Classification of periodontal health, gingival disease, and condition [3].
\r\n\tFinally, I want to emphasize that, in this book, I expect to have excellent contributons on the subjects other than muscle systems, so that the book will be widely read by people interested in non-muscle motile systems as well as by muscle researchers.
",isbn:null,printIsbn:null,pdfIsbn:null,doi:null,price:0,priceEur:null,priceUsd:null,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"862ba53997da17b644b918fe44e97d4a",bookSignature:"Emeritus Prof. Haruo Sugi",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/7021.jpg",keywords:"Musculo-skeletal system, Cardio-vascular system, Porter myosins, Cellular transport, Motile systems, cell division, Contractile ring formation, Mitotic apparatus, Ciliary Movement, Flagellar Movement, Amoeboid movement, Novel motile systems",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"August 13th 2018",dateEndSecondStepPublish:"September 3rd 2018",dateEndThirdStepPublish:"November 2nd 2018",dateEndFourthStepPublish:"January 21st 2019",dateEndFifthStepPublish:"March 22nd 2019",remainingDaysToSecondStep:"3 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"140827",title:"Emeritus Prof.",name:"Haruo",middleName:null,surname:"Sugi",slug:"haruo-sugi",fullName:"Haruo Sugi",profilePictureURL:"https://mts.intechopen.com/storage/users/140827/images/system/140827.jpg",biography:"Haruo Sugi was appointed instructor in the Depertment of Physiology of the University of Tokyoin 1962, and worked at Columbia University and the National Instututes of Health, USA, from 1965 to 1967. He was a professor and chairman of the Department of Physiology, Teikyo University Medical School from 1973 to 2004, when he became emeritus professor. Professor Sugi organized international symposia on muscle contraction seven times, each followed by publication of proceedings. He also edited 4 books. 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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:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"314",title:"Regenerative Medicine and Tissue Engineering",subtitle:"Cells and Biomaterials",isOpenForSubmission:!1,hash:"bb67e80e480c86bb8315458012d65686",slug:"regenerative-medicine-and-tissue-engineering-cells-and-biomaterials",bookSignature:"Daniel Eberli",coverURL:"https://cdn.intechopen.com/books/images_new/314.jpg",editedByType:"Edited by",editors:[{id:"6495",title:"Dr.",name:"Daniel",surname:"Eberli",slug:"daniel-eberli",fullName:"Daniel Eberli"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"57",title:"Physics and Applications of Graphene",subtitle:"Experiments",isOpenForSubmission:!1,hash:"0e6622a71cf4f02f45bfdd5691e1189a",slug:"physics-and-applications-of-graphene-experiments",bookSignature:"Sergey Mikhailov",coverURL:"https://cdn.intechopen.com/books/images_new/57.jpg",editedByType:"Edited by",editors:[{id:"16042",title:"Dr.",name:"Sergey",surname:"Mikhailov",slug:"sergey-mikhailov",fullName:"Sergey Mikhailov"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1373",title:"Ionic Liquids",subtitle:"Applications and Perspectives",isOpenForSubmission:!1,hash:"5e9ae5ae9167cde4b344e499a792c41c",slug:"ionic-liquids-applications-and-perspectives",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/1373.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"71710",title:"Diagnosis and Treatment Plan for Gingival Diseases and Conditions",doi:"10.5772/intechopen.91726",slug:"diagnosis-and-treatment-plan-for-gingival-diseases-and-conditions",body:'\nThe 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 [
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 | \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 | \n|
Perioscan uses BANA (N-benzoyl-DL arginine naphthylamide) hydrolysis carried out by trypsin-like protease | \nDetects trypsin-like protease releasing bacteria, such as | \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 | \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 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 | \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 | \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\n | \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.
Searching strategies for finding targets using appropriate sensing modalities are of great importance in many aspects of life. In the context of national security, there could be a need to find a source of hazardous emissions [1, 2, 3]. Similarly, rescue and recovery missions may be tasked with localising a lost piece of equipment that is emitting weak signals [4]. Biological applications include, for example, protein searching for its specific target site on DNA [5], or foraging behaviour of animals in their search for food or a mate [6, 7]. The objective of search research [8] is to develop optimal strategies for localising a target in the shortest time (on average), for a given search volume and sensing characteristics.
The use of autonomous vehicles in dangerous missions, such as finding a source of hazardous emissions, has become widespread [9, 10, 11]. Existing approaches to the search and localisation in the context of atmospheric releases can be loosely divided into three categories: up-flow motion methods, concentration gradient-based methods and information gain-based methods, also known as
This chapter summarizes our recent results in development of an autonomous infotaxic coordinated search strategy for a group of robots, searching for an emitting hazardous source in open terrain under turbulent conditions. The assumption is that the search platforms can move and sense. Two types of sensor measurements are collected sequentially: (a) the concentration of the hazardous substance; (b) the platform location within the search domain. Due to the turbulent transport of the emitted substance, the concentration measurements are typically sporadic and fluctuating. The searching platforms form a moving sensor network, thus enabling the exchange of data and a cooperative behaviour. The multi-robot infotaxis have already been studied in [16, 17, 20, 24]. However, all mentioned references assumed
We develop an approach where the group of searching robots operate in a fully decentralised coordinated manner. Decentralised operation means that each searching robot performs the computations (i.e., source estimation and path planning) locally and independently of other platforms. Having a common task, however the robotic platforms must perform in a coordinated manner. This coordination is achieved by exchanging the data with immediate neighbours only, in a manner which does not require the global knowledge of the communication network topology. For this reason, the proposed approach is scalable in the sense that the complexities for sensing, communication, and computing per sensor platform are independent of the sensor network size. In addition, because all sensor platforms are treated equally (no leader-follower hierarchy), this approach is robust to the failure of any of the searching agents. The only requirement for avoiding the break-up of the searching formation is that the communication graph of the sensor network remains
First, we describe the measurement model. The concentration measurements are modelled using a Lagrange encounters model developed in [13], based on an open field assumption and a two-dimensional geometry. Let
where
The probability that a sensor at location
Parameter
The motion model of a coordinated group of robots is described next. Let the pose vector of the
For each platform
The measurements of concentration are taken at time instants
Motion of the
where vector
Here,
An example of a formation of
A robotic platform can communicate with another platform of the formation, if their mutual distance is smaller than a certain range
Estimation and robot motion control are carried out using the measurement dissemination-based decentralised fusion architecture [25]. Measurement locations2 and the corresponding measured concentration values, i.e., the triple
Suppose the posterior density function of the source at discrete-time
where
where
is independent of
where the posterior of source strength
Since the conjugate prior of the Poisson distribution is the Gamma distribution [28], the posterior
The parameters of the prior for source strength,
Next, we turn our attention to the posterior of source position
where
The Rao-Blackwellised particle filter (RBPF) fully describes the posterior
Here,
In decentralised multi-robot search, each platform autonomously makes a decision at time
A robot platform
where
Previous studies of search strategies [3, 20] found that the reward function defined as the
where
while
where
Given that
In order to compute
where the product
Thus, (17) is approximated with
Pseudo-code of the routine for the computation of control vector on platform
Algorithm 1 Computation of
1:
2: Compute
3: Create admissible set
4:
5: Compute the future platform location
6: Compute
7: Determine
8: Compute
9: Calculate the expected reward
10:
11: Find
12:
So far, we have explained how platform
We apply decentralised cooperative control based on the average consensus [30, 31]. In a network of collaborating agents, consensus is an iterative protocol designed to reach an agreement regarding a certain quantity of interest. Suppose that every platform, as a node in the communication network, initially has an individual scalar value. The goal of average consensus is for every node in the network to compute the average of initial scalar values, in a completely decentralised manner: by communicating only with the neighbours in the communication graph (without knowing the topology of the communication graph).
In the problem we consider, there is not only a single individual scalar value, but six of them. They include three motion control parameters, i.e., for platform
Let us denote the scalar value of interest by
Ideally, we want every platform in the formation to compute the mean value
Average consensus is an iterative algorithm. At iteration
where
The search continues until the global stopping criterion is satisfied. The local stopping criterion is calculated on each platform independently based on the spread of the local positional particles
The global stopping criterion is computed on each platform using the average consensus algorithm, using (21), but with
We point out that both estimation and control are based on the consensus algorithm. While the cooperative control is using the
The proposed search algorithm has been applied to an experimental dataset, collected by COANDA Research & Development Corporation using their large recirculating water channel. The emitting source was releasing fluorescent dye at a constant rate from a narrow tube. The dataset comprises a sequence of 340 frames of instantaneous concentration field measurements in the vertical plane and is sampled at every 10/23 s. The size of a frame is
An example of the search algorithm running on the experimental data is shown in Figure 2. All physical quantities are in arbitrary units (a.u.). The following environmental/sensing parameters were used:
Experimental dataset: an illustrative run of the decentralised multi-robot search using
Figure 2 displays the top-down view of the search progress at step indices
Using 200 Monte Carlo simulations, the mean search time for the algorithm was 2525 a.u., with a 5th and 95th quantile of 1840 and 3445 a.u., respectively. Note that in all simulations the formation started from the bottom right hand corner indicated in Figure 2(a).
The chapter presented a decentralised infotaxic search algorithm for a group of autonomous robotic platforms. The algorithm allows the platforms to search and locate a source of hazardous emissions in a coordinated manner without the need for a centralised fusion and control system. More precisely, this distributed coordination is achieved only by local exchange of measurement data between neighbouring platforms. Similarly, the movement decisions taken by the platforms were reached using a distributed average consensus algorithm over the whole formation. The key aspect is that individual platforms only require knowledge of their neighbours; the global knowledge of the communication network topology is unnecessary. An advantage of adopted distributed framework is that all platforms are treated equally, making the proposed search algorithm scalable and robust to the failure of a single platform. Numerical results using experimental data confirmed the robust performance of the algorithm. The main limitation of the algorithm is that the environmental parameters (such as diffusivity, the average direction and speed of the wind, particle lifetime), must be known. Future work will explore sensitivity to parametrisation and will aim to develop a team of “search and rescue” robots for further experimentation in realistic environments.
This research was supported in part by the Defence Science and Technology Group through its Strategic Research Initiative on Trusted Autonomous Systems.
IntechOpen - where academia and industry create content with global impact
",metaTitle:"Team",metaDescription:"Advancing discovery in Open Access for the scientists by the scientist",metaKeywords:null,canonicalURL:"page/team",contentRaw:'[{"type":"htmlEditorComponent","content":"Our business values are based on those any scientist applies to their research. We have created a culture of respect and collaboration within a relaxed, friendly and progressive atmosphere, while maintaining academic rigour.
\\n\\nCo-founded by Alex Lazinica and Vedran Kordic: “We are passionate about the advancement of science. As Ph.D. researchers in Vienna, we found it difficult to access the scholarly research we needed. We created IntechOpen with the specific aim of putting the academic needs of the global research community before the business interests of publishers. Our Team is now a global one and includes highly-renowned scientists and publishers, as well as experts in disseminating your research.”
\\n\\nBut, one thing we have in common is -- we are all scientists at heart!
\\n\\nSara Uhac, COO
\\n\\nSara Uhac was appointed Managing Director of IntechOpen at the beginning of 2014. She directs and controls the company’s operations. Sara joined IntechOpen in 2010 as Head of Journal Publishing, a new strategically underdeveloped department at that time. After obtaining a Master's degree in Media Management, she completed her Ph.D. at the University of Lugano, Switzerland. She holds a BA in Financial Market Management from the Bocconi University in Milan, Italy, where she started her career in the American publishing house Condé Nast and further collaborated with the UK-based publishing company Time Out. Sara was awarded a professional degree in Publishing from Yale University (2012). She is a member of the professional branch association of "Publishers, Designers and Graphic Artists" at the Croatian Chamber of Commerce.
\\n\\nAdrian Assad De Marco
\\n\\nAdrian Assad De Marco joined the company as a Director in 2017. With his extensive experience in management, acquired while working for regional and global leaders, he took over direction and control of all the company's publishing processes. Adrian holds a degree in Economy and Management from the University of Zagreb, School of Economics, Croatia. A former sportsman, he continually strives to develop his skills through professional courses and specializations such as NLP (Neuro-linguistic programming).
\\n\\nDr Alex Lazinica
\\n\\nAlex Lazinica is co-founder and Board member of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his Ph.D. in Robotics at the Vienna University of Technology. There, he worked as a robotics 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, co-founded and built the International Journal of Advanced Robotic Systems, the world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career since it proved to be the pathway to the foundation of IntechOpen with its focus on addressing academic researchers’ needs. Alex personifies many of IntechOpen´s key values, including the commitment to developing mutual trust, openness, and a spirit of entrepreneurialism. Today, his focus is on defining the growth and development strategy for the company.
\\n"}]'},components:[{type:"htmlEditorComponent",content:"Our business values are based on those any scientist applies to their research. We have created a culture of respect and collaboration within a relaxed, friendly and progressive atmosphere, while maintaining academic rigour.
\n\nCo-founded by Alex Lazinica and Vedran Kordic: “We are passionate about the advancement of science. As Ph.D. researchers in Vienna, we found it difficult to access the scholarly research we needed. We created IntechOpen with the specific aim of putting the academic needs of the global research community before the business interests of publishers. Our Team is now a global one and includes highly-renowned scientists and publishers, as well as experts in disseminating your research.”
\n\nBut, one thing we have in common is -- we are all scientists at heart!
\n\nSara Uhac, COO
\n\nSara Uhac was appointed Managing Director of IntechOpen at the beginning of 2014. She directs and controls the company’s operations. Sara joined IntechOpen in 2010 as Head of Journal Publishing, a new strategically underdeveloped department at that time. After obtaining a Master's degree in Media Management, she completed her Ph.D. at the University of Lugano, Switzerland. She holds a BA in Financial Market Management from the Bocconi University in Milan, Italy, where she started her career in the American publishing house Condé Nast and further collaborated with the UK-based publishing company Time Out. Sara was awarded a professional degree in Publishing from Yale University (2012). She is a member of the professional branch association of "Publishers, Designers and Graphic Artists" at the Croatian Chamber of Commerce.
\n\nAdrian Assad De Marco
\n\nAdrian Assad De Marco joined the company as a Director in 2017. With his extensive experience in management, acquired while working for regional and global leaders, he took over direction and control of all the company's publishing processes. Adrian holds a degree in Economy and Management from the University of Zagreb, School of Economics, Croatia. A former sportsman, he continually strives to develop his skills through professional courses and specializations such as NLP (Neuro-linguistic programming).
\n\nDr Alex Lazinica
\n\nAlex Lazinica is co-founder and Board member of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his Ph.D. in Robotics at the Vienna University of Technology. There, he worked as a robotics 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, co-founded and built the International Journal of Advanced Robotic Systems, the world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career since it proved to be the pathway to the foundation of IntechOpen with its focus on addressing academic researchers’ needs. Alex personifies many of IntechOpen´s key values, including the commitment to developing mutual trust, openness, and a spirit of entrepreneurialism. Today, his focus is on defining the growth and development strategy for the company.
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