Classification of periodontal health, gingival disease, and condition [3].
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
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Rajesh Banu",coverURL:"https://cdn.intechopen.com/books/images_new/6839.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"218539",title:"Dr.",name:"Rajesh",middleName:null,surname:"Banu",slug:"rajesh-banu",fullName:"Rajesh Banu"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}}},ofsBook:{item:{type:"book",id:"10691",leadTitle:null,title:"Intelligent and Futuristic Computer Animation",subtitle:null,reviewType:"peer-reviewed",abstract:"\r\n\tComputer Animation is a vital component in producing a realistic movie, game or 3D presentation. A conventional method requires a tremendous amount of time and effort, it greatly depends on animator skills to perform rigging, deformation or skin application. This work can be tedious; therefore, artificial intelligence (AI) is expected to help animators build an animation in efficient ways. As an example, artificial intelligence will help animators to synchronize the rigging process from a human actor toward the 3D character. 3D games with Non-Player Character (NPC) strongly correlate with AI because AI can improve an agent's movement and behaviour. A Game Storytelling can be automatically generated based on the player experience or a specific scenario. Besides, the emotional experience can enrich the agent behaviour during the interaction to achieve full mental immersion.
\r\n\r\n\tThis book intends to provide the reader with an inclusive content of computer animation production, motion capture devices, emotional intelligence and behaviour, computer game and finally interactive agent behaviour.
",isbn:"978-1-83969-558-2",printIsbn:"978-1-83969-557-5",pdfIsbn:"978-1-83969-559-9",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"5496e567e838f1eaeafba5f9a776b13a",bookSignature:"Prof. Ahmad Hoirul Basori and Dr. Andi Besse Firdausiah Mansur",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10691.jpg",keywords:"Rigging, Human Motion, Motion Editor, Storytelling, Artificial Intelligence, NPC Control, Emotional Intelligence, Agent Movement, Crowd Modelling, Emotional Contagion, Motion Synthesis, Behaviour Recording",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"February 19th 2021",dateEndSecondStepPublish:"March 19th 2021",dateEndThirdStepPublish:"May 18th 2021",dateEndFourthStepPublish:"August 6th 2021",dateEndFifthStepPublish:"October 5th 2021",remainingDaysToSecondStep:"14 days",secondStepPassed:!1,currentStepOfPublishingProcess:2,editedByType:null,kuFlag:!1,biosketch:"Dr. Basori is a pioneering researcher in Computer Graphics, Facial Animation, Cloth Simulation, Medical Visualization, Haptic Interaction, Man-Machine Interaction, and Robotics. 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From 2013-2016, he has worked as an Assistant Professor in Faculty of Computing and Information Technology Rabigh, King Abdulaziz University. In 2016, he was promoted to Associate Professor rank in Faculty of Computing and Information Technology Rabigh, King Abdulaziz University. He is the member of Editorial boards of several international journals, and he has published more than 100 articles. He is also a member of professional membership IEEE, ACM SIGGRAPH, IAENG and Senior Member of IACSIT. 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From 2013 she is working as an Assistant Professor in Faculty of Computing and Information Technology Rabigh, King Abdulaziz University. 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From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3621",title:"Silver Nanoparticles",subtitle:null,isOpenForSubmission:!1,hash:null,slug:"silver-nanoparticles",bookSignature:"David Pozo Perez",coverURL:"https://cdn.intechopen.com/books/images_new/3621.jpg",editedByType:"Edited by",editors:[{id:"6667",title:"Dr.",name:"David",surname:"Pozo",slug:"david-pozo",fullName:"David Pozo"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"49657",title:"Studies on Obtaining Diglycidyl Ether from Allyl-Glycidyl Ether over the Mesoporous Ti-SBA-15 Catalyst",doi:"10.5772/61881",slug:"studies-on-obtaining-diglycidyl-ether-from-allyl-glycidyl-ether-over-the-mesoporous-ti-sba-15-cataly",body:'Research on the epoxidation of allylic compounds: propylene [1–5], allyl chloride [6–12], allyl alcohol [13–17], methallyl alcohol, crotyl alcohol, and 1-butene-3-ol [18] with hydrogen peroxide over the titanium silicate catalysts have been carried out for over 10 years. There are not many reports concerning the epoxidation of allyl-glycidyl ether (AGE) or diallyl ether (DAE) [19] with hydrogen peroxide over these catalysts. It can be caused by the fact that the epoxidation of AGE and DAE is very complicated, as in addition to the epoxidized ether derivatives, by-products formed by the decomposition of these ethers and their epoxidized derivatives, as well as products of further transformations of these decomposed products, i.e. glycidol and glycerol, are received. Moreover, during epoxidation, the epoxy rings may be opened and diols can be formed. However, due to numerous applications of diglycidyl ether – DGE (production of linear, branched, and cyclic oligoglycerols used in the production of surfactants, preparation of anti-arrhythmia agents, production of components of other pharmaceuticals and medicines, for example, cryptands, preparation of lubricating oil additives, and synthesis of aminoethers), the epoxidation of AGE with hydrogen peroxide over Ti-SBA-15 is very interesting and worth further examinations. The simultaneous utilization of Ti-SBA-15 and a low-cost, environment friendly oxidant - hydrogen peroxide in the epoxidation of AGE, makes this method of DGE production a modern and environment friendly as the only product of hydrogen peroxide transformation is water and Ti-SBA-15 can be easily recovered from reaction mixtures, recycled into the process, and regenerated if it loses its activity [20]. An additional advantage is this process can be carried out in an aqueous medium also.
Until now, only the TS-1 and Ti-MWW titanium silicate materials have been used in the epoxidation of DAE and AGE – with hydrogen peroxide. In the studies performed by Wu et al. [19], AGE was the semi-product which was formed during DAE epoxidation and it underwent among others further transformation to DGE. In the above mentioned research, at the first stage, the epoxidation of DAE with hydrogen peroxide was performed under vigorous stirring in a 20 ml glass flask, connected to a condenser. In the typical run, the appropriate amounts of DAE, solvent (acetonitrile, acetone, water, methanol, ethanol, dioxane), and the catalyst were mixed in the flask and heated to the desired temperature under the agitation. Next, aqueous hydrogen peroxide (30 wt%) was added to the mixture to start the reaction. The reaction was carried out at the temperature of 60°C for 0.5 h in case of Ti-MWW and for 1.5 h in case of TS-1. Both Ti-MWW and TS-1 materials showed different solvent effect. During the examinations over Ti-MWW catalyst, the highest conversion of DAE was obtained for acetonitrile (about 40 mol%) and acetone (about 39 mol%) as the solvents. The selectivity of AGE was the highest for acetonitrile, methanol, ethanol, and dioxane and amounted to about 71–79 mol%. The selectivity of DGE, which was formed as the product of AGE transformation (epoxidation of the next double bond), was the highest for water as the solvent (about 40 mol%). High values of the selectivity of this product also allow to obtain such solvents as: acetonitrile (about 29 mol%) and acetone (about 25 mol%). The efficiency of hydrogen peroxide conversion was the highest for examinations in acetonitrile (about 95 mol%), acetone (about 92 mol%), and dioxane (about 94 mol%). In methanol and in water, the efficiency of hydrogen peroxide conversion amounted to about 82–87 mol%. The lowest value of this function of the process was obtained for ethanol (61 mol%). The total conversion of hydrogen peroxide was the highest in acetonitrile and acetone (about 99–100 mol%). These studies showed that the Ti-MWW catalyst favoured aprotic solvents such as acetonitrile or acetone. A little worse results were obtained for water as the solvent.
During the studies over the TS-1 catalyst, the highest conversion of DAE was obtained in acetone, methanol, and ethanol as the solvents. The selectivity of AGE was usually high and amounted to about 61–89 mol%. This function was the highest for dioxane. The highest values of DGE selectivity were obtained for acetone and methanol: about 22 and 21mol%, respectively. Efficiency of hydrogen peroxide conversion was the highest for acetone and amounted to 70 mol%. The studies over the TS-1 material showed that methanol and acetone were the most effective solvents in this process. The comparison of the results of DAE epoxidation present that Ti-MWW material was more efficient than TS-1 material in catalytic activity, epoxide selectivity, and hydrogen peroxide conversion when choosing acetonitrile or acetone as the solvent [19].
At the second stage, in which only Ti-MWW material was used, also the influence of temperature from 0 to 67°C was tested in the epoxidation of DAE over the Ti-SBA-15 material. The studies were performed in acetone and at the same conditions as in the first stage of these studies. The examinations showed that the selectivities of AGE and DGE changed of about 10 mol% during the rising of temperature (the selectivity of AGE from about 80 to about 70 mol%, and the selectivity of DGE from about 20 to 30 mol%). Conversion of DAE reached 40 mol% above the temperature of 60°C. The efficiency of hydrogen peroxide conversion slightly decreased with increasing temperature as a result of the thermal decomposition of hydrogen peroxide, but the value of this function was higher than 95 mol% [19].
At the third stage, the influence of the Ti-MWW amount and reaction time were studied. The examinations were performed in acetonitrile and at the temperature of 60°C. The studies showed that the more the catalyst was used, the higher the catalytic activity of Ti-MWW material. The DAE conversion raised rapidly within 30 min and then gradually with the time. The decrease in the reaction rate for longer time was mainly caused by the pore blocking by heavy organic species [19].
The comparison of the results obtained for Ti-MWW and TS-1 catalysts show that Ti-MWW material exhibited more benefits in catalytic activity using less harsh reaction conditions [19].
One of the newer titanium silicate catalysts is Ti-SBA-15. It is a mesoporous material, which is much more durable than Ti-MCM-41 catalyst [20, 21]. Greater durability of this catalyst is likely due to its construction – a honeycomb structure, wherein unlike Ti-MCM-41, in Ti-SBA-15 the main cylindrical channels are connected together by transverse channels which introduces additional porosity and, at the same time, strengthens the structure. Furthermore, Ti-SBA-15 is characterized by thicker pore walls, and its synthesis is carried out in the presence of a biodegradable template – Pluronic P123, as opposed to Ti-MCM-41 whose synthesis is carried out in the presence of an ammonium compound (hexadecyltrimethylammonium bromide) and is uncomfortable to the environment due to formation of amines during calcination of this catalyst [22–31]. Our studies on the epoxidation of allylic alcohols over the Ti-SBA-15 catalyst showed that this catalyst is very active in this process and these compounds can be effectively converted to epoxides [18]. This is the main reason why this catalyst has been chosen to conduct the epoxidation of AGE.
Ti-SBA-15 was obtained by the method of Berube et al. [30] and the following raw materials were used in its synthesis: Pluronic P123 (Aldrich, MW = 5800) as structure-directing agent, tetraethylortosilicalite (TEOS 98%, Aldrich) as a silicon source, and tetraisopropyl orthotitanate (TiPOT >98%, Merck) as a titanium precursor. The characterization of Ti-SBA-15 was performed with the following instrumental methods: XRD (X’Pert PRO Philips diffractometer, Co Kα radiation), IR (Shimadzu FTIR-8100 spectrometer, KBr pellet technique), UV-vis (SPECORD M40 type V-530 with the attachment for solid materials measurements), X-ray microanalysis (Oxford X-ray analyzer ISIS 300), SEM (JOEL JSM-6100 instrument), and porosimetric analysis (porosimetry analyzer ASAP Micromeritics).
The XRD pattern of the obtained Ti-SBA-15 catalyst was similar to the literature data [28, 32–33]. For the SBA-15 material are typical: one characteristic very intensive diffraction peak at 2 Theta angle of 1.01° and two weak peaks at 2 Theta angle of 1.75° and 2.05°, corresponding to the (100), (110), and (200) Bragg reflections. These reflections confirm the 2-d hexagonal symmetry (P6mm) of the SBA-15. The IR spectrum of the obtained Ti-SBA-15 was also similar to the literature data [23, 34–35]. To the main bands characterized, this kind of materials belong to: the band at 800 cm–1 which is assigned to symmetric stretching vibrations of Si-O-Si in SiO4 units the same as the band at 1, 000–1, 300 cm–1, the band at 1625-1650 cm-1 which is assigned to adsorbed water molecules, the band at 3, 000–3, 700 cm–1 which is characteristic for surface Si-OH groups and adsorbed water molecules, and the band 957 cm–1 which is associated with Ti=O or Si-O-Ti vibrations. The UV-VIS spectrum of the obtained Ti-SBA-15 catalyst showed an intense absorption band at 211 nm, associated with ligand-to-metal charge transfer from oxygen to Ti of an isolated tetrahedral Ti species. This band is direct evidence for titanium atoms incorporated into the framework of the silica [36]. In this spectrum also a shoulder with a maximum around of 290 nm was present. This band is connected with the presence of Ti atoms in fivefold and sixfold coordination. This fivefold and sixfold coordination is generated through hydration by one or two water molecules of the tetrahedral titanium ion in the first coordination sphere [36]. Moreover, in the spectra was visible a weak band at 340 nm, which is assigned to the presence of anatase in the sample. The obtained UV-VIS spectrum is similar to the literature data [32, 36].
An X-ray microanalysis showed that the amount of Ti in the sample after calcination was 2.9 wt%. According to the porosimetric analysis, the specific surface area of the obtained catalyst amounted to 620 m2/g, the size of the pores achieved was 5.0 nm, and the pore volume was 0.6 cm3/g. The SEM analyses showed that the Ti-SBA-15 catalyst consisted of large and long, branched, pipe-like structures with diameter of about 4 μm. These structures consisted of smaller particles with diameter of about 0.3–0.6 μm and length about 1–2 μm. This morphology is typical for structures such as SBA-15 [28, 37].
In the epoxidation of AGE, the following raw materials were used: AGE (99%, Aldrich), hydrogen peroxide (60 wt% water solution, Chempur), and Ti-SBA-15 catalyst. The initial technological parameters were as follows: the molar ratio of AGE/H2O2 = 1:1, catalyst content 3 wt%, the reaction time 2 h, and intensity of stirring 500 rpm.
The process of AGE epoxidation was carried out in glass vials with the capacity of 12 cm3 equipped with a rubber septum and a capillary. The raw materials were introduced into the vials at the ambient temperature and in the following order: hydrogen peroxide, catalyst, and AGE. Then the vials were closed with the rubber equipped with the capillary, located in a shaker holder and immersed in a water bath having the appropriate temperature. In order to calculate the mass balance, the unreacted hydrogen peroxide was determined by iodometric method and the remaining products and the unreacted AGE were analyzed by the GC method. The analyses were performed on the FOCUS apparatus with a flame-ionization detector fitted with Quadrex capillary columns filled with methyl-phenyl-siloxanes. After calculating the mass balance, the main functions describing the process were determined: the selectivity of transformation to DGE in relation to AGE consumed and also selectivities of the by-products in relation to AGE consumed, the conversion of AGE, and the selectivity of transformation to organic compounds in relation to hydrogen peroxide consumed (effective conversion of H2O2).
The studies on the epoxidation of AGE to DGE was carried out by one-variable method, changing the values of the following parameters: temperature 0–100°C, molar ratio of AGE/H2O2 0.03:1–4:1, content of the Ti-SBA-15 catalyst (0–5 wt%), and reaction time 15–240 min. The main results of the studies on the influence of temperature on the course of AGE epoxidation were presented in Figure 1.
The influence of temperature on the selectivities of the products of AGE epoxidation process: SDGE – the selectivity of DGE, S3A12PD – the selectivity of 3-allyloxy-1, 2-propanediol, and Sglycerol – the selectivity of glycerol (the molar ratio of AGE/H2O2 = 1:1, the content of the catalyst 3 wt%, and the reaction time 120 min).
During the studies on the influence of temperature, only three products were obtained: DGE, 3-allyloxy-1, 2-propanediol (3A12PD), and glycerol. The selectivity of transformation of AGE to the product of epoxidation of the unsaturated bond – DGE, increases during the increase of the temperature from 0 mol% (the temperature of 0°C) to 38 mol% (the temperature of 20°C) and then decreases to 9 mol% (the temperature of 100°C). Figure 1 shows that DGE is not the main product of this process, because for all investigated temperatures the main product of the process is 3A12PD (with exception at the temperature of 0°C at which the reaction does not proceed). The selectivity of this products changes from about 53–54 mol% (the temperatures 10–20°C) to 80–90 mol% (the temperatures 40–100°C).. The selectivity of glycerol amounts to 13 mol% for the temperature of 10°C, and then decreases to about 2 mol% (for the temperatures of 40–100°C). For the description of the process of AGE epoxidation, the reactions presented in Figure 2 can be proposed.
The main reactions of the process of AGE epoxidation.
Figure 2 shows that the process can proceed in the three directions: (1) the epoxidation of allylic group in AGE and formation of DGE, (2) the hydration of the epoxide ring in AGE and formation of 3A12PD, and (3) the formation of glycerol. Moreover, the two first directions are the main directions of the process in low temperatures. The glycerol formation is a very complicated process and this product can be formed as a product of hydrolysis of the ether groups of AGE, DGE, 3A12PD, and, simultaneously, as a result of the secondary reactions of the products of the hydrolysis of these ethers (epoxidation of allylic group in allyl alcohol to glycidol and next hydration of the epoxide ring in glycidol to glycerol). Allyl alcohol and glycidol were not detected in post-reaction mixtures. It shows that these compounds were very reactive at the investigated conditions and right away underwent secondary reactions. The tendency towards the formation of 3A12PD rises during increasing the temperature of the performing process. On the other hand, the selectivities of the DGE and glycerol decrease. It shows that at higher temperatures the epoxidation of AGE to DGE is hindered and the hydrolysis of the ether groups in AGE, DAE, and 3A12PD is stepped or it proceeds very slowly. The main reaction is hydration of the epoxide ring in AGE and formation of 3A12PD. The formation of 3A12PD as the main product in this process can be explained taking into account the acidic character of the mesoporous Ti-SBA-15 material. This character is mainly connected with: (1) the silanol groups located on the surface of this catalyst [19, 38], (2) the species of Ti present on the surface of the catalyst – tetrahedral Ti(IV) active sites, titanium-containing species in the form of dimmers or very small oligomers [38–41], and (3) the active species of titanium with hydrogen peroxide which are formed during the oxidation process, for example, five-membered active complexes – titanium hydroperoxo species with the specific structure, which are formed from tetrahedral Ti(IV) active sites, protic solvent (for example, methanol or water), and hydrogen peroxide and are present on the surface of the catalyst [42].
Among others, the formation of 3A12PD can also be under influence of the active species of titanium with hydrogen peroxide which are formed during the oxidation process and some of them can have the acidic character. A few structures have been proposed until now for explanations of the structures of these active species. Among these structures are: the peroxide structure, the hydroperoxide structure, and superoxide structures (radical species) [40, 42–49]. Indeed, mainly the hydroperoxide structure was described as the structure responsible for the epoxidation of olefinic compounds [45, 47]. It exists in equilibrium with the peroxide structure, which is a dominant structure in the water solution because it is stabilized by water molecules [45]. In the medium in which epoxidation takes place, the excess of olefins causes that the peroxide structure is converted to hydroperoxide structure [45]. Hydroperoxide structures in the presence of protic solvent create the five-membered active complexes – titanium hydroperoxo species which are composed from tetrahedral Ti(IV) active sites, protic solvent (in case of these studies, from water), and hydrogen peroxide[40, 42, 50, 51].
Bhaumik et al. [42] described that under the influence of the titanium hydroperoxo species undergoes acid-catalyzed cleavage of the oxirane rings in the epoxide compounds; this reaction has considerable SN1 character and the nucleophilic attack is easy to occur at the more crowded carbon atom that can best accommodate the positive charge. Taking into account that this data can be propose the possible way of 3A12PD formation from the AGE presented in Figure 3.
The possible way of 3A12PD formation from the AGE, where: R = CH2=CH-CH2-.
Also the hydration of the ether groups in AGE, DGE, and 3A12PD can be explained taking into account the acidic character of various species which are present in the mesoporous Ti-SBA-15 material (silanol groups, species of Ti and titanium hydroperoxo species).
During the studies on the influence of temperature, the conversion of AGE was very low and it changes from 0 mol% (the temperature of 0°C) to about 4–5 mol% for the highest temperatures. The changes of the effective conversion of H2O2 are very similar. Very low values of this function show that at the studied conditions the catalyst was very active in the ineffective decomposition of hydrogen peroxide to water and oxygen, which takes place at the active centres of Ti in the catalyst even at very low temperatures (the total conversion of hydrogen peroxide changed from 83–90 mol%). The ineffective decomposition of hydrogen peroxide over titanium silicate catalysts has been described in a great number of works [52–57], and this phenomenon is typical for these catalysts, for example, it was shown in the literature that titanium hydroperoxo species can decompose hydrogen peroxide molecules via formation of Ti-O* radical and hydroperoxo radical (HOO*) [52]. As the results presented in this work showed, the Ti-SBA-15 catalyst was very active in the decomposition of hydrogen peroxide. The epoxidation of olefinic bonds undergoes slower than the ineffective decomposition of hydrogen peroxide at the five-membered active species. Probably, very small reactivity of the AGE is connected with the steric hindrances connected with the structure of this ether when the molecules of AGE are close to the active species of Ti with hydrogen peroxide. These steric hindrances cause that the decomposition of AGE molecules also takes place. The increased, ineffective decomposition of hydrogen peroxide can be also caused by the presence of TiO2 domains in the structure of the Ti-SBA-15 catalyst. Taking into account the UV-VIS spectrum of the Ti-SBA-15 catalyst used in this work, the broad absorption peak at the 211 cm–1 and the shoulder at the 290 cm–1, which is not only connected with the presence of Ti atoms in fivefold and sixfold coordination [36] but also can be assigned to the oligomerized titanium-oxygen species – formation of Ti-O-Ti bonds by clusterization of octahedrally coordinated titanium ions [46, 58] or to octahedral titanium species in the form of highly dispersed TiO2 particles with the particle size smaller than 5 nm [48]), and the results of the X-Ray microanalysis (amount of Ti 2.9 wt%), it can be assumed that the Ti-SBA-15 catalyst contains the titanium-oxygen species in the form of dimmers or very small oligomers (TiO2 domains, Ti aggregates) [53, 55].
A lot of works present the strategies to increase the oxidant efficiency. The hydrogen peroxide decomposition is strongly dependent on the pH of the reaction mixtures and on the surface concentration of the hydroxyl groups of the catalytic material [52]. The improving of the efficiency of the hydrogen peroxide conversion can be done by: (1) addition of additives such as for example: CH3COOH, KHSO4, KH2PO4, KHF2, Na2SO4, NaHCO3, K2CO3, K3PO4, K2HPO4, or KH2PO4 [52]; (2) slow addition of hydrogen peroxide [52, 55, 57]; (3) choosing of the appropriate solvent for the epoxidation process – the most beneficial are methanol, acetonitrile, and acetone [44, 54, 55] or co-solvent, for example, sulfolane [59]; (4) increasing of the acidity of the catalyst by the addition of metal oxide, for example, of TiO2, and utilization of the appropriate temperature of the calcination [56]; and (5) the surface hydrophobization of mesoporous titanium silicates [46]. We would like to test in our future work some of the ways of improving the efficiency of hydrogen peroxide conversion: choosing the appropriate solvent, additives, and slow addition of hydrogen peroxide.
Taking into account the results of the studies on the influence of temperature on the course of AGE epoxidation, the temperature of 20°C was taken as the most beneficial for the next studies.
The main results of the studies on the influence of the molar ratio of AGE/H2O2 on the course of AGE epoxidation were presented in Figure 4. The studies were performed at the range of molar ratios of AGE/H2O2 0.03:1 – 4:1. The other parameters were as follows: the temperature of 20°C, the content of the catalyst 3 wt%, and the reaction time 120 min.
The influence of molar ratio of AGE/H2O2 on the selectivities of the products of AGE epoxidation process: SDGE – the selectivity of DGE, S3A12PD – the selectivity of 3-allyloxy-1, 2-propanediol, and Sglycerol – the selectivity of glycerol (the temperature 20°C, the content of the catalyst 3 wt%, and the reaction time 120 min).
The studies show that the conversion of AGE was the highest for the lowest molar ratio of reactants and amounted of 11 mol% and next it decreased to 1 mol% for the molar ratio of AGE/H2O2 = 4:1. The effective conversion of H2O2 had very low values independent of the studied molar ratios, even for the molar ratios of AGE/H2O2 > 1. Figure 4 shows that independent of the molar ratio of reactants the main product of the process was 3A12PD, but its selectivity decreased during increasing the molar ratio of reactants. It shows that the excess of hydrogen peroxide or AGE molecules in the reaction mixture does not cause that the epoxidation of AGE is intensified and the hindering of the hydration of epoxide ring in AGE is not observed. The ethers molecules are unstable in reaction medium and underwent decomposition by the hydration of the ether groups. Simultaneously, the results obtained show that the surface of the catalyst independent of the molar ratio of reactants was very active in the reactions of hydration of epoxide rings and ether groups. Also the formed allyl alcohol and glycidol undergo secondary reactions (epoxidation and hydration of the epoxide ring) very easily. On the basis of the results obtained, the molar ratio of AGE/H2O2 = 0.03 was taken as the most beneficial for the next stages of the studies.
The main results of the studies on the influence of the Ti-SBA-15 catalyst content on the course of AGE epoxidation were presented in Figure 5. These studies were performed for the following parameters: the temperature 20°C, the molar ratio AGE/H2O2 = 0.03, and the reaction time of 120 min.
The influence of the Ti-SBA-15 catalyst content on the selectivities of the products of AGE epoxidation process: SDGE – the selectivity of DGE, S3A12PD – the selectivity of 3-allyloxy-1, 2-propanediol, and Sglycerol – the selectivity of glycerol (the temperature 20°C, the molar ratio of AGE/H2O2 = 0.03, and the reaction time 120 min).
The studies show that for the amount of the catalyst of 0 wt% no one reaction proceeded. The conversion of AGE raised from 0 mol% (for 0 wt% of Ti-SBA-15) to 11 mol% (for 3 wt% of Ti-SBA-15) and next did not change. The effective conversion of H2O2 was very low and amounted to about 1 mol%, independent of the studied Ti-SBA-15 content.
Figure 5 shows that during the rising of the content of the catalyst the selectivity of 3A12PD increased from 0 mol% (the Ti-SBA-15 content 0 wt%) to 78 mol% (the Ti-SBA-15 content 5 wt%). It presents that with the increase of the Ti-SBA-15 content, the hydration of the epoxide ring in AGE was intensified, but the hydrolysis at the ether group of AGE, DGE, and 3A12PD was hindered. Only for the Ti-SBA-15 content of 0.5 and 1 wt%, glycerol was present in the post-reaction mixtures. On the other hand, at higher catalyst content, the phenomenon of ineffective decomposition of hydrogen peroxide at the active centers of Ti in the catalyst was intensified and the water molecules obtained during ineffective decomposition of hydrogen peroxide could probably take part in hydration of the epoxide ring in AGE. The content of the catalyst amounting to 3 wt% was chosen as the most beneficial for the last stage of the studies.
The main results of the studies on the influence of the reaction time on the course of AGE epoxidation were presented in Figure 6. These studies were performed for the following parameters: the temperature 20°C, the molar ratio AGE/H2O2 = 0.03, and the Ti-SBA-15 catalyst content 3 wt%.
The influence of the reaction time on the selectivities of the products of AGE epoxidation process: SDGE – the selectivity of DGE, S3A12PD – the selectivity of 3-allyloxy-1, 2-propanediol, and Sglycerol – the selectivity of glycerol (the temperature 20°C, the molar ratio of AGE/H2O2 = 0.03, and the Ti-SBA-15 catalyst content 3 wt%).
The results show that with the prolongation of the reaction time from 15 min to 240 min, the selectivity of DGE decreased from 100 mol% to 25 mol%. Only for the reaction time of 15 min and 50 min, it was possible to obtain only DGE as the product in the post-reaction mixtures. The conversion of AGE increased in the range of the studied reaction time from 3 mol% to 18 mol%, but the effective conversion of H2O2 was very low and amounted to about 1 mol%. Figure 6 presents that for the reaction time of 120 min the second product of this process was established – 3A12PD. Glycerol – the third product of this process appeared in the post-reaction mixture for the reaction time of 240 min. It shows that it is possible to obtain only one product in the post-reaction mixture – DGE (very desirable) only for short reaction time – 15 min. and 60 min. At this reaction time, it is only possible to stop the hydration of the epoxide ring and formation of 3A12PD.
The comparison of our results obtained for the Ti-SBA-15 material with the results obtained previously by Wu et al. for the Ti-MWW and TS-1 materials [19] shows that the main difference between the epoxidation of AGE over Ti-SBA-15 and the epoxidation of DAE and AGE over Ti-MWW and TS-1 is formation of the considerable amounts of 3-allyloxy-1, 2-propanediol over Ti-SBA-15 and low efficiency of hydrogen peroxide conversion for this catalyst. It is probably connected with the pore size of the Ti-SBA-15 mesoporous material and the structure of the surface of this catalyst, especially with the presence of various species of Ti and hydroxyl groups.
The results presented in these studies show that the best conditions established for the epoxidation of AGE to DGE on the Ti-SBA-15 catalyst in water solution are as follows: the temperature of 20°C, the molar ratio of AGE/H2O2 = 0.03:1, the content of the catalyst 3 wt%, and the reaction time of 60 min. At these mild and relatively safe conditions, the selectivity of DGE amounts to 100 mol%; the conversion of AGE and the selectivity of transformation to organic compounds in relation to hydrogen peroxide consumed amount to 4 mol% and 1 mol%, respectively. These studies also show that this process is very complicated because of the secondary reactions which proceed in reaction medium – hydration of epoxide ring in AGE (formation of 3A12PD), hydrolysis at the epoxide group in AGE, DGE, 3A12PD, epoxidation of the formed allyl alcohol, and hydration of the epoxide ring in glycidol and formation of glycerol. However, it is possible to choose such a way of carrying up this process in which only one product – DGE (the most desirable) – is obtained. The process of obtaining DGE is performed at very mild conditions, thus the danger of the explosive decomposition of hydrogen peroxide or compounds with epoxide group is very little, mainly taking into account the very low temperature of this process which amounts 20°C. Hydrogen peroxide used in this process is a relative cheap oxidizing agent and moreover, the methods of production of hydrogen peroxide are still developed and modernized. The method of AGE epoxidation with hydrogen peroxide is also ecologically friendly because only one product of its transformation is water. The presented studies showed that for this process hydrogen peroxide should be used in excess in relation to AGE. Mainly, it is connected with the phenomenon of ineffective decomposition of hydrogen peroxide (not explosive decomposition) at the active centers of Ti in the structure of the catalyst. This phenomenon causes that only a little amount of hydrogen peroxide takes part in epoxidation process and utilization of the excess of hydrogen peroxide in relation to AGE improves effective utilization of hydrogen peroxide molecules in the process of epoxidation. On the other hand, hydrogen peroxide undergoes very easy ineffective decomposition, thus even at the excess of hydrogen peroxide its concentration in reaction mixtures is low. The main cause of this situation is high content of the Ti-SBA-15 catalyst in reaction mixture (3 wt%). There are some possible ways of improving the hydrogen peroxide conversion efficiency by, for example, (1) addition of additives (CH3COOH, KHSO4, KH2PO4, KHF2, Na2SO4, NaHCO3, K2CO3, K3PO4, K2HPO4, or KH2PO4); (2) the changing of the way of hydrogen peroxide addition; (3) choosing the appropriate solvent (methanol, acetonitrile or acetone), or co-solvent (sulfolane); (4) increasing the acidity of the catalyst by the addition of metal oxide, for example, of TiO2, and utilization of the appropriate temperature of the calcination; and 5) the surface hydrophobization of mesoporous titanium silicates. We would like to test in our future works some of the ways of improving the efficiency of hydrogen peroxide conversion: choosing of the appropriate solvent, additives, and slow addition of hydrogen peroxide. A large advantage of the presented process is also performing the process of epoxidation in water solution without any other solvents. Moreover, water was not additionally introduced in the reactor, only with the solution of the oxidizing agent it was formed during the process. Water is now regarded as a very ecological solvent for organic processes.
The gingiva or commonly referred to as gums surround and protect the teeth (Figure 1). Gingival diseases by namesake denote to the diseases affecting the gingival tissues. These diseases have burdened the human race since the early civilization, and this is proof enough to gauge the importance of diagnosing gingival diseases and treating them. Gingival disease if left untreated can progress to periodontal tissues and result in periodontal disease which is easier to diagnose probably due to its chronic and severe nature as compared to gingival disease. No wonder periodontal disease has been mentioned in the literature of ancient Egypt and a step toward preventing it by means of oral hygiene practices deserves its mention in the ancient scriptures [1].
\nThe diagnosis of any disease is based on a proper documentation of case history which requires precise identification of signs and symptoms of disease and also any underlying medical disease/condition which may influence the same. The next step is to correlate clinical, pathological, laboratory and radiological findings. This sequence of steps also holds true for gingival diseases. This chapter attempts to focus on the minute differences in the diagnosis of gingival diseases which becomes cumbersome due to a simple fact that any infection or inflammation usually results in swelling up of the gingiva, bleeding, or formation of ulcers or vesicles. Such symptoms could be due to a single to multiple etiologic agents corresponding to varied diagnoses and treatment regimens [2].
The gingival disease terminology and classification has undergone many changes, and the current classification given at the World Workshop in 2017 classifies gingival condition in health and disease under three broad categories of health, dental biofilm-induced gingivitis, and non-dental biofilm-induced gingival disease [3] (Table 1).
\nGingivitis per se refers to the inflammation of the gingival tissues and is labeled with different diagnostic terms based on the etiology and clinical presentation to aid in formulation of the best-suited treatment. As mentioned above, the broad etiologic factors which result in gingival disease is the dental biofilm, which contain microbes, causing a microbial attack on the gingiva resulting in a dysbiosis amounting to a host response manifested in the form of the inflammatory disease called plaque-induced gingivitis. The plaque microbes have an influence on the gingiva depending upon its quantity and quality of pathogens present. Although the increased plaque burden is almost always associated with gingivitis, there are instances where paucity of plaque can again result in gingivitis due to the effect of modifying factors which make the host response more accentuated and exaggerated as they tend to have a more systemic affect than a local one [2, 4]. These modifying factors include few systemic conditions, factors which increase plaque accumulation and influence of drugs on gingiva. How these factors can affect gingivitis is summarized in Table 2.
\nPeriodontal health and gingival health | \nDental biofilm-induced gingivitis | \nNon-dental biofilm-induced gingival disease | \n||||
---|---|---|---|---|---|---|
Clinical gingival health on an intact periodontium | \nClinical gingival health on a reduced periodontium | \nAssociated only with dental biofilm | \nMediated by systemic or local risk factors | \nDrug-influenced gingival enlargement | \nGenetic/development disorders | \n|
\n | Stable periodontitis | \nNon-periodontitis | \n\n | Specific infections and inflammatory and immune conditions | \n||
\n | Reactive processes | \n|||||
Neoplasms | \n||||||
Endocrine, nutritional, and metabolic diseases | \n||||||
Traumatic lesions | \n||||||
Gingival pigmentation | \n
Classification of periodontal health, gingival disease, and condition [3].
Factor | \nEffect on gingiva | \nSigns and symptoms for diagnosis | \nDiagnosis | \nTreatment [5] | \n
---|---|---|---|---|
Bacterial dental biofilm only | \nMicrobial attack mounts a host response in the form of inflammation | \nMild redness with or without broken line of bleeding | \nIncipient gingivitis | \nOHI | \n
Mild changes in color and texture of the gingiva | \nMild gingivitis | \nOHI +/OP | \n||
Glazing redness, edema, enlargement, bleeding on probing | \nModerate gingivitis | \nOHI + OP | \n||
\n | Overt redness and edema and bleeding on palpation rather on probing | \nSevere gingivitis | \n||
Potential modifying factors of plaque-induced gingivitis | \n||||
Systemic conditions | \n||||
Sex steroid hormones (estrogen and progesterone) (1) Puberty | \nExaggerate the host inflammatory response in the presence of minimal plaque | \nBleeding on probing or bleeding with toothbrushing, mild to moderate redness | \nDiagnostic term not given as not seen frequently in population and if present can be diagnosed as gingivitis associated with puberty | \nOHI + OP | \n
(2) Menstrual cycle | \nExaggerates the host inflammatory response in the presence of minimal plaque | \nMild redness, edema based on severity of inflammation seen during the menstrual cycle | \nDiagnostic term not given as not seen frequently in population and if present can be diagnosed as gingivitis associated with menstrual cycle | \n|
(3) Pregnancy | \nThe hormones exaggerate the host inflammatory response in the presence of minimal plaque | \nDeep gingival probing depths, bleeding on probing or bleeding with toothbrushing, and elevated gingival crevicular fluid flow in pregnancy | \nPregnancy-associated gingivitis | \n\n |
(4) Oral contraceptives | \nThe high-dose hormones in the pills exaggerate the host inflammatory response in the presence of minimal plaque; low dose does not have much effect | \nMild redness, edema based on severity of inflammation seen after 1 to 3 months of use | \nCurrently the dose of oral contraceptives is low; hence diagnostic terms have been removed | \nOHI + OP + reduction of high-dose oral contraceptive Low-dose contraceptive does not require any change | \n
Hyperglycemia | \nHigh blood glucose levels increase the pathogenic bacteria and also form more AGE which affect collagen turnover and healing | \nSigns of inflammation of gingivitis + high blood glucose levels | \nGingivitis associated with diabetes mellitus | \nOHI + OP + maintenance of blood glucose levels by diet restriction/exercise/medication | \n
Leukemia | \nIncreases number of WBCs which accumulate in the gingival tissues and decreases number of platelets which causes bleeding | \nCervical lymphadenopathy, petechiae, ulcers seen in the mucosa, bleeding on slight provocation, swollen, glazed, spongy gingiva, red to deep purple color of gingival lesions | \nGingivitis associated with acute/chronic leukemia | \nTreat leukemia + symptomatic treatment for gingivitis with careful OHI and OP to prevent excessive bleeding | \n
Smoking | \nDirect smoking can cause vasoconstriction of gingival vasculature | \nNo redness, edema, or swelling present. Color may change to blue and pale pink. No gingival changes and pocket depths increase when lesions progress to periodontitis | \nNo gingivitis | \nSmoking cessation | \n
Malnutrition | \nDeficiency of vitamin C affects crosslinking of collagen | \nBleeding on probing, mobility, and swollen gums in severe cases with minimal plaque | \nScurvy | \nVitamin C supplementation + OHI + OP | \n
Oral factors enhancing plaque accumulation | \n||||
Prominent subgingival restoration margins | \nRoughness and closeness of these restorations to gingival tissue cause accumulation of plaque bacteria and irritation | \nLocalized mild redness, bleeding on probing, slight edema in area of restoration | \nGingivitis due to faulty restoration | \nCorrection of restoration + OHI + SRP | \n
Hyposalivation | \nDecreased saliva causes sticking of bacteria on tooth surfaces | \nDental caries, taste changes, halitosis, mucosal and gingival dryness, and gingival inflammation | \nGingivitis associated with hyposalivation | \nOHI + OP+ salivary substitutes | \n
Drug-influenced gingival enlargements | \n||||
Phenytoin, sodium valproate | \nDrugs and plaque cause fibroblasts to increase production of collagen and extracellular connective tissue | \nOnset after 3 months of drug intake, common in anterior gingiva, gingival size increases which starts from interdental papilla and may extend to the margin and attached gingiva in severe cases. The enlarged areas are firm to soft depending upon the presence of gingival inflammation | \nDrug-influenced mild gingival enlargement (if only papilla is involved) Drug-influenced mild gingival enlargement (if papilla and margin is involved) Drug-influenced mild gingival enlargement (if papilla, margin, and attached gingiva is involved) | \nOHI + OP+ drug substitution if required, followed by gingivectomy to correct enlarged gingival tissues | \n
Nifedipine, amlodipine, verapamil, diltiazem, felodipine | \n\n | \n | ||
Cyclosporine | \n\n | \n |
The crude tools used are a questionnaire/interview to collect important aspects of the patient demographics, medical history, current medications, and habits. The next step involves patient examination starting from extraoral structures to any abnormal intraoral findings to specific examination of the gingiva. The gingival disease is visually examined for clinical signs and symptoms using a mouth mirror under ambient lighting of the dental chair, cotton/gauze to dry the tissues, and sometimes the use of three-way air water syringe to wash way the debris for better inspection. Changes in color, contour, consistency, texture, size, position, etc. are noted. This is followed by palpation of the gingiva for any spontaneous bleeding, pain, discharge, blanching, consistency (by checking the resiliency of tissues on applying pressure), and pitting edema. The UNC-15 or the Michigan O periodontal probe with William’s marking is used to check for bleeding on probing, subgingival faulty restorative margins, and the presence of deeper than 5-mm pockets which is the critical probing depth to differentiate between gingivitis and periodontitis. Apart from these traditional tools used, advanced diagnostic aids have been introduced to further confirm the presence of gingival disease (Table 3) [5, 6].
\nAdvanced diagnostic aid for gingival disease | \nMechanism/working | \nInference | \n
---|---|---|
Periotemp probe | \nDetects the difference in subgingival temperature which is reflected by red or green light | \nRed light indicates future periodontal breakdown and increase in periopathogens | \n
New generation of periodontal probes | \nFirst-generation | \nDetects pocket depth using traditional probes | \n
\n | Second-generation | \nPressure-sensitive probe with uniform pressure | \n
\n | Third-generation | \nPressure-sensitive and captures data on computer | \n
\n | Fourth-generation | \nUses 3D technology to detect pocket | \n
\n | Fifth-generation | \nUses 3D technology and ultrasound to detect pocket | \n
Advances in radiography | \nUse of charged-coupled device, complementary metal oxide semiconductor, and cone beam-computed tomography allow digital recording | \nThese are used to detect bone loss and bone defects in 2D and 3D for periodontal defects rather than gingival diseases | \n
Advances in microbial culturing | \nHigh-performance liquid chromatography | \nCan detect bacterial cell wall components | \n
Flow cytometry | \nCan detect various bacteria | \n|
Latex agglutination test | \nCan detect pathogenic antigen, proteins, and antibody by agglutination reaction | \n|
Direct and indirect immunofluorescence | \nCan detect pathogenic antigen, proteins, and antibody by agglutination and adding fluorescent dyes | \n|
Enzyme-linked immunosorbent assay | \nEvalusite can detect P. gingivalis, P. intermedia, and A. actinomycetemcomitans\n | \n|
Nucleic acid and DNA checkerboard hybridization techniques | \nDetects microbes based on matching of unknown sample with known hybridization technique of nuclei acid/DNA | \n|
DNA probe | \nOmnigene can detect P. gingivalis, P. intermedia, A. actinomycetemcomitans, E. corrodens, C. rectus, F. nucleatum\n | \n|
Perioscan uses BANA (N-benzoyl-DL arginine naphthylamide) hydrolysis carried out by trypsin-like protease | \nDetects trypsin-like protease releasing bacteria, such as P. gingivalis, T. denticola, and T. forsythus\n | \n|
\n | IAI Pado Test 4.5 RNA probe test kit uses oligonucleotide probes complementary to conserve fragments of the 16S rRNA gene that encodes the rRNA | \nDetects A. actinomycetemcomitans, P. gingivalis, Tannerella forsythia, and T. denticola\n | \n
\n | MyPerioPath is a DNA test and uses saliva samples | \nTo identify the type and concentration of periodontal bacteria | \n
Advances in biochemical test kits | \nPerio-Check | \nDetects neutral proteases like collagenases in GCF (gingival crevicular fluid) | \n
\n | Prognos-Stik: detects serine proteinase elastase in GCF | \nShows active disease sites | \n
\n | PocketWatch: detects aspartate aminotransferase in GCF | \nDifferentiates active and non-active sites of disease | \n
\n | PerioGard: detects aspartate aminotransferase in GCF | \nDifferentiates active and non-active sites of disease | \n
\n | Perio 2000: detects volatile sulfur compounds | \nTo detect halitosis | \n
\n | Toxicity prescreening assay (TOPAS) | \nDetects bacterial toxins and proteins | \n
\n | Dipstick | \nDetects (matrix metalloproteinase) MMP-8 in GCF | \n
\n | Integrated microfluidic platform for oral diagnostics (IMPOD) | \nSaliva-based detection of MMP-8 | \n
\n | Oral fluid nanosensor test (OFNASET): saliva-based detection of (interleukin) IL-1, IL-8 | \nUsed for detection of salivary biomarkers for oral cancer | \n
\n | Electronic taste chip (ETC) | \nDetects C-reactive protein which is an important biomarker for inflammation | \n
Genetic tests | \nGenetic periodontitis susceptibility trait (PST) test | \nDetects IL-1 polymorphism | \n
\n | MyPerioID | \nSaliva-based detection of genetic susceptibility | \n
Apart from plaque-induced gingivitis, it is imperative to diagnose and differentiate the non-plaque-induced gingival diseases and conditions to provide appropriate treatment and to avoid overtreatment. The etiology of non-plaque-associated gingival disease is usually related to some genetic defect or systemic disorder. In many instances the oral lesions precede the extraoral findings and can help in diagnosing a disease which could affect the full body. Therefore, while diagnosing these conditions, we need to look for other associated conditions to arrive at a correct diagnosis. Table 4 attempts to highlight the clinical features to help arrive at a diagnosis [7, 8, 9, 10, 11].
\nC | \nCr | \nCs | \nT | \nS | \nP | \nL | \nLab & H/P | \nAdd Sym | \nD | \nRx | \n
---|---|---|---|---|---|---|---|---|---|---|
G | \nFlat or rounded | \nFirm and resilient | \nLoss of stippling | \n++ | \nCoronal to CEJ | \nGingival enlargement | \nExcisional biopsy shows fibrous connective tissue | \n\n | Hereditary gingival fibromatosis | \nGingivectomy to contour the topography + OHI | \n
P-R/B-Br | \nBlunted | \nSoft and friable | \nUlcerative | \n−− | \nVaries from papillary destruction to beyond mucogingival junction | \nGingival ulceration | \nBacterial culture for various bacteria types such as Treponema, Selenomonas, Fusobacterium, and Prevotella intermedia. H/P Loss of the epithelium in ulcerated areas | \nLoss of taste, woody sensation in teeth and feeling of extruded teeth accompanied with underlying risk factors such as poor oral hygiene and systemic conditions | \nNecrotizing periodontal disease | \nDebridement of local factors + CHX+ amoxicillin and metronidazole | \n
FR/W | \nNo change | \nSoft and edematous | \nUlcerative/white pseudomembranous | \n+ | \nNo change | \nErythematous | \nBacterial culture for Neisseria gonorrhoeae\n | \nPharyngitis and lymphadenopathy. Other sites: urethra, anus, cervix, oral mucosa | \nGonorrhea | \nSystemic antibiotic therapy | \n
FR | \nNo change | \nEdematous | \nLoss of stippling and ulceration with whitish membrane | \n+ | \nNo change | \nChancre (rare) | \nBacterial culture for Treponema pallidum, followed by serologic reaction tests | \nGenital and skin lesions | \nSyphilis | \nSystemic antibiotic therapy | \n
R-Gy patches | \nNo change | \nFirm | \nNodular/papillary proliferation | \n+ | \nNo change | \nNodular/papillary proliferation | \nPositive delayed hypersensitivity (tuberculin) skin reaction to purified protein derivative (ppd), isolation of mycobacterial antigen from bacterial cultures, and demonstration of acid-fast mycobacteria in clinical specimens. H/P: characteristic multinucleated giant cells and granulomas are diagnostic features | \nCommonly associated with lung infections. Involves floor of the mouth, extraction sites, and lymph nodes | \nTuberculosis | \nRegimens of multiple antibiotics like isoniazid, rifampicin, pyrazinamide, or ethambutol | \n
RP | \nRounded | \nSoft | \nErythematous patch | \n\n | \n | \n | Culture for streptococcal strains. Biopsy | \nUpper respiratory infections | \nStreptococcal gingivitis | \nOHI+ antibiotics | \n
RP | \nNo change | \nSoft and ulcerative | \nSmall vesicles/fibrinous coated ulcer | \n– | \nBlunted papilla sometimes | \nPainful ulcers after vesicle rupture | \n\n | Skin lesions, low-grade fever | \nHand, foot and mouth disease | \nSupportive treatment to correct fever and pain | \n
RP | \nFlat and rounded | \nSoft and edematous | \nUlcerated, loss of stippling | \n+ | \nCoronal or apical to CEJ | \n\n | \n | Lymphadenitis, fever, malaise | \nPrimary herpetic gingivostomatitis | \nAcyclovir and spirin/paracetamol, fluids. Dyclonine hydrochloride 0.5% for anesthesia | \n
RP | \nFlat and rounded | \nSoft and edematous | \nUlcerated | \n+ | \nAttached gingival and hard palate | \n\n | Rarely required. If needed fluorescent staining is more sensitive. HSV isolation of a virus in tissue. Culture is the most positive method of identification. Scraping made from the base of the lesion and stained with giemsa. H/P: Wright’s or Papanicolaou stain and shows syncytium and ballooning. Degeneration of the nucleus | \nFever | \nRecurrent intraoral herpes simplex | \nAcyclovir and aspirin/paracetamol, fluids. Dyclonine hydrochloride 0.5% for anesthesia | \n
BR | \nNo change | \nSoft | \nVesicular | \n+/− | \nDiffuse erythema and isolated small vesicles that rupture quickly leaving ulcerations | \nLesions on skin and mucosa | \nFluorescent-antibody staining of smears using fluorescein-conjugated monoclonal antibodies is more reliable than routine cytology | \nFever, malaise, and skin rash | \nChicken pox (Varicella) | \nAcyclovir/valacyclovir for healing and reducing acute pain. Systemic corticosteroids to prevent postherpetic neuralgia, combination of intralesional steroids and local anesthetics to decrease healing time and prevent postherpetic neuralgia and application of capsaicin | \n
R patches +W halo | \nBlunt or rounded | \nSoft and friable | \nUlcerated | \n— | \nUnilateral vesicles which rupture | \nNecrosis of periodontium and alveolar bone | \nCulture | \nSkin lesion | \nShingles (herpes zoster) | \nOral acyclovir 800 mg five times a day, famciclovir 500 mg three times a day, or valacyclovir 500 mg three times a day | \n
Pi | \nNo change | \nSoft | \nPapules | \n++ | \nRaised nodular or popular lesions | \nMucosal lesions are rare | \n\n | Discrete papules on skin of face and trunk and in genital areas | \n\nMolluscum contagiosum virus | \nCryotherapy/laser | \n
G | \nNo change | \nFirm | \nExophytic and verrucous | \n++ | \n\n | Exophytic papillomatous, verrucous or flat lesions | \n\n | \n | Squamous cell papilloma, condyloma acuminatum, verruca vulgaris, focal epithelial hyperplasia | \nSurgical removal, laser ablation, cryotherapy, and topical application of keratinolytic agents. For smaller lesions, topical application of 25% podophyllum resin to reduce the size. Intralesional injection of interferon-α 1,000,000 iu/cm2 once weekly and subcutaneous injections 3,000,000 iu/cm2 twice weekly | \n
W-R | \nNo change | \nSoft and resilient | \nScrapable lesion | \n+/− | \n\n | Pseudomembrane/erythematous/plaque-like/ nodular | \nH/P: culture of infected tissues or exudates on Sabouraud’s dextrose agar or other appropriate media | \nOral involvement is secondary to serious systemic infection | \nCandidiasis | \nTopical antifungal medications, nystatin, and amphotericin b | \n
BR | \nRounded | \nSoft and friable | \nChronic vegetating painful ulcer | \n++ | \n\n | Nodular, papillary, or granulomatous lesions | \nBiopsy of infected tissue shows small oval yeasts within macrophages and reticuloendothelial cells as well as chronic granulomas, epithelioid cells, giant cells, and occasionally caseation necrosis | \nCavitation of the lung and dissemination of the organism to the liver, spleen, adrenal glands, and meninges | \nHistoplasmosis | \nKetoconazole or itraconazole for 6–12 months | \n
RP | \nViolaceous marginal gingiva in early stage | \nSoft and friable | \nNecrosis and covered with pseudomembrane in advanced cases | \n−− | \n\n | Lesions are necrotic and covered by pseudomembrane | \n\n | Systemic involvement is present. Late stage involves destruction of alveolar bone and facial muscles | \nAspergillosis | \nSystemic antifungals | \n
R+ W streaks | \nNormal | \nSoft | \nLichenoid reaction | \nNo change | \n\n | Lichenoid-like reaction | \nPatch test by placing aluminum disks with known allergens for 48 hours on hairless skin and wait for any inflammation as a positive test. H/P: chronic inflammatory reaction with lichenoid infiltration of lymphocytes | \n\n | Contact allergy | \nTopical corticosteroids | \n
R | \n\n | \n | Velvety texture | \n+ | \nSeen in anterior maxillary gingiva | \n\n | Plasma cells in lamina propria | \n\n | Plasma cell gingivitis | \nTopical corticosteroids | \n
R-W | \n\n | Soft and friable | \nSmooth or disrupted | \n— | \n\n | Round lesion with central red area or pale pink surrounded by red periphery | \nBiopsy an epidermal pattern characterized by lichenoid vasculitis and intraepidermal vesicles and a dermal pattern characterized by lymphocytic vasculitis and subepidermal vesiculation | \nSkin lesions symmetrically present on distal extremities and moving proximally Hand, face, elbow and knees | \nErythema multiforme | \nAnesthetic mouthwash, corticosteroids in severe cases, and acyclovir if associated with HSV | \n
RP-W | \nNormal | \nSoft and friable | \nSmooth and loss of stippling | \nNo change | \nLesions on free and attached gingiva | \nDesquamative gingivitis with vesiculobullous lesions which rupture | \nELISA to detect circulating antibody to desmoglein 1 and 3. Histopathology: suprabasilar acantholysis may be observed | \nBullous lesions on skin | \nPemphigus vulgaris | \nPrednisolone usually given in dosages of 1–2 mg/kg/d and later −− | \n
R area | \nNormal | \nSoft | \nSmooth and loss of stippling | \n— | \nPositive Nikolsky sign: rubbing the gingiva forms bulla | \nDesquamative lesions with bulla formation | \nHistopathology: circulating antibodies not always found by indirect immunofluorescence | \nScarring in ocular lesions | \nPemphigoid | \nSystemic corticosteroids | \n
R-W streaks | \nNormal | \nSoft and resilient | \nSmooth and ulcerative | \nNo change | \n\n | Papular, reticular, plaque type or bullous lesions | \nHyperkeratosis and saw tooth-shaped rete pegs | \nSkin lesions | \nLichen planus | \nTopical corticosteroids or intralesional steroids like 0.05% fluocinonide (Lidex) and 0.05% clobetasol (temovate) | \n
R and W striae | \n\n | \n | Smooth and ulcerative | \n−/+ | \n\n | Central atrophic area with small white dots surrounded by white striae | \nHyperorthokeratosis with keratotic plugs, atrophy of the rete ridges, and liquefactive degeneration of the basal celllayer | \nRed butterfly-shaped photosensitive, scaly, macules on the nose bridge and cheeks | \nLupus erythematosus | \nSystemic immunosuppressant and protection from sunlight | \n
Pl | \nNormal | \nSoft | \n\n | ++ | \n\n | Cobblestone appearance of mucosa and linear ulceration | \nHistopathology | \nIntestinal pain, anal fissures, diarrhea, and labial enlargement | \nCrohn’s disease | \nSteroids and immunosuppressants to decrease progression | \n
RP | \n\n | Soft and friable | \nLoss of stippling | \n++ | \nGingival recession | \nNodules and ulceration. Loosening of teeth | \nHyperglobulinemia, an elevated level of serum angiotensin-converting enzyme, evidence of depressed cellular immunity. H/P: noncaseating epithelioid granulomas in more than one organ system | \nSwelling of salivary glands | \nSarcoidosis | \nSystemic steroids and anti-inflammatory agents | \n
Pi | \nNormal | \nFibrous | \nSmooth | \n+ | \n\n | Exophytic smooth masses | \nH/P: bundles of collagen covered with the epithelium | \n\n | Fibrous epulis | \nExcision and curettage | \n
RP | \nNormal | \nFibrous | \nSmooth | \n++ | \nStart from interdental papilla | \nPedunculated to sessile masses | \nH/P: cellular fibroblastic tissue containing rounded or lobulated masses of calcified cementum-like tissue | \n\n | Calcifying fibroblastic granuloma | \nExcision of lesion | \n
RP | \n\n | \n | \n | + | \n\n | Ulcerated, smooth, and pedunculated mass | \nH/P: discontinuous hyperplastic parakeratinized stratified squamous epithelium and endothelial cells in the connective tissue | \n\n | Pyogenic granuloma | \nExcision of lesion | \n
Pr-Bl-Br | \n\n | Soft | \n\n | ++ | \n\n | Sessile or pedunculated tumor-like process | \nH/P: multinucleated giant cell forming granuloma | \n\n | Peripheral giant cell granuloma | \nSurgical excision | \n
W | \n\n | Corrugated or verrucous surface | \n\n | + | \n\n | Non-removable white spot | \nTissue biopsy. Vital staining with toluidine blue and cytobrush techniques. H/P: dysplastic cells with ++ hyperchromatic nuclei, cellular and nuclear pleomorphism, an ++ nucleo-cytoplasmic ratio, and generalized loss of cellular polarity and orientation | \nHistory of tobacco/alcohol intake | \nLeukoplakia | \nSurgical excision/cryosurgery and laser ablation | \n
R | \n\n | Velvety | \n\n | + | \n\n | Sharply demarcated from surrounding mucosa | \nSame as above | \nMay be associated with oral lichen planus | \nErythroplakia | \nSame as above | \n
R- W patches | \nNo change | \nSoft | \nSmooth | \n++ | \nInvolve keratinized gingiva | \nPainless exophytic mass with nonhealing ulceration | \nDysplastic changes seen in the epithelium and extending into connective tissue and the presence of keratin pearls | \nHistory of tobacco/alcohol intake | \nSquamous cell carcinoma | \nSurgical removal, chemotherapy | \n
RP | \nNo change | \nSoft and edematous | \nSmooth | \n++ | \n\n | Pallor of oral mucosa, pain, petechiae, ecchymosis, gingival bleeding, deep punched out ulcers | \nBlood investigation. Bone marrow biopsy. Tooth mobility | \nDysphagia, facial paralysis, paraesthesia of the face, lips, tongue, and chin, trismus sometimes | \nLeukemia | \nMonitoring of the patient for infection during neutropenic periods and early management of infection. Corticosteroids, adrenocorticotropin, or testosterone modulates the sharp reduction in marrow function. Granulocyte colony-stimulating factor (G-CSF) | \n
P | \nRounded | \nSoft | \nSmooth | \n++ | \n\n | \n | Histopathology will show Reed-Sternberg cells | \nSwollen lymph nodes | \nLymphoma | \nRadiation and chemotherapy plus doxorubicin, bleomycin, vincristine, and dacarbazine for Hodgkin’s lymphoma and cyclophosphamide, vincristine, and prednisone for non-Hodgkin’s | \n
W plaques | \nNo change | \nSoft | \nLoss of stippling | \n+ | \nSeen on facial attached gingiva | \nLeukoplakia-like asymptomatic plaque | \nH/P: dense fibrous connective tissue | \n\n | Frictional keratosis | \nPrevention of deleterious habits | \n
RP | \nNo change | \nSoft and friable | \n\n | — | \nGingival recession | \nSuperficial and horizontal gingival laceration | \nNot much significant | \n\n | Toothbrushing-induced gingival ulceration | \nChanging the brushing technique | \n
R-W | \n\n | \n | \n | — | \n\n | Surface slough or ulceration | \nNot much significant | \n\n | Chemical insult due to etching, chlorhexidine, hydrogen peroxide, acetylsalicylic acid, dentifrice, detergent, calcium hydroxide, etc. | \nRemoval of offending irritant | \n
R | \n\n | \n | \n | — | \n\n | Erythematous lesion that slough a coagulated surface, vesicles and ulceration may be present | \nNot of much significance | \n\n | Burns of mucosa | \nSupportive care and hydration | \n
Br-Bl | \nNo change | \nNo change | \nNo change | \n= | \n\n | \n | Pigmented deposits in the epithelium and connective tissue | \nAddison’s disease, Albright syndrome, Peutz-Jeghers syndrome | \nGingival pigmentation | \nNot required | \n
Br | \nNo change | \nFirm | \nNo change | \n= | \nMandibular facial gingiva | \n\n | H/P: pigmented macules seen in section | \n\n | Smoker’s melanosis | \nSmoking cessation for 2 weeks | \n
Bl-Gy–Br-Bl | \nNo change | \nNo change | \nNo change | \n= | \n\n | Diffuse pigmentation | \n\n | \n | Drug-induced pigmentation (antimalarial, minocycline) | \nCessation of drug if required | \n
Bl-Gy–Br-Bl | \nNo change | \nNo change | \nNo change | \n= | \n\n | \n | H/P: discrete granules in connective tissue | \n\n | Amalgam tattoo | \nRemoval of amalgam debris and replacement of amalgam if required | \n
Clinical features for diagnosis and treatment of non-plaque-induced gingival diseases.
C, color; Cr, contour; Cs, consistency; T, texture; S, size; P, position; L, lesion; lab and H/P, laboratory procedures and histopathology; add sym, additional symptoms; D, diagnosis; Rx, treatment; FR, fiery red; G, same as surrounding gingiva; W, white; PR, pink to reddish; B-Br, black to brown; R-Gy, red to gray; RP, reddish pink; BR, bright red; Pi, pink; Pl, pale pink; Pr, purple; Bl, blue; OHI, oral hygiene instruction; CHX, chlorhexidine; +, slightly increased; ++, increased; −, slightly decreased; −−, decreased; −/+, may increase or decrease; =, remains the same.
The treatment of gingival disease is based on resolving the etiologic factors and maintaining the systemic status of the individual. In the case of plaque-induced gingivitis, the main treatment plan involves removal of plaque and calculus by scaling and root planning, followed by oral hygiene instruction which includes modified bass method of brushing and the use of chemical plaque control agents like 0.2% or 0.02% chlorhexidine gluconate or essential oil mouthwash. In cases of gingival enlargement, initial therapy is focused on removing plaque and calculus, followed by a review on the gingival condition; only if the condition does not improve the drug substitution may be considered, followed by gingivectomy to remove the enlarged gingival tissue. Plaque-induced gingival disease influenced by modifying factors is controlled by reducing the exposure of the modifying factor in addition to removal of plaque and calculus to maintain oral hygiene. The details of the treatment have been mentioned in Table 2. Non-plaque-induced gingival diseases are treated depending on the etiology of the gingival disease. For example, viral lesions are treated by providing antiviral medications in addition to oral hygiene instruction. The details of treatment in brief are mentioned in Table 4. Diagnosis is essential for providing the proper treatment plan and updating recent research which might help prevent undue treatment [8].
\nGingival diseases are an initial starting point of the advanced periodontal disease and in some cases depict the manifestation of an underlying undiagnosed systemic condition. Therefore, the early diagnosis of gingival disease and its treatment are warranted.
\nThe authors declare no conflict of interest.
.
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I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. 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After obtaining a Master's degree in Mechanical Engineering, he continued his PhD studies in Robotics at the Vienna University of Technology. Here he worked as a robotic researcher with the university's Intelligent Manufacturing Systems Group as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and most importantly he co-founded and built the International Journal of Advanced Robotic Systems- world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career, since it was a pathway to founding IntechOpen - Open Access publisher focused on addressing academic researchers needs. Alex is a personification of IntechOpen key values being trusted, open and entrepreneurial. Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. He is an expert in structural, absorptive, catalytic and photocatalytic properties, in structural organization and dynamic features of ionic liquids, in magnetic interactions between paramagnetic centers. The author or co-author of 3 books, over 200 articles and reviews in scientific journals and books. He is an actual member of the International EPR/ESR Society, European Society on Quantum Solar Energy Conversion, Moscow House of Scientists, of the Board of Moscow Physical Society.",institutionString:null,institution:{name:"Semenov Institute of Chemical Physics",country:{name:"Russia"}}},{id:"62389",title:"PhD.",name:"Ali Demir",middleName:null,surname:"Sezer",slug:"ali-demir-sezer",fullName:"Ali Demir Sezer",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62389/images/3413_n.jpg",biography:"Dr. Ali Demir Sezer has a Ph.D. from Pharmaceutical Biotechnology at the Faculty of Pharmacy, University of Marmara (Turkey). He is the member of many Pharmaceutical Associations and acts as a reviewer of scientific journals and European projects under different research areas such as: drug delivery systems, nanotechnology and pharmaceutical biotechnology. Dr. Sezer is the author of many scientific publications in peer-reviewed journals and poster communications. Focus of his research activity is drug delivery, physico-chemical characterization and biological evaluation of biopolymers micro and nanoparticles as modified drug delivery system, and colloidal drug carriers (liposomes, nanoparticles etc.).",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"61051",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"100762",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"St David's Medical Center",country:{name:"United States of America"}}},{id:"107416",title:"Dr.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Texas Cardiac Arrhythmia",country:{name:"United States of America"}}},{id:"64434",title:"Dr.",name:"Angkoon",middleName:null,surname:"Phinyomark",slug:"angkoon-phinyomark",fullName:"Angkoon Phinyomark",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/64434/images/2619_n.jpg",biography:"My name is Angkoon Phinyomark. 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