample types, elastase was mostly bound to insoluble fraction and preferred valine containing synthetic substrate, similar to neutrophil elastase. The elastase measurement required very little manipulation or time and its reproducibility was found to be good. The elastase levels were found to be negligible in edentulous subjects and usually very low in subjects with healthy periodontium. In about 85% of periodontitis cases having at least 1 deep periodontal pocket ( > or = 6 mm), clearly elevated elastases levels were detected in both the saliva and r rinse samples. In advanced periodontitis cases, the colour reaction took place in 0.5 to 2 h. In localized periodontitis cases, 2- to 18-h incubations were required for positive reaction. There was a good correlation between the elastase activity and the number of deep periodontal pockets and the average community periodontal index of the subjects. Elastase activity was not a good indicator of gingivitis. About 45% of gingivitis cases were positive with the elastase test, and the enzyme values were not significantly increased in experimental gingivitis. In a longitudinal study on advanced periodontitis cases, elastase levels dropped dramatically as a result of clinically successful therapy, close to the values of healthy subjects. The oral elastase test could serve as a valuable adjunct in periodontal screening and assessment of treatment efficacy.

Enzyme activity in whole saliva of trypsin‐like protease, elastase‐like protease, general protease, and three glycosidases was measured by colorimetric assays, using synthetic substrates. A study group of 24 adults with advanced periodontitis was compared to a control group of 25 subjects with healthy periodontium. Clinical parameters and levels of enzyme activity were assessed at baseline, after non‐surgical periodontal therapy (at 8 months), following the maintenance phase or periodontal surgery (at 15 months), and after the maintenance phase with or without systemic chemotherapy (at 20 months). The mean values of the proteolytic enzymatic activity and the activity of two glycosidases in whole saliva were significantly higher in the study group than in the control group at baseline. After the initial treatment phase at 8 months, all three proteases were reduced significantly, but the glycosidases were still high. After all treatment phases at 20 months, the activity of both the proteases and glycosidases approximated the values of the healthy group. In the saliva samples collected prior to treatment and following non‐surgical periodontal therapy, the activity of salivary elastase correlated significantly with the number of deep gingival pockets (PD ≥ 6 mm) and with either gingival index (GI) or the percentage of bleeding sites (BOP%). The enzyme activity in whole saliva appears to reflect the status of periodontal health. Salivary elastase shows good potential to serve as a novel adjunct to detect destructive periodontal inflammation and to follow periodontal healing after treatment. J Periodontol 1993;64:297–301.

The aim of the study was to find out which clinical, radiographic and microbiological variables can be used as prognostic criteria for the efficiency of the commonly used initial treatment protocol comprising scaling, root planing and instruction on oral hygiene in advanced adult periodontitis. 46 patients (mean age 48 years) with untreated, advanced periodontitis volunteered for the study. The clinical examination included recordings of plaque, gingival and calculus indices, probing pocket depths, bleeding and suppuration after probing, probing attachment levels and furcation involvements. Infrabony and furcation lesions were assessed from panoramic radiographs. Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis were cultured from the deepest, most inflamed periodontal pockets, from surface of the tongue and from saliva. 3 months after the completion of non‐surgical treatment comprising meticulous scaling and root planing and instruction on oral hygiene, the healing was assessed clinically, and 13 patients were assigned to a maintenance care programme (MC) and 33 to further treatment procedures (FT). Evaluation of the baseline clinical and radiographic data showed a significantly higher %s of 6 mm deep periodontal pockets, surfaces with suppuration, and sites with subgingival calculus, as well as higher numbers of infrabony lesions, in FT‐patients than in MC‐patients. Subgingival A. actinomycetemcomitans was isolated at baseline in 55% of the FT‐patients and in 38% of the MC‐patients, and P. gingivalis in 27% and 23%, respectively. A. actinomycetemcomitans was eradicated by non‐surgical treatment from only one patient. P. gingivalis was detected in 15% of the patients in both groups after treatment. Combining of the clinical and the microbiological baseline data demonstrated that simultaneous presence of multiple deep periodontal pockets (6 mm at 10% of the sites) and subgingival A. actinomycetemcomitans alone or concomitant with P. gingivalis was significantly more prevalent in the FT‐group than in the MC‐group. This simultaneous presence anticipated insufficient response to initial non‐surgical therapy. The results suggest that a treatment regimen more efficient than the traditional one is needed without delay in the treatment of A. actinomycetemcomitans infected generalized, severe periodontal disease in adults.

Severe forms of chronic periodontitis affect up to 10% of adults. Tumour necrosis factor and lymphotoxin‐α genes in the major histocompatibility complex are associated with severe periodontitis. Complement factor C4 is a nearby, polymorphic, functionally relevant gene region. Although associated with chronic mucosal infections, C4 deficiencies have not been assessed in adult periodontitis patients. We tested whether complement levels are systemically altered and C4 deficiencies associated with severe chronic periodontitis. In a case–control study, we analysed levels of plasma C3, and C4, serum classical pathway haemolytic activity, C4 allotypes and C4 gene numbers in 37 patients with severe chronic periodontitis and in 150 voluntary controls. Plasma levels of C3 were higher, and classical pathway haemolytic activity was lower in patients than in controls. Partial C4 gene deficiencies were more frequent in patients than in controls (odds ratio 2.4, 95% confidence interval 1.1–5.5, P = 0.032). Changes in complement levels may reflect chronic, recurring inflammation. C4 gene deficiencies are associated with predisposition to chronic periodontitis.