Gingivitis

Gingivitis
Trench mouth. Necrotizing gingivitis Image courtesy of Professor Peter Anderson DVM PhD and published with permission. © PEIR, University of Alabama at Birmingham, Department of Pathology
ICD-10	K05.0-K05.1

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2] Jaspinder Kaur, MBBS[3]

Synonyms and keywords:

Overview

Gingivitis ("inflammation of the gums") is a terminology referring to the gingival inflammation caused by bacterial biofilms adherent to tooth surfaces which is also known as plaque. It is characterized by a site-specific reversible dental plaque‑induced inflammation of the gingiva without detectable bone loss or clinical attachment loss. It is commonly prevalent among people of all ages from children, adolescents to adults which is readily seen during the dental practices. The etiology of gingivitis is multi‑factorial which usually shows synergistic effect by more than one factor acting together from poor oral hygiene, genetic, socioeconomic, demographic, iatrogenic, to behavioral factors. These plethora of factors seem to influence the staging process; thus, making it complicated to identify the risk factors. An initiating event is plaque formation and accumulation on the dental surface which results in an inflammatory reaction that were initially edematous and become more fibrotic as the condition persists. The earliest clinical sign of gingival inflammation is the transudation of gingival fluid. This thin cellular transudate is gradually superseded by a fluid consisting of serum plus leucocytes. The redness of the gingival margin arises partly from the aggregation and enlargement of blood vessels in the immediate subepithelial connective tissue; and the loss of keratinization of the facial aspects of gingiva. However, gingivitis is commonly painless which rarely leads to spontaneous bleeding; thus, often associated with subtle clinical changes making most patients unaware of the disease or unable to recognize it. However, gingivitis has a clinical significance because it is considered the precursor of periodontitis, a disease characterized by gingival inflammation combined with connective tissue attachment and bone loss. Although, it is a reversible disorder and therapy is aimed primarily at controlling the causative or risk factors to reduce or eliminate inflammation and hence repairing the gingival tissues. Appropriate supportive periodontal maintenance through personal and professional care is important to prevent recurrences. Simple gingivitis is controlled by adequate oral hygienic measures with or without an antibacterial mouth rinse and thorough scaling via professional cleaning with hand or ultrasonic instruments.

Classification

The gingival disease terminology and classification has been upgraded several times over the last decades. In 2017, the American Academy of Periodontology and the European Federation of Periodontology co-sponsored the World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions with an objective to update the previous disease classification established at the 1999 International Workshop for Classification of Periodontal Diseases and Conditions. This workshop concluded the gingivitis case by the presence of gingival inflammation at one or more sites and bleeding on probing as the primary parameter for it's diagnosis.

Table 1: Classification of the gingivitis

Periodontal Health
Clinical health on an intact periodontium Clinical gingival health on a reduced periodontium Stable periodontitis patient Non-periodontitis patient
Gingivitis—Dental Plaque-induced
Associated with biofilm alone Drug-influenced gingival enlargement Mediated by systemic or local risk factors Systemic modifiable risk factors: Smoking, Hyperglycemia, Nutritional factors (Scorbutic Gingivitis), Pharmacological agents (prescription, non-prescription, and recreational), Sex steroid hormones (puberty, menstrual cycle, pregnancy, and oral contraceptives), Hematological conditions. Local predisposing risk factors: Dental plaque biofilm retention factors (e.g., prominent restoration margins), Oral dryness
Gingival Disease—Non-dental Plaque-induced
Genetic and developmental disorders (e.g., hereditary gingival fibromatosis) Specific infections: Bacterial, viral, fungal Inflammatory and immune conditions: Hypersensitivity reactions, Autoimmune diseases of skin and mucous membranes, Granulomatous inflammatory lesions (e.g., orofacial granulomatosis) Reactive processes: Epulides Neoplasms: Premalignancy, Malignancy Endocrine, nutritional, and metabolic diseases (e.g., vitamin deficiencies) Traumatic lesions: Physical/mechanical trauma, Chemical (toxic) burn, Thermal insults Gingival pigmentation: Melanoplakia, Smoker’s melanosis, Drug-induced pigmentation (antimalarials, minocycline), Amalgam tattoo

Stages

• It undergoes through four different stages which were first elaborated by Page and Schroeder in 1976 before final progression to periodontitis in cases of no timely treatment.

Table 2: Progression of the gingivitis through different level of stages

Stage	Differentiating features
Initial: 24-48 hours	It is characterized by the response of local leukocytes and endothelial cells to the plaque formation (a bacterial biofilm). This stage doesn't show any clinical signs of inflammation, but the changes can be seen on the histological sections. The local blood vessels gets dilated under the response of cytokines mediated neuropeptides produced as a result of the metabolic products of tissue invaded bacteria. Systemic neutrophils migrates towards the inflammatory site in response to released cytokines.
Early: 4-7 days	It is characterized by a subsequent increase in the number of neutrophils. The clinical signs of gingivitis such as redness and bleeding from gingival starts appearing. An increase in the gingival crevicular fluid seen. Histology shows the epithelial proliferation to form rete pegs. The complement proteins are activated.
Established: 2-3 weeks	It is characterized by a shift from an innate to an acquired immune response. There is an increase in the number of macrophages, plasma cells, T and B lymphocytes along with increased collagenolytic activity. It shows clinical changes in the color and contour of the gingival with gingival bleeding on probing. It is categorized as moderate to severe stage of gingivitis.
Advanced	This stage results in a final transition to the development of the periodontitis. It is characterized by irreversible tissue attachment and bone loss. The synergistic effect of inflammation and underlying bacterial infection affects the supporting and surrounding tissues of the teeth such as gingival, periodontal ligament, and alveolar bone which thereby results in their damage and eventually tooth loss.

Pathophysiology

• Gingivitis usually originates from the bacterial plaque that accumulates in the spaces between the gums and the teeth, and visible calculus (tartar) formed on the teeth.
• When the teeth are not adequately cleaned by regular brushing and flossing, bacterial plaque accumulates, and gets mineralized by calcium and other minerals in the saliva which transform them into a hard material called calculus harboring bacteria and irritating the gingiva.
• As the bacterial plaque biofilm becomes thicker, an anoxygenic environment develops which allows more pathogenic bacteria to flourish and release toxins and initiates gingival inflammation.
• Alternatively, excessive injury to the gums caused by very vigorous brushing may further lead to a cycle of recession, inflammation and infection.
• The superseded infection usually begins when the immune system of the body gets weakened due to some local or systemic conditions.
• Over the years, this inflammation and infection can cause deep pockets between the teeth and gums, and subsequent bone loss around the teeth thereby resulting in a periodontitis.

Local factors

• Crowding of teeth makes the plaque difficult to remove completely.
• Malaligned teeth which often require orthodontic correction further adds on to the difficulty in cleansing.
• A dental prosthesis that is inadequately fitted or improperly finished can act as a nidus for the plaque accumulation.
• Eruptive gingivitis: In children, tooth eruption is also frequently associated with gingivitis, as plaque accumulation tends to increase in the area where primary teeth are exfoliating, and moreover, an oral hygiene is difficult to be maintained in the areas where permanent teeth are erupting.

Infectious gingivitis

• A low-grade injury to the local tissues such as fractured teeth, overhanging restorations, overextended flanges of the denture, and faulty fixed dental prosthesis with poor pontic design (saddle pontic) or over contoured margins act as a predisposing factor to it.

Hypersensitive reaction

• An allergens in the form of chewing gum, toothpaste, cinnamon, mint, red pepper, etc. can trigger the plasma cells infiltration in the gingiva, and causes plasma cell gingivitis.

Nutritional gingivitis

• Dietary habits with a higher intake of refined carbohydrates and an increased ratio of omega-6 to omega-3 fatty acids can initiate the inflammatory process through activation of NFkB and oxidative stress.

Hormonal gingivitis

• This form of gingivitis occurs during pregnancy, puberty, or steroid therapy.
• Pregnancy: An increase in the level of circulating female sex hormones are responsible for causing pregnancy gingivitis.
• Puberty: Gingival inflammation occurs even without the presence of plaque. This is referred to as puberty gingivitis. It has been observed that during adolescence, gingivitis appears earlier in girls (eleven to thirteen years) than in boys (thirteen to fourteen years).

It has been found that in the cytoplasm of the cells of the gingiva, receptors for both estrogens and testosterone that have a high affinity for these hormones are present. The receptors for estrogen are specifically present in the basal and spinous layers of the epithelium. In the connective tissue, such receptors are found in the fibroblasts and endothelial cells of small vessels. Therefore, the gingiva is an easy target organ for these steroid hormones resulting in gingivitis.

Drug induced gingivitis

• The mechanism behind this gingival inflammation is thought to be the ability of the metabolites of these drugs to induce the proliferation of fibroblasts.
• An imbalance between the synthesis and the degradation of the extracellular matrix leads to the accumulation of immature proteins in the extracellular matrix, particularly collagen which subsequently results in gingivitis.

Causes

• The etiology of gingivitis is multifactorial which includes factors from local, systemic, genetic to behavioral giving synergistic effect in some cases. The most common cause is an inadequate oral hygiene that leads to dental plaque formation.

Causes by Organ System

Table 3: System wise causative factors of the gingivitis

System involved	Causative factors
Chemical/Poisoning	Bismuthia, gold sodium thiomalate, lead, mercury(II) chloride
Dental	Acute necrotizing ulcerative gingivitis, aphthous ulcer, bad breath, Chediak-Higashi syndrome, dental plaque, dentures, inadequate oral hygiene, pericoronitis, periodontitis, Riggs' disease, trench mouth, Vincent's angina
Dermatologic	Bismuthia, Chediak-Higashi syndrome, epidermolysis bullosa, Kindler syndrome, linear IgA bullous dermatosis, systemic lupus erythematosus
Pharmaceutical agents adverse effects	Acitretin, amlodipine, amsacrine, antihypertensives, articaine, auranofin, bevacizumab, bexarotene, cidofovir, cocaine, cyclosporine, diltiazem, eprosartan, estrogen and progestin (oral contraceptives) (patient information), felodipine, fentanyl, fluvoxamine, gadoteridol, interferon alfa-2b, interferon alfacon-1, interferon beta-1a, itraconazole, lamotrigine, leflunomide, leuprolide, methotrexate, misoprostol, moclobemide, mycophenolate, nabumetone, niacin, nicardipine, nifedipine, nitrendipine, nystatin, octreotide, omacetaxine, pantoprazole, pentamidine, pentostatin, phenytoin, rasagiline, sildenafil, sunitinib, tiagabine, tiotropium, venlafaxine, verapamil, zaleplon, zonisamide
Ear Nose Throat	Acute necrotizing ulcerative gingivitis, aphthous ulcer, chronic mouth breathing, trench mouth, Vincent's angina
Endocrine	Diabetes mellitus, osteoporosis
Gastroenterologic	Pancreatic cancer, Shwachman-Diamond syndrome
Genetic	Chediak-Higashi syndrome, chronic granulomatous disease, epidermolysis bullosa, Kindler syndrome, leukocyte adhesion deficiency, Shwachman-Diamond syndrome
Hematologic	Congenital neutropenia, cyclic neutropenia, immune neutropenia, langerhans cell histiocytosis, leukemia, Shwachman-Diamond syndrome
Infectious Disease	Acute necrotizing ulcerative gingivitis, aphthous ulcer, biofilm, cancrum oris, herpes simplex virus infection, HIV, lichen planus, lung abscess, noma, pasteurellaceae, pemphigoid, periodontitis, Riggs' disease, trench mouth, Vincent's angina, viral infections
Musculoskeletal/Orthopedic	Osteoporosis
Nutritional/Metabolic	Malnutrition, vitamin C deficiency
Obstetric/Gynecologic	Pregnancy
Oncologic	Langerhans cell histiocytosis, leukemia, pancreatic cancer
Pulmonary	Chronic mouth breathing, lung abscess, sarcoidosis
Renal/Electrolyte	Systemic lupus erythematosus
Rheumatology/Immunology/Allergy	Chronic granulomatous disease, graft-versus-host disease, langerhans cell histiocytosis, leukocyte adhesion deficiency, linear IgA bullous dermatosis, sarcoidosis, systemic lupus erythematosus
Reproductive	Puberty

Causes in Alphabetical Order

Table 4: Alphabetical presentation of the causative factors of the gingivitis

A	B	C	D	E
Acitretin Acute necrotizing ulcerative gingivitis Amlodipine Amsacrine Antihypertensives Aphthous ulcer Arteriosclerosis Articaine Auranofin	Bad breath Bevacizumab Bexarotene Biofilm Bismuthia	Cancrum oris Chediak-Higashi syndrome Chronic granulomatous disease Chronic mouth breathing Cidofovir Cocaine Congenital neutropenia Cyclic neutropenia Cyclosporine	Dental plaque Dentures Diabetes mellitus Diltiazem	Epidermolysis bullosa Eprosartan Estrogen and progestin (oral contraceptives) (patient information)
F	G	H	I	K
Felodipine Fentanyl Fluvoxamine	Gadoteridol Gold sodium thiomalate Graft-versus-host disease	Herpes simplex virus infection HIV	Immune neutropenia Inadequate oral hygiene Interferon alfa-2b Interferon alfacon-1 Interferon beta-1a Itraconazole	Kindler syndrome
L	M	N	O	P
Lamotrigine Langerhans cell histiocytosis Lead Leflunomide Leukemia Leukocyte adhesion deficiency Leuprolide Lichen planus Linear IgA bullous dermatosis Lung abscess	Malnutrition Mercury(II) chloride Methotrexate Misoprostol Moclobemide Mycophenolate	Nabumetone Niacin Nicardipine Nifedipine Nitrendipine Noma Nystatin	Octreotide Omacetaxine Osteoporosis	Pancreatic cancer Pantoprazole Pasteurellaceae Pemphigoid Pentamidine Pentostatin Pericoronitis Periodontitis Phenytoin Pregnancy Puberty
R	S	T	V	Z
Rasagiline Riggs' disease	Sarcoidosis Shwachman-Diamond syndrome Sildenafil Sunitinib Systemic lupus erythematosus	Tiagabine Tiotropium Trench mouth	Venlafaxine Verapamil Vincent's angina Viral infections Vitamin C deficiency	Zaleplon Zonisamide

Differentiating Gingivitis from other Diseases

Table 5: Enumerate the conditions mimicking the gingivitis

Differentiating condition	Differentiating sign and symptoms	Differentiating features
Oral lichen planus	A chronic inflammatory mucocutaneous disease which commonly manifests on the gingiva and is characterised by red, nonswollen gingivae with painful atrophic/ulcerative lesions. White papular, reticular and plaque-type lesions, usually asymptomatic, may also be found as the only sign of gingival involvement or occur at the periphery of the atrophic lesions. It is generally nonresponsive to routine oral hygiene procedures. It may also develop on oral mucosa (50%-70% of cases), other mucosal surfaces and on skin of extremities. Oral lesions may occur in the absence of skin lesions.	Direct immunofluorescence is negative for all autoantibodies but positive for fibrinogen fluorescence outlining the basement membrane zone with irregular extensions into the superficial lamina propria (shaggy appearance). Histopathology reveals a dense lymphocytic infiltrate with possible changes to the epithelium.
Pemphigoid	A group of chronic, mucocutaneous autoimmune disorders in which autoantibodies are directed toward components of the basement membrane and characterized by bullae and blisters that rupture leaving superficial painful, persistent ulcerations. The average age of onset is 50 to 60 years. Since healing may occasionally leave scars, ocular involvement may lead to conjunctival scarring and blindness. The oral lesions usually do not result in scarring. If only mucous membranes are affected, the term mucous membrane pemphigoid (MMP) is used. Gingival involvement is characterized by the clinical pattern known as desquamative gingivitis or by localized bullous formation quickly evolving into painful and persisting erosions.	Linear band of IgG, C3, and sometimes other immunoglobulins as well as fibrin at the basement membrane zone. Indirect immunofluorescence (IIF) is negative, but salt-split-skin IIF is positive in up to 50% of the cases.
Pemphigus	A group of autoimmune diseases characterized by formation of intraepithelial bullae in skin and mucous membranes. The average age of onset is 50 years and it is rarely seen in children. A positive Nikolsky sign is seen (top layers of skin slide over lower layers when rubbed). The typical oral lesions are chronic, superficial, ragged irregular painful erosions. Gingival involvement usually appears in the form of desquamative gingivitis. Since the bulla formation is located in the spinous cell layer, the chance of finding an intact bulla on the oral mucosa is quite small. Lesions may develop on mucosal surfaces earlier than they develop on the skin, although skin lesions are more common. Conjunctival involvement is uncommon and, unlike pemphigoid, the ocular lesions of pemphigus do not produce scarring.	Direct immunofluorescence is positive for intercellular IgG and C3 between epithelial cells; no linear reactivity along basement membrane zone. IFF is positive.
Lupus erythematosus	Oral mucosal lesions resemble erosive lichen planus with erosions and striae but also demonstrate atrophy with fine white stippling not seen in erosive lichen planus. Systemic lupus erythematosus may also give rise to gingival ulceration and increased plaque-induced gingivitis secondary to Sjogren syndrome. It can give rise to desquamative gingivitis.	Direct immunofluorescence is positive for IgM, IgG, and/or C3 in a shaggy or granular band at the basement membrane zone. Serum ANAs and antidouble-stranded DNA usually occur in SLE.
Desquamative gingivitis	A clinical reaction pattern produced by several disorders that involve the gingiva. This pattern is characterized by an extensive desquamation and/or erosion of the affected gingival, particularly in the buccal aspect of anterior teeth. Often marginal gingival is unaffected in the absence of plaque accumulation.	Biopsy reveals in about 80% of cases features that are diagnostic of mucous membrane pemphigoid and oral lichen planus. Less frequently biopsy shows features that are diagnostic of pemphigus vulgaris, linear IgA disease, epidermolysis bullosa acquisita, systemic lupus erythematosus, chronic ulcerative stomatitis, and paraneoplastic pemphigus.
Drug-influenced gingival enlargement	Patients have a 1- to 3-month minimum history of therapy with phenytoin, cyclosporine, or calcium-channel blockers such as nifedipine and less commonly amlodipine, verapamil, felodipine, and diltiazem. Gingiva is often of normal color with enlargement ranging from focal to extensive enlargement that covers most of the teeth and may impair mastication of food. In the presence of secondary inflammation caused by dental plaque, the gingiva may be reddened, puffy, and painful.	Diagnosis is by clinical oral exam and review of medical history. Treatment options are usually oral hygiene maintenance, gingival surgery and rarely substituting an acceptable alternative drug.
Primary herpetic gingivostomatitis	Primary herpetic gingivostomatitis has a bimodal age distribution of 2-3 years and >60 years. Clusters of small vesicles coalesce to form blisters that rupture to leave painful mucosal ulcerations. The gingivae are enlarged, very erythematous, and painful. The gingival features can be in a form similar to necrotizing gingivitis, but gingival lesions are less severe and without significant hemorrhage. More significantly, other mucosal surfaces are likely involved with clusters of painful ruptured vesicles. Affected patients may be febrile, have cervical lymphadenopathy and occasionally skin rashes. Recurrent herpetic gingivostomatitis is characterized by the same clinical findings, but it is rare in immunocompetent subjects.	No specific tests are needed. Cytologic smear may confirm viral inclusions. The disease is self-limiting, lasting up to 2 weeks in immunocompetent patients.
Allergic reactions	Allergic reactions occasionally occur after the use of mouthwashes,toothpastes, or chewing gums. The allergens responsible for such reactions may be flavor additives (e.g., cinnamon) or preservatives, or may be contained in materials or drugs used by dentists or in foods, natural products, or lipsticks. Clinically, the allergic reaction appears as a swollen red area, sometimes with painful ulcerations or white striae. This disorder can affect other mucosal surfaces where the allergen makes contact. Plasma cell gingivitis is a distinctive form of allergic reaction characterized by a dense inflammatory infiltrate consisting predominantly of plasma cells.	Withdrawal of suspected offending agent brings relief within 1 week. Patch testing may be useful.
Leukemia	Leukemia presents in the oral cavity with spontaneous hemorrhage, petechiae and possible pain. Gingival enlargement is most likely with acute myeloid leukemia. Ulcers may be present on the gingival and the mucosal surfaces. Gingival manifestations are more common in acute than chronic leukemia.	CBC and blood film will usually establish the leukemic type.
Gingival candidosis	Gingival candidosis (formerly known as linear gingival erythema and associated with HIV infection) is characterized by a distinct 2- to 3-mm linear band of pronounced erythema along the gingival margin directly adjacent to the teeth, often with a granular surface, that does not respond to conventional oral hygiene procedures.	Diagnosis of candidosis can be accomplished on the basis of culture, smear, and biopsy. Nonresponse to standard therapy is suggestive. Confirm HIV status. Some cases are associated with oral candidosis.
Primary and metastatic carcinoma	Most gingival carcinomas, both primary and metastatic, present with localized exophytic masses rather than diffuse pseudoinflammatory changes generally associated with gingivitis.	Radiology and biopsy. Primary gingival carcinoma usually shows squamous epithelial carcinoma; findings for metastatic disease are indicative of the primary carcinoma.
Foreign body gingivitis	Gingival inflammation associated with foreign bodies located in the connective tissue deep to the sulcular epithelium. It often presents as a red or combined red-white lesion frequently misdiagnosed as oral lichen planus. Pain or sensitivity is a common finding and the lesion does not resolve with optimization of oral hygiene. Foreign bodies can originate from a wide variety of dental materials.	Diagnosis is from history and clinical features. Biopsy demonstrates a nonspecific pattern of chronic or subacute mucositis and a foreign body (but in some cases the foreign material may be too fine to be detected). When granulomatous inflammation is microscopically found (approximately 20% of cases) and a foreign body is not detected, the clinician must search for signs and symptoms of granulomatous diseases (Crohn disease, sarcoidosis, tuberculosis, orofacial granulomatosis).
Orofacial granulomatosis	An idiopathic disorder due to an abnormal immune reaction. Lips are frequently affected and show a nontender, persistent enlargement. The tongue may develop fissures, edema, erosions, paresthesia, and taste alteration. Gingival lesions present as swelling and slight erythema mimicking plaque-induced gingivitis, or as painful erosions.	Biopsy reveals a nonspecific granulomatous inflammation associated with negative stains for organisms and no foreign body. Local and systemic granulomatous diseases must be considered in the differential diagnosis.
Pyostomatitis vegetans	A relatively rare, pustular disorder of the oral mucosa associated with inflammatory bowel diseases, particularly ulcerative colitis or Crohn disease. The typical lesions of this disorder are multiple, painless, yellow-white, vegetative mucosal folds, and microabscesses, which may be present on both gingival and oral mucosa.	Biopsy reveals an acantholytic appearance of the epithelium due to the presence of numerous eosinophils, often forming intraepithelial microabscesses. Direct immunofluorescence rules out chronic bullous oral diseases.
Linear IgA disease	Oral lesions present as desquamative gingivitis alone or in association with vesicles, painful erosions, and ulceration. Lesions affect the hard and soft palates, tonsillar pillars, buccal mucosa, tongue, and gingiva. Oral lesions occur always in the presence of skin lesions.	Direct immunofluorescence is characterized by linear deposition of IgA along the dermoepidermal basement membrane zone. Circulating anti-basement membrane IgA may be detected using IIF in approximately 30% of patients. Exclusive oral lesions showing linear IgA staining at the basement membrane zone should be considered mucous membrane pemphigoid not linear IgA disease.
Wegener granulomatosis	Oral involvement is rare. When present, it is considered an early sign of disease. Characteristic lesions include dramatic gingival hyperplasia with short bulbous, friable, and hemorrhagic projections beginning in the interdental papillae, commonly referred to as "strawberry gingivitis". The upper gingivae are the most commonly affected site in the mouth.	Biopsy shows leukocytoclastic vasculitis. In oral biopsies, owing to the paucity of large vessels, vasculitis may be difficult to demonstrate. Gingival biopsy specimens usually show prominent vascularity with extensive red blood cell extravasation. Circulating perinuclear antineutrophil cytoplasmic antibody (p-ANCA) or cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA) may be detected. Indirect immunofluorescence (IIF) is positive for c-ANCA. A positive reaction for proteinase 3, the major antigen for c-ANCA that resides in the azurophilic granules of neutrophils, is needed to confirm the positive IIF for c-ANCA.
Erythema multiforme	Acute onset of symmetrically distributed cutaneous target lesions often accompanied by mucus membrane involvement. Gingival involvement is extremely rare but may give rise to desquamative gingivitis and/or gingival ulceration. Patients may have a recent history of HSV infection, mycoplasma infection, drug therapy (e.g., anticonvulsants and antibiotics) or immunisation.	Histopathology is rarely helpful as the features are usually nonspecific. Hence diagnosis is based on clinical features and exclusion of other vesiculo-erosive disorders.
Agranulocytosis	Gingiva appears as necrotizing gingivitis, but patient has a history of exposure to drugs that cause decreased granulocyte production, such as anticancer chemotherapeutic agents, or a history of congenital disease associated with decreased levels of granulocyte-specific colony-stimulating factor (G-CSF). Malaise, fever, pharyngitis, and painful stomatitis may accompany necrotic, punched-out ulcerations of multiple mucosal surfaces.	Discontinuation of the suspect drug leading to resolution within 2 weeks may be diagnostic. CBC shows granulocytopenia (<500 cells/mm^3) and normal erythrocytes and platelets.
Histoplasmosis	Very rare. Oral lesions may occur with disseminated form of the disease in older or immunocompromised patients. They appear as chronic ulcers with firm rolled margins and may resemble oral carcinoma of the gingiva.	Biopsy reveals granulomatous inflammation with periodic acid-Schiff and Gomori methenamine silver-positive fungi, morphologically consistent with Histoplasma capsulatum infection. Nonculture methods include zymogen-based colorimetric assays to detect (13)-beta-D-glucan and molecular methods to detect fungal DNA.
Cyclic neutropenia	Cyclic neutropenia is a rare hematological disorder seen in children as a uniformly episodic fever, cervical lymphadenopathy, pharyngitis, and mucosal ulcerations that are most severe in the gingiva. The average cycle length is 21 ± 3 days, with a range of 14 to 40 days. Alveolar bone loss (from maxillary or mandibular bones) and tooth mobility may develop.	Sequential CBCs show neutrophil counts <500/m^3 for 3-5 days during 3 successive cycles.

Epidemiology and Demographics

• Gingivitis is the commonest periodontal disease that is found to be more prevalent in males as compared to females as it has been found that females tend to follow better oral care regimes and thus in maintaining oral hygiene.
• Women: There have been studies that found gingivitis to be more prevalent in pregnant women as compared to non-pregnant women. Also, the severe form of gingivitis has been found to be predominant in pregnant women.
• It is commonly seen in children and adults and prevalent worldwide. .
• Young population: Gingivitis occurs in half the population by the age of 4 or 5 years, and the incidence continues to increase with age. The prevalence of gingivitis peaks at close to 100% at puberty, but after puberty it declines slightly and stays constant into adulthood. Some children exhibit severe gingivitis at puberty. Puberty-associated gingivitis is related to increases in steroid hormones.
• Socioeconomic status: Studies have found gingivitis to be more prevalent in people with low socioeconomic status as people with high socioeconomic status tend to show a more positive attitude towards the maintenance of oral hygiene. Also, they have better access to health care options.

Risk Factors

• Risk factor is defined as an environmental, behavioral, or biologic factor which directly increases the probability of a disease occurring and if absent or removed, reduces the disease probability.

Table 6: List the risk factors for gingivitis

Modifiable risk factors	Non-modifiable risk factors
Smoking Diabetes mellitus Microorganisms Socio-economic status Psychological stress Nutritional deficiency Cardiovascular disease Obesity Drug-Induced Disorders Use of orthodontic appliances	Genetic factors Osteoporosis Ageing Hematological disorders such as chronic leukemia Female Hormonal Alterations Pregnancy Mouth breathing Crowded teeth Tooth fracture Defective dental restorations

Complications

• Recurrence of gingivitis
• Periodontitis
• Infection or abscess of the gingiva or the jaw bones
• Trench mouth (bacterial infection and ulceration of the gums)

Acute Necrotizing Ulcerative Gingitivitis (ANUG or Trench mouth)

• Chronic gingivitis can progress to ANUG if not treated and when the patient neglects oral hygiene completely or when the immune system of the patient is compromised.
• The condition is commonly seen in developing countries where the living conditions are poor.
• IT occurs most frequently in smokers and debilitated patients who are under stress. Other risk factors are poor oral hygiene, nutritional deficiencies, immunodeficiency (eg, HIV/AIDS, use of immunosuppressive drugs), and sleep deprivation. Some patients also have oral candidiasis.
• The aetiology of ANUG is the overgrowth of a particular type of pathogenic bacteria (fusiform-spirochete variety) but risk factors such as stress, poor nutrition and a compromised immune system can exacerbate the infection
• It is categorized under a severe form of gingivitis associated with pain, gingival bleeding, and ulceration. It is characterized by marked gingival edema, spontaneous bleeding, or bleeding in response to minimal local trauma. It may be associated with localized pain, altered taste (metallic taste mostly), and halitosis.
• Ulcerations, which are pathognomonic, are present on the dental papillae and marginal gingiva. These ulcerations have a characteristically punched-out appearance and are covered by a gray pseudomembrane. Similar lesions on the buccal mucosa and tonsils are rare. Swallowing and talking may be painful. Regional lymphadenopathy often is present.
• Treatment: It includes debridement, rinses (eg, hydrogen peroxide, chlorhexidine) and improved oral hygiene. If debridement is delayed (eg, if a dentist or the instruments necessary for debridement are unavailable), oral antibiotics (eg, amoxicillin 500 mg every 8 hours, erythromycin 250 mg every 6 hours, or tetracycline 250 mg every 6 hours) may help to provide relief and can be continued until 72 hours after symptoms resolve.

Prognosis

• Gingivitis, if identified and treated, can easily be resolved as the condition is reversible in its early stages.
• However, chronic gingivitis, if left untreated, can progress to periodontitis and can ultimately result in bone destruction, causing tooth loss.

Clinical presentation

• Onset: It can be acute or chronic, and can be either localized or generalized which is categorized as follows:
  • Marginal gingivitis: An inflammation confined to the gingival margin.
  • Papillary gingivitis: It involves interdental papillae.
  • Diffuse gingivitis: It has diffuse involvement of the gingival margin, attached gingiva, and interdental papillae.

Clinical symptoms

The symptoms of gingivitis are as follows:

• Swollen gums
• Mouth sores
• Bright-red, or purple gums
• Shiny gums
• Gums that are painless, except when pressure is applied
• Gums that bleed easily, even with gentle brushing,and especially when you floss
• Gums that itch with varying degrees of severity
• Receding gumline

Clinical signs

Table 7: Elaborates the clinical signs of gingivitis seen on the physical examination

Medical condition	Clinical signs on examination
Bacterial dental biofilm only	Incipient gingivitis: Mild redness with or without broken line of bleeding Mild gingivitis: Mild changes in color and texture of the gingiva Moderate gingivitis: Glazing redness, edema, enlargement, bleeding on probing Severe gingivitis: Overt redness and edema and bleeding on palpation rather on probing
Plaque-induced gingivitis	Clinical signs on examination
Puberty	Bleeding on probing or bleeding with toothbrushing, mild to moderate redness
Menstrual cycle	Mild redness, edema based on severity of inflammation seen during the menstrual cycle
Pregnancy	Deep gingival probing depths, bleeding on probing or bleeding with toothbrushing, and elevated gingival crevicular fluid flow in pregnancy
Oral contraceptives	Mild redness, edema based on severity of inflammation seen after 1 to 3 months of use
Hyperglycemia	Signs of inflammation of gingivitis + high blood glucose levels
Leukemia	Cervical lymphadenopathy, petechiae, ulcers seen in the mucosa, bleeding on slight provocation, swollen, glazed, spongy gingiva, red to deep purple color of gingival lesions
Smoking	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
Malnutrition	Bleeding on probing, mobility,and swollen gums in severe cases with minimal plaque
Prominent subgingival restoration margins	Localized mild redness, bleeding on probing, slight edema in area of restoration
Hyposalivation	Dental caries, taste changes, halitosis, mucosal and gingival dryness, and gingival inflammation
Drug-influenced gingival enlargements	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

• A detailed history taking and physical examination (Table) should be performed.
• Clinical evaluation: Finding erythematous and friable tissue at the gum lines confirms the diagnosis of gingivitis. To detect early gingival disease, some dentists frequently measure the depth of the pocket around each tooth. Depths < 3 mm are normal; deeper pockets are at high risk of gingivitis and periodontitis.
• Laboratory test: Not routinely required.
• Radiographs: As gingivitis is a soft tissue disease, radiographic evaluation is not helpful. However, it should be done to rule out periodontitis or other differential disorder.

Treatment

• Treatment approach: An interprofessional approach is required to identify the causes of gingivitis and to intervene at an early stage before its progression to periodontitis.
• Aim: To restore the inflamed tissues to clinical health and then to maintain clinically healthy gingivae and subsequently preventing periodontitis. Periodontitis has also been linked to diabetes, arteriosclerosis, osteoporosis, pancreatic cancer and pre-term low birth weight babies.
• Stepwise approach:
  • A dentist or dental hygienist will perform a thorough cleaning of the teeth and gums and remove localized factors initiating the inflammatory response. This includes scaling to thoroughly remove biofilm and deposits on the tooth structure and laser decontamination of the sulcus if possible. The removal of plaque is usually not painful, and the inflammation of the gums should be gone between one and two weeks.
  • Ensure oral hygiene reinforcement by twice daily tooth brushing and once daily interdental cleaning (with an interdental brush or dental floss) and adjunctive chemical plaque control agents (such as chlorhexidine or essential oil-containing mouthwash).
  • Address the modifiable systemic or local factors by changing the medication if drug induced; prescribing supplements in case of nutritional deficiency; and an indentification of faulty prosthesis should be done and replaced.
  • In severe cases, patients can also be prescribed antibiotics.

Prevention

• Oral hygiene: Maintenance of a good oral hygiene can prevent the formation of plaque and gingivitis. Patients should be taught the correct brushing technique, frequency of brushing (twice daily) along with the use of floss.
  • Brushing: Brushing after meals helps remove food debris and plaque trapped between your teeth and gums. Don’t forget to include your tongue, bacteria loves to hide there.
  • Floss: Flossing at least once a day helps remove food particles and plaque between teeth and along the gum line that your toothbrush can’t quite reach.
  • Swish with mouthwash: Mouthwash and gel containing antiseptic and anti-inflammatory properties can also be advised to the patient.
• Balanced diet: An importance of a balanced diet should be emphasized.
• Dentist visit: A routine cleaning by a dentist or hygienist at 6-month to 1-year intervals can help minimize gingivitis. Patients with systemic disorders predisposing to gingivitis require more frequent professional cleanings (from every 2 weeks to every 3 months).
• Know your risk: Age, smoking, diet and genetics can all increase your risk for periodontal disease. If you are at increased risk, be sure to talk with your dental professional.

External links

• Gingivitis - Medline plus

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