Human Gingivitis Research Articles

Extraction and characterization of the smooth-type lipopolysaccharide from Fusobacterium nucleatum JCM 8532 and its biological activities.

The lipopolysaccharide (LPS) of Fusobacterium nucleatum JCM 8532 was isolated by hot-phenol water extraction. Most of the LPS was extracted in the phenolic phase and shown to be the smooth-type, whereas the aqueous phase contained mainly rough-type LPS. The chemical composition of the LPS was similar to that reported in other studies, but D-quinovosamine, which may be a major component of O-antigenic polysaccharide, and 3-deoxy-D-manno-2-octulosonic acid (Kdoi) were detected for the first time by gas chromatography-mass spectrometry. The biological activities of smooth-type LPS, including limulus activity, lethal toxicity, pyrogenicity, and B lymphocyte mitogenicity, were comparable to those of entero-bacterial LPS. Smooth-type LPS inhibited the cell growth and DNA synthesis of adult and fetal human gingival fibroblasts in a dose-dependent manner, suggesting that LPS may play a role in the occurrence of human gingivitis.

Microbial vitality of supragingival dental plaque during initial stages of experimental gingivitis in humans.

Although vital plaque micro-organisms are part of the natural ecosystem in the oral cavity they are also the key factor in the development of diseases induced by the human dental plaque. In a previous study (9) the portion of vital bacteria related to the total number of plaque micro-organisms (i.e. the microbial vitality) appeared low in small plaque samples. The objective of this investigation was to determine the exact relationship of microbial vitality and age of supragingival plaque during the early phases of human dental plaque formation. Between intervals of optimal oral hygiene, thirteen participants refrained from all oral hygiene measures for periods of 1, 2, 4, 8, 24 and 72 h. Plaque was completely sampled from a defined area situated on the vestibular surface of the teeth 13, 14, 15, 23, 24 and 25. The pooled plaque from these areas was immediately processed. Total bacterial counts (BC) as enumerated by darkfield microscopy, and colony-forming units (CFU) were recorded. The microbial vitality was calculated indirectly as plating efficiency (PE = CFU per BC) and directly assessed using a vital fluorescence (VF) technique. In the 1 h old plaque samples the median values of PE and VF were 29% and 18%, respectively. Thereafter, the microbial vitality increased significantly with plaque age. The 24 h old plaque samples yielded values of 77% (PE) and 62% (VF). It was concluded that the microbial vitality of the early dental plaque investigated was considerably lower compared to that of a more mature plaque.

Microcirculatory dynamics in experimental human gingivitis.

The purpose of this study was to determine the changes that occur in the gingival microcirculation during the development of experimental gingivitis in humans. There have been no studies published to date combining videomicroscopy and laser Doppler flowmetry to study vascular dynamics in experimental gingivitis. Alterations occurring in the microcirculation of the marginal gingiva in 10 (18-30-year-old), healthy male humans when they suspended oral hygiene procedures in a proscribed area for 12-16 days were monitored. A partial mouth, experimental gingivitis model was employed. Gingival health was evaluated before and after the experimental period by assessing gingival and plaque indices and gingival crevicular fluid volume. Gingival vascular monitoring included measurement of red blood cell velocity in individual gingival microvessels via videomicroscopy and measurement of regional gingival blood flow using laser doppler flowmetry. The number of vessels visible in a given microscopic field in a given subject and the number of vessels exhibiting flow were also determined from the videotapes. Systemic cardiovascular and respiratory parameters were monitored to ensure that gingival vascular changes were not secondary to systemic changes. Gingivitis developed in all subjects; significant increases (Student t-test, p < 0.05) were seen in plaque index, gingival index, bleeding on probing and crevicular fluid volume. No change in superficial capillary blood velocity and a significant decrease in gingival regional blood flow were seen with gingivitis. A significant increase in the number of vessels visible in microscopic fields and a decrease in the % of vessels exhibiting flow were observed. Gingival microcirculation exhibited a dramatic, dynamic change in response to the development and progression of gingivitis.

Changes in crevicular fluid levels of interleukin-1 beta, leukotriene B4, prostaglandin E2, thromboxane B2 and tumour necrosis factor alpha in experimental gingivitis in humans.

We conducted a study to determine the sequence of cytokine and lipid mediator activation within the periodontium during the development of experimental gingivitis in humans. Crevicular fluid samples were collected from 7 previously cleaned, healthy patients at baseline, 1, 2, 3 and 4 weeks following the cessation of all oral hygiene measures. Gingival and plaque scores were taken at each visit to follow the development of gingivitis and plaque retention. Crevicular fluid samples were assayed in quadruplicate for prostaglandin E2 (PGE2), thromboxane B2 (TxB2), leukotriene B4, interleukin-1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF alpha) by RIAs or ELISAs, maintaining site pairing to examine temporal changes. Redness scores (expressed as mean percentage of sites with redness present) increased almost linearly from a baseline value of zero to approximately 40% at 1 week, 59% at 2 weeks, 83% at 3 weeks and 100% at 4 weeks. The mean % of sites with bleeding on probing increased gradually from zero at baseline to 5% at 3 weeks and then rose abruptly to 25% at 4 weeks. CF-PGE2 and CF-TxB2 levels remained fairly stable at baseline levels for the first 3 weeks then rose sharply by 2.5- and 2-fold, respectively, at 4 weeks. CF-LTB4 levels increased 2-fold by 1 week and 4-fold by 4 weeks. The CF levels of IL-1 beta increased abruptly from mean baseline values of 16.5 +/- 9.3 ng/ml to 131 +/- 76.0 ng/ml at 1 week and remained at this level for the duration of the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Gingivitis/Stomatitis in Cats

Any alteration in the balance of bacterial challenge versus the host's ability to resist and repair will result in oral lesions that are similar in appearance. The bacterial cause of gingivitis and periodontitis in humans and in all other animals in which it has been studied is firmly established, and specific species of predominantly gram-negative anaerobes have been implicated. Naturally occurring or acquired immunopathologies are likely to result in premature dental disease. When oral disease is associated with the accumulation of plaque, a positive response can be achieved by reducing the bacterial challenge to the host through the maintenance of oral hygiene by timely professional dental prophylaxis and home care. Disease that is the result of atypical immune responses, however, can be much more difficult to manage. Such oral disease can occur with either immune deficiencies or exaggerated immune responses, and it is likely that multiple mechanisms are active concurrently. In any case, gram-negative anaerobes present in plaque are likely to be a major contributing factor. Therefore patients with chronic refractory gingivitis-stomatitis must be considered to be plaque intolerant. Only with a frequent regimen of aggressive and thorough professional dental treatment plus meticulous oral home care on a daily basis can one expect to keep these cases in remission. Because this is often unrealistic, the only other way to keep these patients free of disease is by total dental extraction. The tissues that are colonized by the causative organisms must be eliminated. All root tips and bony sequestra must be removed and healing with intact epithelium accomplished before these cases will go into remission. Edentulous feline patients that continue to have signs of gingivostomatitis have been found to have an area of nonhealed bony sequestrum and chronic osteomyelitis. Once effective debridement has been accomplished and epithelial healing completed, nonresponsive cases can be expected to go into remission (Color Plate 2, Figure 7). It is hoped that as more is learned about this frustrating problem, the many factors influencing feline oral disease will be scientifically documented. In the future, actual diagnoses can be systematically made early on in disease, and treatment will be more than just symptomatic.

Vascular expansion in chronic periodontitis

Animal studies have demonstrated expansion and remodelling of gingival blood vessels in inflamed gingival tissues. However, there is a paucity of information, regarding the vascular response in human gingivitis and periodontitis. In this study, gingival biopsies were obtained from 51 separate patients. Fifteen minimally inflamed, 16 gingivitis and 20 periodontitis specimens were studied. Gingival biopsies were divided into five fields, and a quantitative survey of vascular changes was performed. In fields adjacent to the bacterial plaque irritant, vessel profiles were increased in number with the development of the advanced periodontal lesion. The diameter of blood vessels throughout the entire thickness of gingival biopsies was found to increase with advancing periodontal disease. It is concluded that considerable remodelling of the gingival vasculature occurs in chronic periodontitis, and that this may contribute to the tissue destruction seen in this disease.

Dentifrices containing new agents for the control of plaque and gingivitis: microbiological aspects

Antimicrobial agents have been proposed as playing an important role in controlling plaque and gingivitis. Unfortunately, a large number of potential compounds are unsuitable for use in dentifrices because they lack "substantivity", produce undesirable side-effects, or are incompatible with toothpaste ingredients. New agents that have been successfully incorporated into dentifrices include plant extracts, phenolic compounds and metal salts. Several products are currently being based on the phenol, Triclosan. Triclosan has a broad spectrum of antimicrobial activity against yeasts and oral bacteria. To enhance its clinical efficacy, Triclosan has been combined either with a co-polymer or with another compatible antimicrobial agent, zinc citrate. The co-polymer acts to increase the oral retention of Triclosan, and has resulted in further reductions in salivary bacterial counts in vivo. Zinc salts also have antimicrobial activity, and at low concentrations, can inhibit glycolysis and bacterial proteases. In mixed culture chemostat studies, Triclosan selectively inhibited Gram-negative periodontopathic bacteria; additive effects were obtained when zinc citrate and Triclosan were combined. In an experimental human gingivitis study, a zinc citrate/Triclosan dentifrice reduced plaque accumulation and gingivitis compared to a placebo paste; the ratio of anaerobic/aerobic bacteria and the proportions of Actinomyces species in plaque were also reduced. The prolonged use of a zinc citrate/Triclosan dentifrice neither significantly altered the ecology of supragingival plaque nor led to the selection of Triclosan-resistant bacteria. The data suggest that dentifrices containing new antimicrobial agents could be of clinical relevance in the prevention and control of plaque and gingivitis.

Transition dynamics in experimental gingivitis in humans

This study was conducted in order to investigate the dynamics of the gingival inflammatory status during periods of plaque accumulation and thorough oral hygiene. After a period of prophylaxis, 42 volunteers were asked to abstain from all oral hygiene measures for 2 weeks, whereafter oral hygiene was reinstituted. In the absence of oral hygiene, plaque was found at virtually all sites after 7 days and the number of sites with gingivitis increased simultaneously. A reduction in gingival inflammation occurred subsequent to plaque removal. During phases of both plaque accumulation and thorough oral hygiene, sites were found to convert from non-inflamed to inflamed status concurrently, as in the reverse direction. No association between plaque and gingivitis was revealed. The gingival status of a single site was a poor predictor of its status on the subsequent occasion. The proportion of inflamed sites converting to non-inflamed status was greater than the proportion of non-inflamed sites converting to inflamed status at any time. The estimated incidence rate remained fairly constant during both the plaque accumulation phase and the oral hygiene phase, whereas the estimated recovery rate was considerable lower during the plaque accumulation phase compared to oral hygiene phase. The clinical appearance is the outcome of the dynamics between these rates. The steady-state prevalences derived from the estimated "incidence" and "recovery" rates were quite similar to the actual findings after 14 d of plaque accumulation and the subsequent 10 d of thorough oral hygiene.

Relationships of serum opsonins and complement in human experimental gingivitis.

This study assessed the phagocytosis of polymorphonuclear neutrophils and the opsonic capacity of serum in experimental human gingivitis. Relationships were sought among these two measurements, clinical indices of gingivitis and complement-related opsonins. Measurements of chemiluminescence provided an index of phagocytosis and of opsonic capacity. Test group Plaque Index scores were higher than the control group on Days 7, 14, and 21, while the Gingival Index of the test group was elevated only on Day 21. Phagocytosis of test subjects' PMNs and opsonic capacity of their sera were no different from that of the controls'. Levels of C3 in both nonactivated and activated sera of the test group were significantly lower than that of the control group only on Day 14. In the test group, differences of per cent C3 conversion occurred between Days 14 and 21, and Plaque Index scores were inversely correlated with the order of per cent C3 data on these same days. Our results also indicate that complement contributes significantly to the serum opsonic capacity. The levels of developing plaque and subsequent gingival inflammation are apparently related to the degree of complement activation.

Effects of octenidine mouthrinse on plaque formation and gingivitis in humans.

Octenidine, a new bispyridine mouthrinse, has been shown to prevent plaque formation in humans over a seven‐day period. The purpose of the present study was to determine the effects of octenidine on plaque and gingivitis development in humans using a 21‐day experimental gingivitis model. Eighty‐eight subjects with a Plaque Index (PII) and Gingival Index (GI) ≤ 0.4 were randomly assigned to 4 coded formulations: 1) 0.1% octenidine in mouthwash vehicle used 3 times a day (TID), 2) 0.1% octenidine in mouthwash vehicle used twice a day (BID), placebo rinse once a day, 3) 0.1% octenidine in water used 3 times a day, and 4) mouthwash vehicle alone used 3 times a day (VEH). Each subject refrained from all mechanical plaque control and rinsed morning, noon, and evening under supervision with 15 ml of assigned formulation for 60 s. At 0, 7, 14, and 21 days, Pit, GI, and mucosal tolerance were assessed. Tooth stain was measured at day 0 and twice at day 21 (prior to and immediately following a single toothbrushing).By day seven of the rinse phase, significant mucosal irritation had occurred in several subjects in the octenidine in water group. Therefore, that group was discontinued from the study and the remaining 66 subjects continued. The mean PII increased in the VEH group from a mean of 0.13 at day 0 to 1.08, 1.39, and 1.69 at days 7, 14, and 21, respectively. In contrast, the mean PII of the TID and BID groups did not increase over the 21 day period (0.14 and 0.10, 0.18 and 0.22, 0.15 and 0.16, 0.12 and 0.16 at day 0, 7, 14, and 21 for TID and BID, respectively). Although the TID and BID groups did not statistically differ at any point, both groups demonstrated significantly less plaque accumulation than the VEH group at days 7, 14, and 21 (p &lt; 0.000001). Gingivitis, as measured by GI, increased significantly in the VEH group from a mean of 0.14 at day 0, to 0.58, 0.84 and 0.98 at day 7, 14, and 21. Both the TID and BID groups demonstrated a small increase in mean GI, rising from 0.12 and 0.16 at day 0 to 0.21 and 0.24, 0.29 and 0.27, and 0.32 and 0.31 at days 7, 14, and 21 for TID and BID, respectively. Again, the TID and BID groups were not different while both had significantly less gingivitis than the VEH group at days 7, 14, and 21 (p 0.000002). Stain, observed in 26 subjects in the TID and BID groups at day 21, was removed by a single toothbrushing in all but 5 subjects. No significant adverse reactions were observed in the remaining subjects. These results demonstrate that octenidine, when used as the only means of oral hygiene for 21 days, will significantly inhibit the development of plaque and gingivitis.

Gingival sulcular leukocytes in periodontitis and in experimental gingivitis in humans.

Leukocytes may play an important defensive role against plaque microorganisms in the periodontium. The aim of the present study was to characterize some functional and morphological aspects of sulcular leukocytes in periodontitis and in experimental gingivitis in humans. In a cross‐sectional study, cells were collected from periodontal pockets or from gingivitis (control) sites of patients with periodontitis. In a longitudinal study, cells were obtained from experimental or from control sites during a split‐mouth experimental gingivitis. Leukocytes were examined for cell numbers, viability, phagocytic function, and morphology.The cell numbers in periodontal pockets were higher than in control sites but the cell viability had a tendency to decrease. A significant decrease was also observed in the percent of leukocytes capable of phagocytizing Candida albicans in vitro in periodontitis sites compared to gingivitis sites. In the experimental gingivitis, the cell numbers showed a significant increase from day 0 to day 21 of the non‐brushing period in the experimental sites when compared to the control sites. However, the cell viability did not vary significantly between the experimental and the control sites during the experimental period. No significant variations were observed in the leukocyte in vitro phagocytic function during the same period. Polymorphonuclear leukocytes collected from the sulcus presenting different clinical situations showed various degrees of phagocytosis, loss of lysosomes, and cell lysis, but no correlation could be established between these observations and the clinical status.

The role of ascorbic acid deficiency in human gingivitis—A new hypothesis

Periodontal disease is one of the most prevalent health problems in the world and is the major cause of tooth loss in the adult population. Its two major subdivisions are gingivitis where disease is confined to the gingiva, and periodontitis where disease is present both in the gingiva and the supporting periodontal tissues. During the first stage there is a vasculitis of vessels subjacent to the junctional epithelium which is followed by exudation of fluid from the gingival sulcus and migration of leukocytes. There is variable expression of this stage throughout the mouth with new areas of involvement appearing in place of healed areas. Mast cells which are present in the gingival connective tissues may participate in this inflammatory response by liberating histamine. Ascorbic acid deficiency has been shown to be a conditioning factor in the development of gingivitis. When humans are placed on ascorbic acid deficient diets there is increased edema, redness and swelling of the gingiva. These changes have been attributed to deficient collagen production by gingival blood vessels. However, this may be due to an antihistamine role of ascorbic acid. This vitamin may act to directly detoxify histamine or effect a change in the level of enzymes responsible for histamine metabolism. This could occur through the influence of ascorbic acid in altering cyclic AMP (c-AMP) levels. Such changes in the level of this regulatory molecule could result in increased histamine-N-methyl transferase and other enzymes responsible for the breakdown of histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Experimental gingivitis in humans. A clinical and histologic investigation.

AN EXPERIMENTAL GINGIVITIS STUDY was carried out to relate the clinical parameters (plaque and gingival index) to the histologic appearance of the associated gingival lesions. Fifteen third-year dental students took part in the study. Following the withdrawal of oral hygiene, biopsies were taken on days 0, 4, 8 and 21 of the experimental period. A statistically significant association was found between the plaque and gingival indices and the various time intervals throughout the experimental period (P less than 0.001). At day 0, although all sites had a GI of 0, all but 2 of the 15 specimens showed some degree of inflammation. Histologically, these lesions consisted of over 60% lymphocytes, while plasma cells comprised less than 5% of the infiltrating population. Although the degree of inflammation increased both clinically and histologically throughout the experimental period, the nature of the infiltrate did not change significantly. Lymphocytes remained as the dominant cell type. In fact, no association was seen between the degree of inflammation and the nature of the infiltrating cells.

Histopathology of initial gingivitis in humans. A pilot study.

The present study concerns the inflammatory alterations in the gingival margin during initial gingivitis in 11-13 year old human subjects. At day 0 of the experiment, all participants had clean teeth and healthy gingiva. All active oral hygiene measures were excluded for 4 days. From upper and lower premolars, which were extracted for orthodontic reasons, contralateral gingival biopsies, including the tooth and the adjacent gingiva, were obtained on days 0 and 4. The presence of inflammatory cells in the junctional epithelium and the adjacent connective tissue was determined quantitatively in semi-thin sections. The collagen content of the gingival margin was also determined. From day 0 to day 4 there was only a slight increase in the number of neutrophilic granulocytes in the junctional epithelium and adjacent connective tissue, while a more pronounced increase was found in the number of mononuclear leukocytes. A loss of collagen was noticed in 4 of the subjects, while 2 did not show any changes in collagen content. The inflammatory reaction seen in the present study differs somewhat from that observed in adult humans and adult dogs. The results correspond more to the reaction seen in juvenile dogs.

Effect of a new anti-plaque agent (CK-0569A) on developing plaque and gingivitis in man.

This study investigated the effect of 1,4-bis[3-(n-hexylcarbamylguanidine)propyl]piperazine dimethanesulfonic acid salt (CK-0569A), used as a mouthrinse, on the development of plaque and gingivitis in humans. Fourteen dental students participated in a double-blind cross-over study. At the start of each of the two 14-day periods of mouthrinsing (one period with CK-0569A and one period with a placebo solution) the participants were examined for the presence of plaque (P1I) and gingivitis (GI). In addition, supragingival plaque samples were obtained and analyzed by darkfield microscopy. Clinical examination of plaque and gingivitis was repeated 4, 7 and 14 days after the start of the no-toothbrushing periods. Bacterial samples were obtained after 7 and 14 days of trial. The results demonstrated that a mouthrinse containing CK-0569A prevented the colonization of motile + curved rods and spirochetes in developing plaque. Furthermore, rinsing twice daily with 0.1% solution CK-0569A significantly reduced the amount of dental plaque formed and retarded the development of gingivitis.

Periodontal disease in gnotobiotic rats.

The present investigation was carried out in order to assess the development of periodontal disease in germfree rats infected with microorganisms associated with human gingivitis, periodontitis and periodontosis lesions. One hundred and forty gnotobiotic rats of the Spraque‐Dawley strain were weaned 21 days after birth and then randomly divided into five groups (four experimental groups and one control) consisting of 28 animals each. After weaning the animals of the experimental groups were infected with one of the following strains; strain I (Actinomyces naeslundii), strain 1073 (Eikenella corrodens), strain 381 (Bacteroides asaccharolyticus), strain 4 (Capnocytophage sputigena). Animals were sacrificed to provide specimens for examination 14, 28, 56 and 84 days after infection. Germ‐free controls were sacrificed at the same time intervals.The degree of alveolar bone loss was assessed on defleshed and dried jaws. Microscopic assessments regarding loss of connective tissue attachment, degree of bone resorption, and degree of impaction of hair and bedding material were determined in histological sections. In addition, a morphometric analysis of the gingival tissues was carried out using a standardized morphometric test procedure.The results showed that germfree rats monoinfected with different bacteria associated with human periodontal diseases may suffer severe breakdown of the periodontal tissues. The degree of breakdown tended to increase with increasing experimental time. However, periodontal tissue destruction was obviously related to the impaction of hair and bedding material. In fact, only in areas with severe impaction of foreign material could gross destruction of the supporting apparatus be recognized.

Studies of host responses during experimental gingivitis in humans

To determine if the early accumulation of plaque in experimental gingivitis is associated with systemic alterations in acute phase serum proteins, immunoglobulins and complement, serial serum specimens were obtained from experimental subjects and matched controls. Therre were no singnificant changes in acute phase reactants (C‐reactive protein, transferrin, alpha‐1‐antitrypsin) or IgG, IgA or IgM. Total hemolytic complement (CH50) and C4 quantitative levels rose significantly in the experimental subjects 21 days after discontinuing oral hygiene, but not in the controls. There were no significant changes in C3 or Factor B levels in either group. Thus, there was no evidence of gross activation of the complement system by either pathway (e.g. consumptive depletion). On the other hand, functional analysis of the sera for spontaneous, complement derived, neutrophil chemotactic activity (SCA) revealed the following: (1) significant elevation in SCA occurred in the experimental subjects 3 and 21 days after discontinuing oral hygiene (compared to the Day 0 baseline value) but did not occur in the controls; (2) the elevated SCA was C5‐dependent; and (3) elevated serum SCA at days 3 and 21 was correlated with the enhancement of plaque mediated lysosomal release from polymorphonuclear leukocytes, incubated with aliquots of these sera. The data suggest that subtle degrees of systemic complement activation occur in experimental gingivitis but are only detected by sensitive, functional assays.

Studies of host responses during experimental gingivitis in humans

The aim of the study was to find out whether autologous supragingival plaques collected at various times during the development of experimental gingivitis in men differ in their potential to induce PMN responses in vitro. Ten subjects refrained from all oral hygiene for a period of 21 days. At day 0, Day 3 and Day 21 after cressation of oral hygiene clinical indices (plaque index, gingival index, gingival crevicular fluid flow) were assessed plaque was collected at day 3 and Day 21 after cessation of Oral hygiene clinical indices (plaque index, gingival index, gingival crevicular fluid flow) were assessed plaque was collected at Day 3 and Day 21. PMNs, isolated from peripheral blood 1–2 months after the non‐brushing period were incubated with the various autologous plaques in the presence or the absence of autologous serum. Supernatants of cell cultures were monitored for extracellular release of lysosomal constituents, viz. lysozyme, myeloperoxidase and lactoferrin. There was no difference in the amounts of lysozyme, myeloperox dase and lactoferrin. There was no difference in the amounts of lysozyme or myeloperoxidase released by PMNs. The inclusion of fresh serum enhanced PMN release reactions but there was no significant differences in the relative capacity of Day 0, Day3 and Day 21 sera to modulate PMN responses. A statistically significant positive correlation was established betwen the magnitude of lactoferrin release from PMNs exposed to Day 3 plaque and the gingival fluid flow recorded on Day3. Lactoferrin is segregated in the specific granules of the PMNs which also contain other cationic proteins, collagenases and neutral proteinases. These data suggest that a possible causal relationship may exit between the release of PMN constituents and the development of inflammation during the early phases of gingivitis.

Bacteriology of human experimental gingivitis: effect of plaque and gingivitis score.

The plaque flora isolated from discrete dentogingival sites during a human gingivitis experiment was analyzed as a function of the plaque score and of the gingivitis score. When the gingivitis score was plotted as a function of the plaque score, a nonbleeding gingivitis was associated with a proportional increase in the Actinomyces sp. at the expense of the Streptococcus sp. In particular, the percentage of Actinomyces israelii increased significantly, while the percent Streptococcus sanguis decreased significantly. A. israelii also increased significantly when a bleeding gingivitis developed. When the plaque score was plotted as a function of the gingivitis score, A. israelii increased significantly as the nonbleeding gingivitis developed, but A. viscosus and Bacteroides melaninogenicus increased significantly when the bleeding gingivitis developed. The availability of a sufficient number of plaques with a plaque score of 2.0 permitted the examination of the interrelationship of gingivitis and flora minus the effect of plaque biomass. The bacteriological profile showed that when bleeding occurred, the levels and proportions of A. viscosus and B. melaninogenicus increased significantly. These findings raise the possibility that proportional changes in the gingival plaque flora may uniquely contribute to the development of gingival inflammation in this experimental model.

Reduction of the formation of dental plaque and gingivitis in humans by crude mutanase

The effect of a Trichoderma harzianum enzyme preparation containing mutanase (alpha-1,3 glucan glucanohydrolase) on plaque accumulation and composition and on occurrence of gingivitis was assessed in 20 persons in a double-blind cross-over investigation. The enzyme preparation was administered in chewing gum. Two test periods of 1 week were preceded by scaling and cleansing of the teeth, oral hygiene instruction, and controlled hygiene for at least 3 weeks. Oral hygiene measures were discontinued during the test periods, while the persons chewed six pieces of chewing gum per day, one half using enzyme-containing gum, and the other half using placebo gum. The test periods were identical, only enzyme gum was used instead of placebo, or vice versa. Evaluations of plaque and gingivitis showed that less plaque had accumulated and less gingivitis developed during the enzyme than during the placebo period, but bacteriologic studies of interproximal plaque did not reveal differences that could explain the clinical findings. Treatment with the enzyme preparation caused some local side effects, but no primary skin irritation, delayed hypersensitivity, nor anti-enzyme IgE was detected in any of the persons.