Open access peer-reviewed chapter

Diagnosis and Treatment Plan for Gingival Diseases and Conditions

By Anahita Punj and Manav Chaturvedi

Submitted: October 2nd 2019Reviewed: February 12th 2020Published: April 8th 2020

DOI: 10.5772/intechopen.91726

Downloaded: 51

Abstract

The prevalence of gingival and periodontal disease is manifold and has not been highlighted much due to its asymptomatic and milder symptoms. It is usually given its due importance when the gingival disease progresses to advanced periodontal disease, displays symptoms of dull pain and tooth mobility, and is associated with pus discharge. The starting point of periodontal disease is usually gingival disease which is a reversible condition. It is therefore necessary to diagnose gingival diseases at an early stage to prevent its progression to irreversible periodontal disease. The diagnosis of gingival disease becomes cumbersome due to its similarity in the presentation of signs and symptoms. Gingival diseases can occur due to microbial attack from the plaque biofilm which is usually bacterial in nature. There are other viral, fungal, and immune-mediated mechanisms which can result in gingival diseases. Some systemic conditions also influence the gingiva which allows for diagnosing systemic diseases and treating these conditions appropriately. It is said that oral cavity is the mirror of the body, and in that sense the gingiva is the biggest surface where any changes or manifestations could be observed.

Keywords

  • gingivitis
  • gingival disease
  • diagnosis
  • treatment

1. Introduction

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].

Figure 1.

The 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].

2. Gingival disease terminology

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).

2.1 Diagnosis of plaque-induced gingivitis

Gingivitis 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.

Periodontal health and gingival healthDental biofilm-induced gingivitisNon-dental biofilm-induced gingival disease
Clinical gingival health on an intact periodontiumClinical gingival health on a reduced periodontiumAssociated only with dental biofilmMediated by systemic or local risk factorsDrug-influenced gingival enlargementGenetic/development disorders
Stable periodontitisNon-periodontitisSpecific infections and inflammatory and immune conditions
Reactive processes
Neoplasms
Endocrine, nutritional, and metabolic diseases
Traumatic lesions
Gingival pigmentation

Table 1.

Classification of periodontal health, gingival disease, and condition [3].

FactorEffect on gingivaSigns and symptoms for diagnosisDiagnosisTreatment [5]
Bacterial dental biofilm onlyMicrobial attack mounts a host response in the form of inflammationMild redness with or without broken line of bleedingIncipient gingivitisOHI
Mild changes in color and texture of the gingivaMild gingivitisOHI +/OP
Glazing redness, edema, enlargement, bleeding on probingModerate gingivitisOHI + OP
Overt redness and edema and bleeding on palpation rather on probingSevere gingivitis
Potential modifying factors of plaque-induced gingivitis
Systemic conditions
Sex steroid hormones (estrogen and progesterone)
(1) Puberty
Exaggerate the host inflammatory response in the presence of minimal plaqueBleeding on probing or bleeding with toothbrushing, mild to moderate rednessDiagnostic term not given as not seen frequently in population and if present can be diagnosed as gingivitis associated with pubertyOHI + OP
(2) Menstrual cycleExaggerates the host inflammatory response in the presence of minimal plaqueMild redness, edema based on severity of inflammation seen during the menstrual cycleDiagnostic term not given as not seen frequently in population and if present can be diagnosed as gingivitis associated with menstrual cycle
(3) PregnancyThe hormones exaggerate the host inflammatory response in the presence of minimal plaqueDeep gingival probing depths, bleeding on probing or bleeding with toothbrushing, and elevated gingival crevicular fluid flow in pregnancyPregnancy-associated gingivitis
(4) Oral contraceptivesThe high-dose hormones in the pills exaggerate the host inflammatory response in the presence of minimal plaque; low dose does not have much effectMild redness, edema based on severity of inflammation seen after 1 to 3 months of useCurrently the dose of oral contraceptives is low; hence diagnostic terms have been removedOHI + OP + reduction of high-dose oral contraceptive
Low-dose contraceptive does not require any change
HyperglycemiaHigh blood glucose levels increase the pathogenic bacteria and also form more AGE which affect collagen turnover and healingSigns of inflammation of gingivitis + high blood glucose levelsGingivitis associated with diabetes mellitusOHI + OP + maintenance of blood glucose levels by diet restriction/exercise/medication
LeukemiaIncreases number of WBCs which accumulate in the gingival tissues and decreases number of platelets which causes bleedingCervical lymphadenopathy, petechiae, ulcers seen in the mucosa, bleeding on slight provocation, swollen, glazed, spongy gingiva, red to deep purple color of gingival lesionsGingivitis associated with acute/chronic leukemiaTreat leukemia + symptomatic treatment for gingivitis with careful OHI and OP to prevent excessive bleeding
SmokingDirect smoking can cause vasoconstriction of gingival vasculatureNo redness, edema, or swelling present. Color may change to blue and pale pink. No gingival changes and pocket depths increase when lesions progress to periodontitisNo gingivitisSmoking cessation
MalnutritionDeficiency of vitamin C affects crosslinking of collagenBleeding on probing, mobility, and swollen gums in severe cases with minimal plaqueScurvyVitamin C supplementation + OHI + OP
Oral factors enhancing plaque accumulation
Prominent subgingival restoration marginsRoughness and closeness of these restorations to gingival tissue cause accumulation of plaque bacteria and irritationLocalized mild redness, bleeding on probing, slight edema in area of restorationGingivitis due to faulty restorationCorrection of restoration + OHI + SRP
HyposalivationDecreased saliva causes sticking of bacteria on tooth surfacesDental caries, taste changes, halitosis, mucosal and gingival dryness, and gingival inflammationGingivitis associated with hyposalivationOHI + OP+ salivary substitutes
Drug-influenced gingival enlargements
Phenytoin, sodium valproateDrugs and plaque cause fibroblasts to increase production of collagen and extracellular connective tissueOnset 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
Drug-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)
OHI + OP+ drug substitution if required, followed by gingivectomy to correct enlarged gingival tissues
Nifedipine, amlodipine, verapamil, diltiazem, felodipine
Cyclosporine

Table 2.

Diagnosis based on etiology, modifying factors, and clinical features [2, 4].

OHI, oral hygiene instruction, OP, oral prophylaxis.

2.2 Tools used for gingival diagnosis

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].

Advanced diagnostic aid for gingival diseaseMechanism/workingInference
Periotemp probeDetects the difference in subgingival temperature which is reflected by red or green lightRed light indicates future periodontal breakdown and increase in periopathogens
New generation of periodontal probesFirst-generationDetects pocket depth using traditional probes
Second-generationPressure-sensitive probe with uniform pressure
Third-generationPressure-sensitive and captures data on computer
Fourth-generationUses 3D technology to detect pocket
Fifth-generationUses 3D technology and ultrasound to detect pocket
Advances in radiographyUse of charged-coupled device, complementary metal oxide semiconductor, and cone beam-computed tomography allow digital recordingThese are used to detect bone loss and bone defects in 2D and 3D for periodontal defects rather than gingival diseases
Advances in microbial culturingHigh-performance liquid chromatographyCan detect bacterial cell wall components
Flow cytometryCan detect various bacteria
Latex agglutination testCan detect pathogenic antigen, proteins, and antibody by agglutination reaction
Direct and indirect immunofluorescenceCan detect pathogenic antigen, proteins, and antibody by agglutination and adding fluorescent dyes
Enzyme-linked immunosorbent assayEvalusite can detect P. gingivalis, P. intermedia, and A. actinomycetemcomitans
Nucleic acid and DNA checkerboard hybridization techniquesDetects microbes based on matching of unknown sample with known hybridization technique of nuclei acid/DNA
DNA probeOmnigene can detect P. gingivalis, P. intermedia, A. actinomycetemcomitans, E. corrodens, C. rectus, F. nucleatum
Perioscan uses BANA (N-benzoyl-DL arginine naphthylamide) hydrolysis carried out by trypsin-like proteaseDetects trypsin-like protease releasing bacteria, such as P. gingivalis, T. denticola, and T. forsythus
IAI Pado Test 4.5 RNA probe test kit uses oligonucleotide probes complementary to conserve fragments of the 16S rRNA gene that encodes the rRNADetects A. actinomycetemcomitans, P. gingivalis, Tannerella forsythia, and T. denticola
MyPerioPath is a DNA test and uses saliva samplesTo identify the type and concentration of periodontal bacteria
Advances in biochemical test kitsPerio-CheckDetects neutral proteases like collagenases in GCF (gingival crevicular fluid)
Prognos-Stik: detects serine proteinase elastase in GCFShows active disease sites
PocketWatch: detects aspartate aminotransferase in GCFDifferentiates active and non-active sites of disease
PerioGard: detects aspartate aminotransferase in GCFDifferentiates active and non-active sites of disease
Perio 2000: detects volatile sulfur compoundsTo detect halitosis
Toxicity prescreening assay (TOPAS)Detects bacterial toxins and proteins
DipstickDetects (matrix metalloproteinase) MMP-8 in GCF
Integrated microfluidic platform for oral diagnostics (IMPOD)Saliva-based detection of MMP-8
Oral fluid nanosensor test (OFNASET): saliva-based detection of (interleukin) IL-1, IL-8Used for detection of salivary biomarkers for oral cancer
Electronic taste chip (ETC)Detects C-reactive protein which is an important biomarker for inflammation
Genetic testsGenetic periodontitis susceptibility trait (PST) testDetects IL-1 polymorphism
MyPerioIDSaliva-based detection of genetic susceptibility

Table 3.

Diagnostic tools for gingival disease [5, 6].

2.3 Diagnosis of non-plaque-induced gingival diseases

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].

CCrCsTSPLLab & H/PAdd SymDRx
GFlat or roundedFirm and resilientLoss of stippling++Coronal to CEJGingival enlargementExcisional biopsy shows fibrous connective tissueHereditary gingival fibromatosisGingivectomy to contour the topography + OHI
P-R/B-BrBluntedSoft and friableUlcerative−−Varies from papillary destruction to beyond mucogingival junctionGingival ulcerationBacterial culture for various bacteria types such as Treponema, Selenomonas, Fusobacterium, and Prevotella intermedia.
H/P Loss of the epithelium in ulcerated areas
Loss of taste, woody sensation in teeth and feeling of extruded teeth
accompanied with underlying risk factors such as poor oral hygiene and systemic conditions
Necrotizing periodontal diseaseDebridement of local factors + CHX+ amoxicillin and metronidazole
FR/WNo changeSoft and edematousUlcerative/white pseudomembranous+No changeErythematousBacterial culture for Neisseria gonorrhoeaePharyngitis and lymphadenopathy. Other sites: urethra, anus, cervix, oral mucosaGonorrheaSystemic antibiotic therapy
FRNo changeEdematousLoss of stippling and ulceration with whitish membrane+No changeChancre (rare)Bacterial culture for Treponema pallidum, followed by serologic reaction testsGenital and skin lesionsSyphilisSystemic antibiotic therapy
R-Gy patchesNo changeFirmNodular/papillary proliferation+No changeNodular/papillary proliferationPositive 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
Commonly associated with lung infections.
Involves floor of the mouth, extraction sites, and lymph nodes
TuberculosisRegimens of multiple antibiotics like isoniazid, rifampicin, pyrazinamide, or ethambutol
RPRoundedSoftErythematous patchCulture for streptococcal strains. BiopsyUpper respiratory infectionsStreptococcal gingivitisOHI+ antibiotics
RPNo changeSoft and ulcerativeSmall vesicles/fibrinous coated ulcerBlunted papilla sometimesPainful ulcers after vesicle ruptureSkin lesions, low-grade feverHand, foot and mouth diseaseSupportive treatment to correct fever and pain
RPFlat and roundedSoft and edematousUlcerated, loss of stippling+Coronal or apical to CEJLymphadenitis, fever, malaisePrimary herpetic gingivostomatitisAcyclovir and spirin/paracetamol, fluids. Dyclonine hydrochloride 0.5% for anesthesia
RPFlat and roundedSoft and edematousUlcerated+Attached gingival and hard palateRarely 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
FeverRecurrent intraoral herpes simplexAcyclovir and aspirin/paracetamol, fluids. Dyclonine hydrochloride 0.5% for anesthesia
BRNo changeSoftVesicular+/−Diffuse erythema and isolated small vesicles that rupture quickly leaving ulcerationsLesions on skin and mucosaFluorescent-antibody
staining of smears using fluorescein-conjugated monoclonal antibodies is more reliable than routine cytology
Fever, malaise, and skin rashChicken pox (Varicella)Acyclovir/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
R patches +W haloBlunt or roundedSoft and friableUlceratedUnilateral vesicles which ruptureNecrosis of periodontium and alveolar boneCultureSkin lesionShingles (herpes zoster)Oral acyclovir 800 mg five
times a day, famciclovir 500 mg three times a day, or
valacyclovir 500 mg three times a day
PiNo changeSoftPapules++Raised nodular or popular lesionsMucosal lesions are rareDiscrete papules on skin of face and trunk and in genital areasMolluscum contagiosum virusCryotherapy/laser
GNo changeFirmExophytic and verrucous++Exophytic papillomatous, verrucous or flat lesionsSquamous cell papilloma, condyloma acuminatum, verruca vulgaris, focal epithelial hyperplasiaSurgical 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
W-RNo changeSoft and resilientScrapable lesion+/−Pseudomembrane/erythematous/plaque-like/ nodularH/P: culture of infected tissues or exudates on Sabouraud’s dextrose agar or other appropriate mediaOral involvement is secondary to serious systemic infectionCandidiasisTopical antifungal medications, nystatin, and amphotericin b
BRRoundedSoft and friableChronic vegetating painful ulcer++Nodular, papillary, or granulomatous lesionsBiopsy 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
Cavitation of the lung and dissemination of the organism
to the liver, spleen, adrenal glands, and meninges
HistoplasmosisKetoconazole or itraconazole for 6–12 months
RPViolaceous marginal gingiva in early stageSoft and friableNecrosis and covered with pseudomembrane in advanced cases−−Lesions are necrotic and covered by pseudomembraneSystemic involvement is present. Late stage involves destruction of alveolar bone and facial musclesAspergillosisSystemic antifungals
R+ W streaksNormalSoftLichenoid reactionNo changeLichenoid-like reactionPatch 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
Contact allergyTopical corticosteroids
RVelvety texture+Seen in anterior maxillary gingivaPlasma cells in lamina propriaPlasma cell gingivitisTopical corticosteroids
R-WSoft and friableSmooth or disruptedRound lesion with central red area or pale pink surrounded by red peripheryBiopsy
an epidermal pattern
characterized by lichenoid vasculitis and intraepidermal vesicles and a dermal pattern characterized by lymphocytic vasculitis
and subepidermal vesiculation
Skin lesions symmetrically present on distal extremities and moving proximally
Hand, face, elbow and knees
Erythema multiformeAnesthetic mouthwash, corticosteroids in severe cases, and acyclovir if associated with HSV
RP-WNormalSoft and friableSmooth and loss of stipplingNo changeLesions on free and attached gingivaDesquamative gingivitis with vesiculobullous lesions which ruptureELISA to detect circulating antibody to desmoglein 1 and 3.
Histopathology:
suprabasilar acantholysis may be observed
Bullous lesions on skinPemphigus vulgarisPrednisolone usually given in dosages of 1–2 mg/kg/d and later −−
R areaNormalSoftSmooth and loss of stipplingPositive Nikolsky sign: rubbing the gingiva forms bullaDesquamative lesions with bulla formationHistopathology: circulating antibodies not always found by indirect immunofluorescenceScarring in ocular lesionsPemphigoidSystemic corticosteroids
R-W streaksNormalSoft and resilientSmooth and ulcerativeNo changePapular, reticular, plaque type or bullous lesionsHyperkeratosis and saw tooth-shaped rete pegsSkin lesionsLichen planusTopical corticosteroids or intralesional steroids like 0.05% fluocinonide
(Lidex) and 0.05% clobetasol (temovate)
R and W striaeSmooth and ulcerative−/+Central atrophic area with small white dots surrounded by white striaeHyperorthokeratosis with keratotic plugs, atrophy of the rete ridges, and liquefactive degeneration of the basal celllayerRed butterfly-shaped photosensitive, scaly, macules on the nose bridge and cheeksLupus erythematosusSystemic immunosuppressant and protection from sunlight
PlNormalSoft++Cobblestone appearance of mucosa and linear ulcerationHistopathologyIntestinal pain, anal fissures, diarrhea, and labial enlargementCrohn’s diseaseSteroids and immunosuppressants to decrease progression
RPSoft and friableLoss of stippling++Gingival recessionNodules and ulceration.
Loosening of teeth
Hyperglobulinemia, an elevated level of serum angiotensin-converting enzyme, evidence of
depressed cellular immunity.
H/P: noncaseating epithelioid
granulomas in more than one organ system
Swelling of salivary glandsSarcoidosisSystemic steroids and anti-inflammatory agents
PiNormalFibrousSmooth+Exophytic smooth massesH/P: bundles of collagen covered with the epitheliumFibrous epulisExcision and curettage
RPNormalFibrousSmooth++Start from interdental papillaPedunculated to sessile massesH/P: cellular fibroblastic tissue containing rounded
or lobulated masses of calcified cementum-like tissue
Calcifying fibroblastic granulomaExcision of lesion
RP+Ulcerated, smooth, and pedunculated massH/P: discontinuous hyperplastic parakeratinized stratified squamous epithelium and endothelial cells in the connective tissuePyogenic granulomaExcision of lesion
Pr-Bl-BrSoft++Sessile or pedunculated tumor-like processH/P: multinucleated giant cell forming granulomaPeripheral giant cell granulomaSurgical excision
WCorrugated or verrucous surface+Non-removable white spotTissue 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
History of tobacco/alcohol intakeLeukoplakiaSurgical excision/cryosurgery and laser ablation
RVelvety+Sharply demarcated from surrounding mucosaSame as aboveMay be associated with oral lichen planusErythroplakiaSame as above
R- W patchesNo changeSoftSmooth++Involve keratinized gingivaPainless exophytic mass with nonhealing ulcerationDysplastic changes seen in the epithelium and extending into connective tissue and the presence of keratin pearlsHistory of tobacco/alcohol intakeSquamous cell carcinomaSurgical removal, chemotherapy
RPNo changeSoft and edematousSmooth++Pallor of oral mucosa, pain, petechiae, ecchymosis, gingival bleeding, deep punched out ulcersBlood investigation.
Bone marrow biopsy.
Tooth mobility
Dysphagia, facial paralysis, paraesthesia of the face, lips, tongue, and chin, trismus sometimesLeukemiaMonitoring 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)
PRoundedSoftSmooth++Histopathology will show Reed-Sternberg cellsSwollen lymph nodesLymphomaRadiation and chemotherapy plus doxorubicin,
bleomycin, vincristine, and dacarbazine for Hodgkin’s lymphoma and cyclophosphamide, vincristine, and prednisone for non-Hodgkin’s
W plaquesNo changeSoftLoss of stippling+Seen on facial attached gingivaLeukoplakia-like asymptomatic plaqueH/P: dense fibrous connective tissueFrictional keratosisPrevention of deleterious habits
RPNo changeSoft and friableGingival recessionSuperficial and horizontal gingival lacerationNot much significantToothbrushing-induced gingival ulcerationChanging the brushing technique
R-WSurface slough or ulcerationNot much significantChemical insult due to etching, chlorhexidine, hydrogen peroxide, acetylsalicylic acid, dentifrice, detergent, calcium hydroxide, etc.Removal of offending irritant
RErythematous lesion that slough a coagulated surface, vesicles and ulceration may be presentNot of much significanceBurns of mucosaSupportive care and hydration
Br-BlNo changeNo changeNo change=Pigmented deposits in the epithelium and connective tissueAddison’s disease, Albright syndrome, Peutz-Jeghers syndromeGingival pigmentationNot required
BrNo changeFirmNo change=Mandibular facial gingivaH/P: pigmented macules seen in sectionSmoker’s melanosisSmoking cessation for 2 weeks
Bl-Gy–Br-BlNo changeNo changeNo change=Diffuse pigmentationDrug-induced pigmentation (antimalarial, minocycline)Cessation of drug if required
Bl-Gy–Br-BlNo changeNo changeNo change=H/P: discrete granules in connective tissueAmalgam tattooRemoval of amalgam debris and replacement of amalgam if required

Table 4.

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.

3. Treatment of gingival disease

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].

4. Conclusions

Gingival 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.

Conflict of interest

The authors declare no conflict of interest.

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Anahita Punj and Manav Chaturvedi (April 8th 2020). Diagnosis and Treatment Plan for Gingival Diseases and Conditions, Oral Diseases, Gokul Sridharan, Anil Sukumaran and Alaa Eddin Omar Al Ostwani, IntechOpen, DOI: 10.5772/intechopen.91726. Available from:

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