**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**.


classifies gingival condition in health and disease under three broad categories of health, dental biofilm-induced gingivitis, and non-dental biofilm-induced gingival

**Periodontal health and gingival health Dental biofilm-induced gingivitis Non-dental**

Associated only with dental biofilm

Mediated by systemic or local risk factors

Druginfluenced gingival enlargement

Clinical gingival health on a reduced periodontium

> Nonperiodontitis

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

Stable periodontitis **biofilm-induced gingival disease**

Genetic/ development disorders

Specific infections and inflammatory and immune conditions Reactive processes Neoplasms Endocrine, nutritional, and metabolic diseases

Traumatic lesions

Gingival pigmentation

*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*

disease [3] (**Table 1**).

**Figure 1.**

*Oral Diseases*

*regimens [2].*

Clinical gingival health on an intact periodontium

**Table 1.**

**32**

#### *Oral Diseases*


**2.2 Tools used for gingival diagnosis**

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

*OHI, oral hygiene instruction, OP, oral prophylaxis.*

**Factor Effect on gingiva Signs and**

*DOI: http://dx.doi.org/10.5772/intechopen.91726*

*Diagnosis and Treatment Plan for Gingival Diseases and Conditions*

Roughness and closeness of these restorations to gingival tissue cause accumulation of plaque bacteria and irritation

causes sticking of bacteria on tooth surfaces

Drugs and plaque cause fibroblasts to increase production of collagen and extracellular connective tissue

Hyposalivation Decreased saliva

Drug-influenced gingival enlargements

Prominent subgingival restoration margins

Phenytoin, sodium valproate

Nifedipine, amlodipine, verapamil, diltiazem, felodipine Cyclosporine

**Table 2.**

**35**

**symptoms for diagnosis**

Localized mild redness, bleeding on probing, slight edema in area of restoration

Dental caries, taste changes, halitosis, mucosal and gingival dryness, and gingival inflammation

Onset 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

**Diagnosis Treatment [5]**

Correction of restoration + OHI + SRP

OHI + OP+ salivary substitutes

OHI + OP+ drug substitution if required, followed by gingivectomy to correct enlarged gingival tissues

Gingivitis due to faulty restoration

Gingivitis associated with hyposalivation

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)

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


#### **Table 2.**

**Factor Effect on gingiva Signs and**

exaggerate the host inflammatory response in the presence of minimal

(3) Pregnancy The hormones

(4) Oral contraceptives

*Oral Diseases*

plaque

effect

levels increase the pathogenic bacteria and also form more AGE which affect collagen turnover and healing

Hyperglycemia High blood glucose

Leukemia Increases number of WBCs which accumulate in the gingival tissues and decreases number of platelets which causes bleeding

Smoking Direct smoking can cause

Malnutrition Deficiency of

**34**

vasoconstriction of gingival vasculature

vitamin C affects crosslinking of collagen

Oral factors enhancing plaque accumulation

The high-dose hormones in the pills exaggerate the host inflammatory response in the presence of minimal plaque; low dose does not have much

**symptoms for diagnosis**

Deep gingival probing depths, bleeding on probing or bleeding with toothbrushing, and elevated gingival crevicular fluid flow in pregnancy

Mild redness, edema based on severity of inflammation seen after 1 to 3 months

of use

Signs of inflammation of gingivitis + high blood glucose levels

Cervical lymphadenopathy, petechiae, ulcers seen in the mucosa, bleeding on slight provocation, swollen, glazed, spongy gingiva, red to deep purple color of gingival lesions

No 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

Bleeding on probing, mobility, and swollen gums in severe cases with minimal plaque

**Diagnosis Treatment [5]**

associated with menstrual cycle

Currently the dose

OHI + OP + reduction of highdose oral contraceptive Low-dose contraceptive does not require any change

OHI + OP + maintenance of blood glucose levels by diet restriction/ exercise/ medication

Treat leukemia + symptomatic treatment for gingivitis with careful OHI and OP to prevent excessive bleeding

supplementation + OHI + OP

No gingivitis Smoking cessation

Scurvy Vitamin C

of oral contraceptives is low; hence diagnostic terms have been removed

Gingivitis associated with diabetes mellitus

Gingivitis associated with acute/chronic leukemia

Pregnancyassociated gingivitis

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

#### **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 intro-

**Mechanism/working Inference**

Shows active disease sites

of disease

of disease

Toxicity prescreening assay (TOPAS) Detects bacterial toxins and proteins Dipstick Detects (matrix metalloproteinase)

Electronic taste chip (ETC) Detects C-reactive protein which is an

MyPerioID Saliva-based detection of genetic

To detect halitosis

MMP-8 in GCF

Differentiates active and non-active sites

Differentiates active and non-active sites

Saliva-based detection of MMP-8

important biomarker for inflammation

Used for detection of salivary biomarkers for oral cancer

Detects IL-1 polymorphism

susceptibility

Prognos-Stik: detects serine proteinase

PocketWatch: detects aspartate aminotransferase in GCF

*Diagnosis and Treatment Plan for Gingival Diseases and Conditions*

Perio 2000: detects volatile sulfur

Integrated microfluidic platform for oral

Oral fluid nanosensor test (OFNASET): saliva-based detection of (interleukin)

PerioGard: detects aspartate aminotransferase in GCF

elastase in GCF

*DOI: http://dx.doi.org/10.5772/intechopen.91726*

compounds

IL-1, IL-8

*Diagnostic tools for gingival disease [5, 6].*

diagnostics (IMPOD)

Genetic tests Genetic periodontitis susceptibility trait (PST) test

duced to further confirm the presence of gingival disease (**Table 3**) [5, 6].

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

**2.3 Diagnosis of non-plaque-induced gingival diseases**

a diagnosis [7–11].

**37**

**Table 3.**

**Advanced diagnostic aid for gingival disease**


#### **Table 3.**

**Advanced diagnostic aid for gingival disease**

*Oral Diseases*

New generation of periodontal probes

Advances in radiography

Advances in microbial culturing

Advances in biochemical test

kits

**36**

**Mechanism/working Inference**

Red light indicates future periodontal breakdown and increase in

These are used to detect bone loss and bone defects in 2D and 3D for periodontal defects rather than gingival

and antibody by agglutination reaction

Detects microbes based on matching of unknown sample with known hybridization technique of nuclei acid/

*P. intermedia*, *A. actinomycetemcomitans*, *E. corrodens*, *C. rectus*, *F. nucleatum*

Detects trypsin-like protease releasing bacteria, such as *P. gingivalis, T. denticola*, and *T. forsythus*

Detects *A. actinomycetemcomitans, P. gingivalis*,*Tannerella forsythia*, and

To identify the type and concentration

collagenases in GCF (gingival crevicular

and antibody by agglutination and adding fluorescent dyes

Can detect bacterial cell wall

periopathogens

probes

pressure

computer

detect pocket

diseases

components

*P. intermedia*, and *A. actinomycetemcomitans*

DNA

*T. denticola*

fluid)

of periodontal bacteria

First-generation Detects pocket depth using traditional

Second-generation Pressure-sensitive probe with uniform

Third-generation Pressure-sensitive and captures data on

Fourth-generation Uses 3D technology to detect pocket Fifth-generation Uses 3D technology and ultrasound to

Flow cytometry Can detect various bacteria

Latex agglutination test Can detect pathogenic antigen, proteins,

Direct and indirect immunofluorescence Can detect pathogenic antigen, proteins,

Enzyme-linked immunosorbent assay Evalusite can detect *P. gingivalis*,

DNA probe Omnigene can detect *P. gingivalis*,

Perio-Check Detects neutral proteases like

temperature which is reflected by red or

Use of charged-coupled device, complementary metal oxide semiconductor, and cone beamcomputed tomography allow digital

High-performance liquid chromatography

Nucleic acid and DNA checkerboard

Perioscan uses BANA (N-benzoyl-DL arginine naphthylamide) hydrolysis carried out by trypsin-like protease

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

saliva samples

MyPerioPath is a DNA test and uses

hybridization techniques

Periotemp probe Detects the difference in subgingival

green light

recording

*Diagnostic tools for gingival disease [5, 6].*

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].

#### **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 [7–11].


**C**

**39**

RP

RP

RP

 Flat and

Soft and

Ulcerated, loss of

+

 Coronal or apical

to CEJ

rounded

RP

 Flat and

Soft and

Ulcerated

+

 Attached

Rarely required.

Fever

Recurrent intraoral

Acyclovir and aspirin/

paracetamol,

Dyclonine hydrochloride

0.5% for anesthesia

 fluids.

herpes simplex

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

shows syncytium and

ballooning. Degeneration

of the nucleus

BR

 No change Soft

 Vesicular

+/

Diffuse

Lesions on skin and

Fluorescent-antibody

Fever, malaise, and

Chicken pox (Varicella)

for healing and reducing

acute pain.

Systemic

to prevent postherpetic

neuralgia,

combination of

corticosteroids

Acyclovir/valacyclovir

skin rash

staining of smears using

fluorescein-conjugated

monoclonal antibodies is

more reliable than

routine cytology

mucosa

erythema and

isolated small

vesicles that

rupture quickly

leaving

ulcerations

 stain and

gingival and hard

palate

rounded

edematous

edematous

stippling

 No change Soft and

ulcerative

fibrinous coated

ulcer

Small vesicles/

–

Blunted papilla

Painful ulcers after

vesicle rupture

sometimes

 Rounded

 Soft

 Erythematous

 patch

 **Cr**

 **Cs**

 **T**

**S**

 **P**

**L**

**Lab & H/P** and granulomas are

diagnostic features

Culture for streptococcal

Upper respiratory

Streptococcal

 gingivitis

 OHI+ antibiotics

infections

Skin lesions, low-

Hand, foot and mouth

Supportive treatment to

correct fever and pain

*DOI: http://dx.doi.org/10.5772/intechopen.91726*

disease

grade fever

Lymphadenitis,

Primary herpetic

Acyclovir and spirin/

paracetamol,

Dyclonine hydrochloride

0.5% for anesthesia

*Diagnosis and Treatment Plan for Gingival Diseases and Conditions*

 fluids.

gingivostomatitis

fever, malaise

strains. Biopsy

**Add Sym**

**D**


#### *Diagnosis and Treatment Plan for Gingival Diseases and Conditions DOI: http://dx.doi.org/10.5772/intechopen.91726*

**C**

**38**

G

 Flat or

Firm and

Loss of stippling

 ++

 Coronal to CEJ Gingival enlargement

rounded

P-R/B-Br

Blunted

 Soft and friable

Ulcerative

Varies from papillary

Gingival ulceration

 Bacterial culture for

Loss of taste, woody

sensation in teeth

various bacteria types

such as *Selenomonas*,

*Fusobacterium*,

*Prevotella intermedia*.

H/P Loss of the epithelium in ulcerated

areas

FR/W

FR

R-Gy

No change Firm

Nodular/papillary

+

 No change

Nodular/papillary

Positive delayed

Commonly

Tuberculosis

Regimens of multiple antibiotics like isoniazid,

rifampicin,

pyrazinamide,

ethambutol

 or

associated with lung

infections.

Involves floor of the

mouth, extraction

sites, and lymph

nodes

hypersensitivity

(tuberculin) skin

reaction to purified protein derivative (ppd),

isolation of mycobacterial

antigen from bacterial

cultures, and

demonstration

fast mycobacteria clinical specimens. H/P: characteristic

multinucleated

 giant cells

 of acid-

 in

proliferation

proliferation

patches

 No change Edematous

 Loss of stippling

+

 No change

 Chancre (rare)

 Bacterial culture for *Treponema pallidum*, followed by serologic

reaction tests

and ulceration with

whitish membrane

 No change Soft and

edematous

Ulcerative/white

+

 No change

 Erythematous

 Bacterial culture for *Neisseria gonorrhoeae*

pseudomembranous

 and

*Treponema*,

and feeling of

extruded teeth

accompanied

underlying risk

factors such as poor

oral hygiene and

systemic conditions

Pharyngitis and

Gonorrhea

Systemic antibiotic

therapy

lymphadenopathy.

Other sites: urethra,

anus, cervix, oral

mucosa

Genital and skin

Syphilis

Systemic antibiotic

therapy

lesions

 with

destruction to

beyond

mucogingival

junction

resilient

 **Cr**

 **Cs**

 **T**

**S**

 **P**

**L**

**Lab & H/P**

 Excisional biopsy shows

fibrous connective tissue

**Add Sym**

**D** Hereditary gingival

Gingivectomy

the topography + OHI

 to contour

*Oral Diseases*

fibromatosis

Necrotizing periodontal

Debridement

factors + CHX+ amoxicillin and

metronidazole

 of local

disease


**C**

**41**

W-R

BR

 Rounded

 Soft and

Chronic vegetating

++

Nodular, papillary, or

Biopsy of infected tissue

Cavitation of the

Histoplasmosis

 Ketoconazole

itraconazole for 6–

12 months

*DOI: http://dx.doi.org/10.5772/intechopen.91726*

 or

> lung and

> shows small oval yeasts

within macrophages

reticuloendothelial

as well as chronic granulomas, epithelioid

cells, giant cells, and

occasionally caseation

necrosis

RP

 Violaceous

Soft and

Necrosis and

Lesions are necrotic

Systemic

Aspergillosis

Systemic antifungals

> involvement is

present. Late stage involves destruction of alveolar bone and

facial muscles

Contact allergy

 Topical

corticosteroids

and covered by pseudomembrane

marginal

friable

covered with pseudomembrane

in advanced cases

gingiva in

early stage

> R+ W

Normal

 Soft

 Lichenoid reaction

 No

Lichenoid-like

Patch test by placing aluminum disks with

known allergens for

48 hours on hairless skin

and wait for any

inflammation

positive test.

H/P: chronic inflammatory

with lichenoid

infiltration of

lymphocytes

 reaction

 as a

reaction

change

streaks

 cells

organism

to the liver, spleen, adrenal glands, and

meninges

*Diagnosis and Treatment Plan for Gingival Diseases and Conditions*

 and

dissemination

 of the

granulomatous

lesions

friable

painful ulcer

 No change Soft and

resilient

 **Cr**

 **Cs**

 **T** Scrapable lesion

 +/

**S**

 **P**

**L** Pseudomembrane/

H/P: culture of infected

tissues or exudates on

Sabouraud's dextrose

agar or other appropriate

media

erythematous/plaque-

like/ nodular

**Lab & H/P**

**Add Sym** Oral involvement is

Candidiasis

Topical antifungal

medications,

and amphotericin

 nystatin,

 b

secondary to serious

systemic infection

**D**


#### *Diagnosis and Treatment Plan for Gingival Diseases and Conditions DOI: http://dx.doi.org/10.5772/intechopen.91726*

**C**

**40**

R

Blunt or

Soft and

Ulcerated

—

Unilateral

Necrosis of

Culture

Skin lesion

Shingles (herpes

Oral acyclovir 800 mg

five

times a day, famciclovir

500 mg three times a

day, or

valacyclovir 500 mg

three times a day

zoster)

periodontium

alveolar bone

 and

vesicles which

rupture

patches

rounded

friable

+W

halo

Pi

G

 No change Firm

 Exophytic and

++

Exophytic

papillomatous,

verrucous or flat

lesions

verrucous

 No change Soft

 Papules

++

 Raised nodular

Mucosal lesions are

Discrete papules on

*Molluscum contagiosum*

Cryotherapy/laser

virus

skin of face and trunk and in genital

areas

Squamous cell

Surgical removal, laser

ablation, cryotherapy, and topical application of keratinolytic agents.

For smaller lesions, topical application of

25% podophyllum

to reduce the size. Intralesional injection of

interferon-α

1,000,000 iu/cm2 once

weekly and

subcutaneous

3,000,000 iu/cm2 twice

weekly

 injections

 resin

papilloma, condyloma

acuminatum,

vulgaris, focal epithelial

hyperplasia

 verruca

rare

or popular

lesions

 **Cr**

 **Cs**

 **T**

**S**

 **P**

**L**

**Lab & H/P**

**Add Sym**

**D**

**Rx**

intralesional steroids and

*Oral Diseases*

local anesthetics to decrease healing time

and prevent postherpetic neuralgia and application

of capsaicin


**C**

**43**

Pl

RP

Soft and

Loss of stippling

 ++

 Gingival

Nodules and

Hyperglobulinemia,

elevated level of serum angiotensin-converting

enzyme, evidence of

depressed cellular

immunity.

H/P: noncaseating

epithelioid

granulomas in more than

one organ system

Pi

RP

RP

+

Ulcerated, smooth,

H/P: discontinuous

Pyogenic granuloma

 Excision of lesion

hyperplastic

parakeratinized

squamous epithelium and endothelial cells in

the connective tissue

 stratified

and pedunculated

mass

 Normal

 Fibrous

 Smooth

++

 Start from

Pedunculated

 to

H/P: cellular fibroblastic

Calcifying fibroblastic

Excision of lesion

granuloma

tissue containing

rounded

or lobulated masses of

calcified

tissue

cementum-like

interdental

sessile masses

papilla

 Normal

 Fibrous

 Smooth

+

Exophytic smooth

H/P: bundles of collagen

Fibrous epulis

Excision and curettage

> covered with the

epithelium

masses

 an

Swelling of salivary

Sarcoidosis

Systemic steroids and

*DOI: http://dx.doi.org/10.5772/intechopen.91726*

anti-inflammatory

agents

*Diagnosis and Treatment Plan for Gingival Diseases and Conditions*

glands

ulceration.

Loosening of teeth

recession

friable

 Normal

 Soft

++

Cobblestone

Histopathology

Intestinal pain, anal

Crohn's disease

 Steroids and immunosuppressants

decrease progression

 to

fissures, diarrhea,

and labial enlargement

appearance of mucosa

and linear ulceration

 **Cr**

 **Cs**

 **T**

**S**

 **P**

**L**

**Lab & H/P** degeneration

celllayer

 of the basal

the nose bridge and

cheeks

**Add Sym**

**D**


#### *Diagnosis and Treatment Plan for Gingival Diseases and Conditions DOI: http://dx.doi.org/10.5772/intechopen.91726*

**C**

**42**

R R-W

Soft and

Smooth or

—

Round lesion with central red area or pale pink surrounded

by red periphery

friable

disrupted

 **Cr**

 **Cs**

 **T** Velvety texture

 +

 Seen in anterior maxillary gingiva

**S**

 **P**

**L**

**Lab & H/P** Plasma cells in lamina

propria

Biopsy

Skin lesions

Erythema multiforme

 Anesthetic mouthwash,

corticosteroids

cases, and acyclovir if

associated with HSV

 in severe

symmetrically

an epidermal pattern

characterized

lichenoid vasculitis and

intraepidermal

and a dermal pattern

characterized

lymphocytic vasculitis

and subepidermal

vesiculation

RP-W

R area Normal

R-W

Normal

 Soft and

Smooth and

No

Papular, reticular,

Hyperkeratosis

tooth-shaped

 rete pegs

 and saw

Skin lesions

 Lichen planus

Topical

or intralesional steroids like 0.05% fluocinonide

(Lidex) and 0.05%

clobetasol (temovate)

corticosteroids

plaque type or bullous

lesions

change

resilient

ulcerative

streaks

R and

Smooth and

/+

Central atrophic area

Hyperorthokeratosis

Red butterflyshaped

Lupus

erythematosus

 Systemic immunosuppressant

protection from sunlight

 and

with keratotic plugs,

atrophy of the rete

photosensitive,

scaly, macules on

ridges, and liquefactive

with small white dots

surrounded by white

striae

ulcerative

W

striae

 Soft

 Smooth and loss of

—

Positive

Desquamative

 lesions

Histopathology:

Scarring in ocular

Pemphigoid

Systemic

corticosteroids

lesions

circulating antibodies not

always found by indirect

immunofluorescence

Nikolsky sign:

with bulla formation

> rubbing the

gingiva forms

bulla

stippling

 Normal

 Soft and

Smooth and loss of

No

Lesions on free

Desquamative

ELISA to detect

Bullous lesions on

Pemphigus vulgaris

 Prednisolone given in dosages of 1–

2 mg/kg/d and later 

 usually

skin

circulating antibody to

desmoglein 1 and 3.

Histopathology:

suprabasilar acantholysis

may be observed

gingivitis with

vesiculobullous

lesions which rupture

change

and attached

gingiva

friable

stippling

 by

 vesicles

moving proximally

Hand, face, elbow

and knees

 by

present on distal

extremities and

**Add Sym**

**D** Plasma cell gingivitis

 Topical

corticosteroids

*Oral Diseases*


**C**

**45**

P

W

No change Soft

 Loss of stippling

 + —

Gingival

Superficial and

Not much significant

> horizontal gingival

laceration

Surface slough or

Not much significant

ulceration

recession

—

 Seen on facial

Leukoplakia-like

H/P: dense fibrous

connective tissue

asymptomatic

 plaque

attached gingiva

plaques

RP

R-W

R

—

Erythematous

that slough a

coagulated surface,

vesicles and ulceration may be

present

 lesion

Not of much significance

 No change Soft and

friable

 Rounded

 Soft

 Smooth

++

Histopathology

Reed-Sternberg

 cells

 will show

Swollen lymph

Lymphoma

Radiation and chemotherapy

doxorubicin,

bleomycin, vincristine,

and dacarbazine for Hodgkin's lymphoma

*DOI: http://dx.doi.org/10.5772/intechopen.91726*

and

vincristine, and

prednisone for non-

Hodgkin's

*Diagnosis and Treatment Plan for Gingival Diseases and Conditions*

Frictional keratosis

 Prevention of deleterious

habits

Toothbrushing-induced

Changing the brushing

technique

gingival ulceration

Chemical insult due to

Removal of offending

irritant

etching, chlorhexidine,

hydrogen peroxide,

acetylsalicylic

dentifrice, detergent, calcium hydroxide, etc.

Burns of mucosa

 Supportive care and

hydration

 acid,

cyclophosphamide,

 plus

nodes

 **Cr**

 **Cs**

 **T**

**S**

 **P**

**L**

**Lab & H/P**

**Add Sym**

**D**

**Rx**

stimulating factor (G-

CSF)


#### *Diagnosis and Treatment Plan for Gingival Diseases and Conditions DOI: http://dx.doi.org/10.5772/intechopen.91726*

**C**

**44**

Pr-Bl-Br

W

Corrugated

+

or

verrucous

surface

 **Cr**

 **Cs** Soft

 **T**

**S**

++

 **P**

**L** Sessile or pedunculated

H/P:

multinucleated

> tumor-

giant cell forming

granuloma

like process Non-removable

Tissue biopsy. Vital

History of tobacco/

Leukoplakia

Surgical excision/

cryosurgery and laser

ablation

alcohol intake

staining with toluidine

blue and cytobrush

techniques.

H/P: dysplastic cells with

++ nuclei, cellular and

nuclear

an ++ nucleo-cytoplasmic

and generalized loss of

cellular polarity and

orientation

R R- W

No change Soft

 Smooth

++

 Involve keratinized

mass with nonhealing

ulceration

gingiva

patches

RP

 No change Soft and

edematous

Smooth

++

Pallor of oral mucosa,

pain, petechiae, ecchymosis, gingival

bleeding, deep

punched out ulcers

Velvety

+

Sharply demarcated

Same as above

May be associated

Erythroplakia

Same as above

> with oral lichen

planus

History of tobacco/

Squamous cell

Surgical removal,

chemotherapy

carcinoma

alcohol intake

from surrounding

mucosa

Painless exophytic

Dysplastic changes seen

in the epithelium and

extending into

connective tissue and the

presence of keratin pearls

Blood investigation.

Dysphagia, facial

Leukemia

Monitoring of the

patient for infection

during neutropenic

periods and early

management

infection.

Corticosteroids,

adrenocorticotropin,

testosterone modulates

the sharp reduction in

marrow function. Granulocyte colony-

 or

 of

paralysis,

paraesthesia of the

face, lips, tongue, and chin, trismus

sometimes

Bone marrow biopsy.

Tooth mobility

 ratio,

pleomorphism,

hyperchromatic

white spot

**Lab & H/P**

**Add Sym**

**D** Peripheral giant cell

Surgical excision

*Oral Diseases*

granuloma


#### **Table 4.**

*Clinical features for diagnosis and treatment of non-plaque-induced gingival diseases.*

**3. Treatment of gingival disease**

*DOI: http://dx.doi.org/10.5772/intechopen.91726*

*Diagnosis and Treatment Plan for Gingival Diseases and Conditions*

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

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

2

1 Department of Periodontics, Army College of Dental Sciences, Secunderabad,

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

research which might help prevent undue treatment [8].

The authors declare no conflict of interest.

\* and Manav Chaturvedi

\*Address all correspondence to: anahitapunj@gmail.com

**4. Conclusions**

**Conflict of interest**

**Author details**

1

2 Partha Dental, Hyderabad, India

provided the original work is properly cited.

Anahita Punj

India

**47**

warranted.

.
