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Sanguinarine, a new antiplaque agent: retention and plaque specificity.

Sanguinarine, a component of sanguinaria extract, was investigated for anti-plaque activity and retention in the oral cavity. Oral rinses containing sanguinaria extract showed antiplaque activity in humans. Uptake and retention levels of sanguinarine in plaque and saliva were determined by high-pressure liquid chromatography and sanguinarine levels in plaque were higher than in vitro minimum inhibitory concentrations against oral aerobic and anaerobic bacteria. Further, sanguinarine was able to disclose plaque with the aid of long-wave ultraviolet light and was retained longer than erythrosine and sodium fluorescein as shown by measurement of plaque area. It was concluded that sanguinarine has a high specificity and retention in dental plaque. The plaque-retentive properties in combination with antimicrobial action may be responsible for its clinical anti-plaque efficacy.

Adolescent↗

Selective modulation of protein kinase A and protein kinase C activities in epidermal growth factor (EGF)-stimulated MCF-7 breast cancer cells.

In human MCF-7 breast cancer cells, both protein kinase A (PKA) and different members of the protein kinase C (PKC) family are stimulated upon binding of epidermal growth factor (EGF) to cell surface receptors. Selective stimulation of calcium-dependent PKCs with 10(-6) to 10(-9) M Thymeleatoxin significantly increased the proliferation rate of MCF-7 cells over 5 days in culture. This stimulation was blocked by the PKC antagonist Chelerythrine. In contrast, selective activation of PKA by addition of 1 mM dibutyryl cyclic AMP (dBcAMP) did not affect the proliferation rate of MCF-7 cells. Similarly, activation of the adenylate cyclase by 1 microM Forskolin and inhibition of PKA by the cyclic AMP analogue Rp-cAMPS did not modulate the proliferation rate of these cells. Activation of PKC stimulated the expression of the immediate early gene c-fos but c-myc expression was not significantly enhanced. On the other hand, PKA activation increased both c-myc and c-fos expression in MCF-7 cells. These results suggest that PKA activation and c-myc expression are not obligatory for proliferation of MCF-7 cells.

Alkaloids↗

A new phenylpropanoid ester from the bark of Zanthoxylum scandens (Rutaceae).

The alkaloids norchelerythrine, magnoflorine and (-)(S)-O-methylbalfourodinium cation were isolated from Zanthoxylum scandens bark collected in Vietnam, together with the flavanone glycoside hesperidin and the phenylpropanoids (E)-O-geranylconiferyl alcohol and (E)-O-geranylconiferyl alcohol (9Z, 12Z)-linoleate. This latter is a novel compound whose structure was elucidated on the basis of its spectral data and confirmed by chemical correlation.

Alkaloids↗

Recent advances in targeting regulators of apoptosis in cancer cells for therapeutic gain.

Apoptosis is a fundamental cellular death process that is essential for normal tissue homeostasis, whose deregulation is associated with several human disease states, including cancer. Increased understanding of cancer biology has led to the hypothesis that although cancer cells are inherently resistant to the engagement of apoptosis due to the deregulation of molecular components of core apoptotic machinery or of survival signalling cascades, they are primed to die as a result of microenvironmental and oncogenic proapoptotic stress. Recently, deeper insight into the molecular regulation of apoptosis and, specifically, into its deregulation in cancer has led to the development of promising therapies to restore apoptosis and enable selective tumour cell kill. It is hoped that these mechanism-based therapies will exhibit less problematic toxicity profiles than those of conventional agents. Moreover, the development of tailored therapies directed at malignancies bearing specific alterations in apoptotic or survival signalling components may be used in combination approaches to overcome the resistance to other forms of treatment.

Alkaloids↗

Protein kinase C dependent and independent mechanisms controlling rat trophoblast cell DNA synthesis and differentiation.

Trophoblast giant cells are the steroidogenic cells of the rat placenta. In this study, the role of protein kinase C signalling pathways in the control of DNA synthesis and differentiation-dependent progesterone biosynthesis by trophoblast cells were investigated. Rcho-1 trophoblast cells, derived from a rat choriocarcinoma, can be experimentally manipulated to proliferate or differentiate and provide a useful model for studying trophoblast giant cell endocrine differentiation. The role of protein kinase C signal transduction was examined through the treatment of Rcho-1 trophoblast cells with isoquinolinesulfonamide derivatives (H7, a protein kinase C inhibitor; HA1004, a control compound), chelytherine (a protein kinase C inhibitor), and phorbol esters (protein kinase C activators). Treatment with H7 significantly attenuated DNA synthesis in proliferating and differentiating trophoblast cells and accelerated the acquisition of progesterone biosynthetic capabilities by trophoblast cells. Treatment with HA1004, the related but functionally distinct isoquinolone, did not significantly affect trophoblast DNA synthesis or proliferation and only weakly increased progesterone accumulation. Chelytherine significantly inhibited trophoblast cell proliferation but failed to influence trophoblast progesterone production significantly. The phorbol ester, 12-O-tetradecanoylphorbol acetate, did not significantly influence progesterone accumulation. H7 did not significantly influence the concentration of either P450scc or the mRNA encoding it in Rcho-1 trophoblast cells, or the transcriptional activity of the P450scc gene. The results indicate that signalling pathways sensitive to protein kinase C are involved in the control of trophoblast cell proliferation. Differentiation-dependent production of progesterone is sensitive to H7 but appears to be independent of protein kinase C and occurs at a stage other than P450scc expression.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Pharmacological preconditioning with bradykinin affords myocardial protection through NO-dependent mechanisms.

Bradykinin (BK) is one of the triggers of ischemic preconditioning. Protein kinase C (PKC) and mitochondrial ATP-dependent potassium (K(ATP)) channels are central factors in cardioprotection afforded by BK. However, the role of nitric oxide (NO) in the early phase protection of preconditioning with BK is not well understood. We assessed the signaling pathway of the early phase protection of pharmacological preconditioning afforded by BK. Isolated perfused rat hearts (n = 8/group) were subjected to 30-minute global ischemia and 50-minute reperfusion. Left ventricular systolic pressure (LVSP) was recorded prior to the global ischemia and at the end of reperfusion. Preconditioning with BK was induced by two cycles of 5-minute infusion of BK (0.5 micromol/L) and 5-minute washout prior to the global ischemia. To examine participants in the signaling pathway, 5-hydroxydecanoate (5-HD, 200 micromol/L), chelerythrine (CH, 5 micromol/L), or N(omega)-nitro-L-arginine methyl ester (L-NAME, 50 mmol/L) was added to the perfusate for 5 minutes prior to the infusion of BK. Pharmacological preconditioning by BK improved postischemic recovery of LVSP (+ 45.1% versus control, P < 0.01). Protection by BK was abolished by coadministration of CH, 5-HD, or L-NAME. BK affords myocardial protection in the early phase of pharmacological preconditioning through a pathway that includes endogenous NO, PKC, and mitochondrial K(ATP) channels.

Alkaloids↗

Down-regulation of connexin43 in early myocardial ischemia and protective effect by ischemic preconditioning in rat hearts in vivo.

Connexin 43 (Cx43), a primary component of gap junctions, contributes to intercellular electrochemical communication. Cx43 undergoes dephosphorylation in early ischemia. We examined whether Cx43 is degraded in association with dephosphorylation during early myocardial ischemia and whether ischemic preconditioning (IP) affects the degradation after rat coronary artery occlusion. Male Sprague-Dawley rats underwent coronary artery occlusion for 1, 2, or 3 hours, or for 1 hour following treatment either with a calcineurin inhibitor (cyclosporine A), proteasome inhibitor (PSI), or lysosomal inhibitor (E64c), or following IP alone or after protein kinase C (PKC) inhibitor (chelerythrine) pretreatment. The IP was afforded by three cycles of 3 minute ischemia and 5 minute reperfusion. A large portion of the phosphorylated Cx43 (pCx43) in the membrane fraction was dephosphorylated, while a small portion was degraded at 1 hour of ischemia. The effects of the inhibitors were dephosphorylation and degradation by calcineurin and proteasome/lysosome, respectively. IP suppressed the decrease in pCx43 and increase in dCx43, while only the former was inhibited by the PKC inhibitor chelerythrine. The Cx43 mRNA level was reduced at 3 hours, but not at 1 hour of ischemia, irrespective of IP. We believe that Cx43 is dephosphorylated and degraded in early ischemia, whereas Cx43 transcription was suppressed at a later phase of ischemia.

Alkaloids↗

Dual concentration-dependent effects of phorbol 12, 13-dibutyrate on spontaneous and acetylcholine-induced electrical responses recorded from isolated circular smooth muscle of the guinea-pig stomach antrum.

Intracellular recordings of electrical activity were made from circular smooth muscle cells in small segments of tissue isolated from the guinea-pig stomach antrum. Every cell that was impaled exhibited a rhythmic generation of slow potentials. Experiments were carried out to test the effects of three different concentrations (1, 10 and 100 nM) of phorbol 12, 13-dibutyrate (PDBu) on these slow potentials and on the responses produced by acetylcholine (ACh), in the presence of nifedipine and N(omega)-nitro-L-arginine (nitroarginine), known inhibitors of L-type Ca-channels and nitric oxide synthase, respectively. The resting membrane potential was -62 +/- 7 mV, while the frequency and amplitude of the slow potentials were 1.6 +/- 0.1 cycle per min (cpm) and 33 +/- 1 mV, respectively. Application of 1 nM PDBu increased the frequency of slow potentials, with no significant change in the membrane potential and amplitude of slow potentials. At a concentration of 100 nM, PDBu depolarized the membrane by about 6 mV, and either decreased the amplitude and frequency of the slow potentials or abolished them. The amplitude and frequency of the slow potentials were not significantly changed in the presence of 10 nM PDBu. In the presence of chelerythrine (1-2 microM), a known inhibitor of protein kinase C (PKC), the increase in frequency of slow potentials by 1 nM PDBu and depolarization produced by 100 nM PDBu were not elicited. The increase in frequency of slow potentials by 100 nM ACh was inhibited by PDBu, in a concentration-dependent manner, and ACh-responses were abolished in the presence of 100 nM PDBu. These results indicate that PDBu has dual actions on the spontaneous activity of antral circular muscle, with low concentrations increasing and high concentrations inhibiting the frequency of the slow potentials. The former may be produced by activation of protein kinase C (PKC). As the ACh-induced excitation of slow potentials is inhibited by PDBu, a possible causal relationship between the inhibition and over-activation of PKC is considered.

Acetylcholine↗

Involvement of protein kinase C-related anti-apoptosis signaling in radiation-induced apoptosis in murine thymic lymphoma(3SBH5) cells.

Protein kinase C (PKC; also known as PRKC) is known to be an important participant in radiation-induced apoptosis. However, its role is not fully clarified. Using 3SBH5 cells, which are radiation-sensitive thymic lymphoma cells, the involvement and functions of PKC were assessed in radiation- induced apoptosis. PMA (phorbol 12-myristate 13-acetate), a PKC activator, inhibited the radiation-induced apoptosis in 3SBH5 cells. On the other hand, chelerythrine, a PKC inhibitor, potentiated apoptosis. In addition, Gö6976, a classical PKC (cPKC) inhibitor, which specifically inhibits PKC (alpha and betaI), also promoted apoptosis. Interestingly, post-treatment (20 min after irradiation) with Gö6976 had no effect on the radiation-induced apoptosis. These results suggest that cPKC is activated early after irradiation for anti-apoptosis signaling and contributes to the balance between cell survival and death. Indeed, an increase of cPKC activity involving PKC (alpha, betaI and betaII) was observed in the cytosolic fraction 3 min after irradiation with 0.5 Gy. However, no translocation of cPKC was observed in the cells after irradiation. Our findings indicate that activation of cPKC (alpha or beta) soon after irradiation is critical to the understanding of the regulation of radiation-induced apoptosis in radiation-sensitive cells.

Alkaloids↗

Multiple signal transduction pathways regulate clusterin (gp 80) gene expression in MDCK cells.

Clusterin (gp 80, apolipoprotein J, TRPM-2) is a widely expressed multifunctional glycoprotein. Its demonstrated and proposed functions include the transport of lipids and membrane fragments, the inhibition of the cytolytic action of the terminal complement complex and the modulation of cell-cell interactions. The expression of the gene is enhanced during tissue injury and remodelling and by hormone-withdrawal-induced apoptosis of prostate and mammary cells. We show here that, in the kidney-derived epithelial cell line MDCK, clusterin mRNA is repressed by glucocorticoids and by progesterone. Treatment with epidermal growth factor also represses clusterin gene expression in MDCK cells. Incubation with 12-O-tetradecanoyl-phorbol-13-acetate, which activates protein kinase C (PKC), induces clusterin mRNA, while chelerythrine, an inhibitor of PKC, represses clusterin gene expression, suggesting that the clusterin gene responds to signalling pathways involving PKC. These results open up the possibility of studying the complex regulation of the clusterin gene by multiple signal transduction pathways within a single cell type, and most importantly, of characterizing interactions between the individual signal transduction cascades.

1-Methyl-3-isobutylxanthine↗

The role of protein kinase C in GH secretion induced by GH-releasing factor and GH-releasing peptides in cultured ovine somatotrophs.

The involvement of protein kinase C (PKC) in the action of GH-releasing factor (GRF) and synthetic GH-releasing peptides (GHRP-2 and GHRP-6) was investigated in ovine somatotrophs in primary culture. In partially purified sheep somatotrophs, GRF and GHRP-2 caused translocation of PKC activity from the cytosol to the cell membranes and caused GH release in a dose- and time-dependent manner. GHRP-6 did not cause PKC translocation. The PKC inhibitors, calphostin C, staurosporine and chelerythrine, partially reduced GH release in response to GRF and GHRP-2 at doses which selectively inhibit PKC activity. These inhibitors totally abolished GH release caused by phorbol 12-myristate 13-acetate (PMA). Down-regulation of PKC by the treatment of cells with phorbol 12,13-dibutyrate for 16 h caused a significant (P < 0.001) reduction in total PKC activity and totally abolished PKC translocation in response to a challenge with GRF, GHRP-2 or PMA. In addition, down-regulation abolished GH release in response to GRF, GHRP-2 or GHRP-6. Treatment of cells with H89, a selective PKA inhibitor, totally blocked GH release caused by either GRF or GHRP-2 and partially reduced PMA-induced GH release. H89 had no effect on PKC translocation caused by GRF, GHRP-2 or PMA and did not affect GH release caused by GHRP-6. These data suggest that GHRP-2 and GRF activate PKC in addition to stimulating adenylyl cyclase activity. Although the cAMP-protein kinase A (PKA) pathway is the major signalling pathway employed by GRF and GHRP-2, the activation of PKC may potentiate signalling via the cAMP-PKA pathway in ovine GH secretion. Importantly, the effect of PMA in increasing the secretion of GH from ovine somatotrophs is effected, in part, by up-regulation of the cAMP-PKA pathway. We conclude that there is cross-talk between the PKC pathway and the cAMP-PKA pathway in ovine somatotrophs during the action of GRF or GHRP.

Alkaloids↗

Antisense knockout of HOXB4 blocks 1,25-dihydroxyvitamin D3 inhibition of c-myc expression.

The expression of c-myc is decreased by 1,25-(OH)2D(3) during HL-60 cell differentiation. Concomitantly, 1,25-(OH)2D(3) increases the expression and DNA binding activity of HOXB4, a homeobox gene. HOXB4 binds to the c-my c gene at sites involved in blocking c-myc transcription elongation. In this study, a phosphorothioate antisense oligonucleotide targeted against HOXB4 was examined for its effect on 1,25-(OH)2D(3) inhibition of c-myc expression. Alone, 1,25-(OH)2D(3) (20 nM) increased HOXB4 levels by 103+/-7% (mean+/-s.e., n=3) and decreased c-myc levels by 89+/-5% (mean+/-s.e.m., n=3) at 48 h of treatment. HOXB4 antisense treatment completely blocked the induction of HOXB4 by 1,25-(OH)2D(3). In addition, HOXB4 antisense partially blocked 1,25-(OH)2D(3)-mediated decrease in c-myc levels (46+/-6% inhibition) and promotion of HL-60 cell differentiation (20+/-2% and 25+/-3% inhibition as assessed by nitroblue tetrazolium and non-specific esterase assays respectively). The data further establish that HOXB4 levels are regulated by 1,25-(OH)2D(3) and reveal that HOXB4 participates in the down-regulation of c-myc expression.

Alkaloids↗

Local anti-infective therapy: pharmacological agents. A systematic review.

BACKGROUND: It is well recognized that periodontal diseases are bacterial in nature. An essential component of therapy is to eliminate or control these pathogens. This has been traditionally accomplished through mechanical means (scaling and root planing [SRP]), which is time-consuming, difficult, and sometimes ineffective. Over the past 20 years, locally delivered, anti-infective pharmacological agents, most recently employing sustained-release vehicles, have been introduced to achieve this goal. RATIONALE: This systematic review evaluates literature-based evidence in an effort to determine the efficacy of currently available anti-infective agents, with and without concurrent SRP, in controlling chronic periodontitis. FOCUSED QUESTION: In patients with chronic periodontitis, what is the effect of local controlled-release anti-infective drug therapy with or without SRP compared to SRP alone on changes in clinical, patient-centered, and adverse outcomes? SEARCH PROTOCOL: MEDLINE, the Cochrane Central Trials Register, and Web of Science were searched. Hand searches were performed of the Journal of Clinical Periodontology, Journal of Periodontology, and Journal of Periodontal Research. Searches were performed for articles published through April 2002. In addition, investigators contacted editors of the above-mentioned journals and companies sponsoring research on these agents for related unpublished data and studies in progress. SELECTION CRITERIA INCLUSION CRITERIA: Studies included randomized controlled clinical trials (RCT), and case-controlled and cohort studies at least 3 months long. Therapeutic interventions had to include 1) SRP alone; 2) local anti-infective drug therapy and SRP; or 3) local anti-infective drug therapy alone. Included studies had to report patient-based mean values and measures of variation for probing depth (PD) and/or clinical attachment levels (CAL) for both test and control groups. EXCLUSION CRITERIA: Studies were excluded if they: 1) included data from a previously published article; 2) included daily rinsing with chlorhexidine (CHX); or 3) had unclear descriptions of randomization procedures, examiner masking, or concomitant therapies. DATA COLLECTION AND ANALYSIS: For the meta-analysis, PD and CAL were expressed as summary mean effects with 95% confidence intervals (CI) for the effect, and analyzed using a standardized difference between SRP alone and experimental agent groups. The results were assessed with both fixed-effects and random-effects models. Studies were ranked according to the York system. MAIN RESULTS: 1. Thirty-two studies were included (28 RCT, 2 cohort, and 2 case-control), incorporating a total patient population of 3,705 subjects. 2. Essentially all studies reported substantial reductions in gingival inflammation and bleeding indices, which were similar in both control and experimental groups. 3. A meta-analysis completed on 19 studies that included SRP and local sustained-release agents compared with SRP alone indicated significant adjunctive PD reduction or CAL gain for minocycline (MINO) gel, microencapsulated MINO, CHX chip and doxycycline (DOXY) gel during SRP compared to SRP alone. 4. Use of antimicrobial irrigants or anti-infective sustained-release systems as an adjunct to SRP does not result in significant patient-centered adverse events. REVIEWERS' CONCLUSIONS: 1. In some populations, anti-infective agents in a sustained-release vehicle alone can reduce PD and bleeding on probing (BOP) equivalent to that achieved by SRP alone. 2. No evidence was found for an adjunctive effect on reduction of PD and BOP of therapist-delivered CHX irrigation during SRP compared to SRP alone. 3. Additional RCTs are needed which evaluate the effectiveness of these therapies in all forms of periodontitis. 4. The study protocol for future RCTs should include appropriate statistical analyses and complete data sets to facilitate future evidence-based reviews. 5. Alternative surrogate parameters to PD and CAL need to be identified and validated such as microbial, inflammatory, or tissue-destructive markers that could be used in conjunction with clinical parameters to help determine the patient's response to emerging technologies that target the infectious and/or inflammatory aspects of periodontitis. 6. Future Phase IV clinical trials should be designed that evaluate local anti-infective therapies in conjunction with SRP in a manner consistent with current standards of care and evaluate cost-effectiveness. 7. The use of local anti-infective agents in at-risk patient populations and for the treatment of at-risk disease sites needs to be validated in randomized controlled clinical trials. 8. Several local anti-infective agents combined with SRP appear to provide additional benefits in PD reduction and CAL gain compared to SRP alone. The decision to use local anti-infective adjunctive therapy remains a matter of individual clinical judgment, the phase of treatment, and the patient's status and preferences.

Alkaloids↗

Viadent, ethanol, and pH effects upon gingival epithelial-like cells, in vitro.

Interest has recently been directed towards the use of antiplaque mouthrinses. Most published material concerns the antimicrobial effects of these agents rather than their effects upon oral tissue. This study was conducted to evaluate the effect of a sanguinarine-containing mouthrinse called Viadent upon epithelial-like gingival cells. The cells were grown for 24 hours in supplemented Earle's medium, with and without different Viadent dilutions. Cell counts were made with a hematocytometer. It was found that 50% of the cells were inhibited at 1.2% Viadent. In similar studies, it was found that 70% ethanol and two pH buffers were less toxic than Viadent. Exposure of preformed cell monolayers to Viadent also showed significant inhibition. The relative toxicity of different antiplaque agents may be compared using such cells as a model system. In conclusion, it was observed that Viadent significantly affected gingival cell growth in vitro, that viable cell numbers were greatly reduced by short time exposure, and that the toxic effect of Viadent could only partially be accounted for by ethanol content and/or pH.

Adult↗

Six-month effects of a sanguinarine dentifrice on plaque and gingivitis.

A six-month, double-blind clinical trial was conducted to determine the effectiveness of a sanguinarine-containing dentifrice in reducing plaque and gingival inflammation. One hundred twenty adult volunteers were randomly assigned to a control or experimental group. The test dentifrice contained 750 mcg/g of sanguinaria extract. A dentifrice of similar composition without sanguinarine was used as the placebo. Plaque and gingival inflammation scores were recorded for four surfaces on each of 12 index teeth at baseline, one-, three, and six-months. Matched pair t-test analyses showed no significant differences between experimental and control groups for mean six-month changes in plaque and gingival inflammation scores in analyses using all 48 sites per subject or in analyses of only the 24 interproximal sites. No long-term reduction was demonstrated in plaque or gingival inflammation with the use of a sanguinarine-containing dentifrice.

Adult↗

Clinical effect of a sanguinaria dentifrice on plaque and gingivitis in adults.

A clinical trial was conducted to evaluate the effects of a sanguinaria-zinc chloride dentifrice on the prevention of plaque formation and gingivitis. A total of 59 young adults, 18 to 30 years of age, either performed supervised brushing with a 0.075% sanguinaria-0.05% zinc chloride dentifrice, a 0.24% sodium fluoride dentifrice, or rinsed daily with a 0.05% NaF solution. Clinical evaluations for plaque and gingivitis were performed after 7, 14, and 21 days of the test regimen. After 21 days, all subjects resumed twice daily supervised brushing and flossing and post-test evaluations were conducted after two weeks. The results showed that after 7, 14, and 21 days both groups using dentifrices had significantly less plaque and gingivitis than the group using the rinse, and there were no significant differences between the two groups using either the sanguinaria-ZnCl2 or the NaF dentifrices.

Adolescent↗

A clinical comparison of antibacterial mouthrinses: effects of chlorhexidine, phenolics, and sanguinarine on dental plaque and gingivitis.

This study compared the clinical efficacy of three mouthrinses containing either 0.12% chlorhexidine, phenolic compounds, or sanguinarine, which were used unsupervised, in a placebo-controlled, double-blind study of 6 months' duration. The study was conducted according to ADA clinical guidelines for evaluation of antigingivitis agents and was completed by 481 adults. Following baseline exams and a prophylaxis, subjects were randomly divided into treatment groups matched for age, gender, and gingivitis severity, and were instructed to use the rinses in accordance with manufacturer's directions. Followup examinations evaluated supragingival plaque, gingivitis, and gingival bleeding. Compared to placebo at 6 months, the group rinsing with 0.12% chlorhexidine had significantly less gingivitis (31% reduction), gingival bleeding (39% reduction), and plaque (49% reduction) and was significantly better than any of the other treatment groups (P less than 0.05). Both the phenolic and sanguinarine groups showed moderate, yet significant, reductions in plaque compared to placebo (24% and 12% respectively) yet were significantly less effective than the 0.12% chlorhexidine rinse (P less than 0.05). However, neither the phenolic nor sanguinarine rinses were significantly different than placebo in their effects on gingivitis or gingival bleeding. These results support previous published results on the superiority of 0.12% chlorhexidine when used in conjunction with professional care and as an adjunct to routine oral hygiene practices.

Adult↗