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") (gingiva) around the teeth is a general term for gingival diseases affecting the gingiva (gums). As generally used, the term gingivitis refers to gingival inflammation induced by bacterial biofilms (also called plaque) adherent to tooth surfaces.

Pathophysiology

Gingivitis is usually caused by bacterial plaque that accumulates in the spaces between the gums and the teeth and in calculus (tartar) that forms on the teeth. These accumulations may be tiny, even microscopic, but the bacteria in them produce foreign chemicals and toxins that cause inflammation of the gums around the teeth. This inflammation can, over the years, cause deep pockets between the teeth and gums and loss of bone around teeth otherwise known as periodontitis.

Since the bone in the jaws holds the teeth into the jaws, the loss of bone can cause teeth over the years to become loose and eventually to fall out or need to be extracted because of acute infection. Regular cleanings (correctly termed periodontal debridement, scaling or root planing) below the gum line, best accomplished professionally by a dental hygienist or dentist, disrupt this plaque biofilm and remove plaque retentive calculus (tartar) to help prevent inflammation. Once cleaned, plaque will begin to grow on the teeth within hours. However, it takes approximately 3 months for the pathogenic type of bacteria (typically gram negative anaerobes and spirochetes) to grow back into the deep pockets and restart the inflammatory process. Calculus (tartar) may start to reform within 24 hours. Ideally, scientific studies show that all people with deep periodontal pockets (greater than 5mm) should have the pockets between their teeth and gums cleaned by a dental hygienist or dentist every 3-4 months.

People with a healthy periodontium (gums, bone and ligament) or people with gingivitis only require periodontal debridement every 6 months. However, many dental professionals only recommend periodontal debridement (cleanings) every 6 months, because this has been the standard advice for decades, and because the benefits of regular periodontal debridement (cleanings) are too subtle for many patients to notice without regular education from the dental hygienist or dentist. If the inflammation in the gums becomes especially well-developed, it can invade the gums and allow tiny amounts of bacteria and bacterial toxins to enter the bloodstream. The patient may not be able to notice this, but studies suggest this can result in a generalized increase in inflammation in the body cause possible long term heart problems. Periodontitis has also been linked to diabetes, arteriosclerosis, osteoporosis, pancreatic cancer and pre-term low birth weight babies.

Sometimes, the inflammation of the gingiva can suddenly amplify, such as to cause a disease called Acute Necrotizing Ulcerative Gingitivitis (ANUG), otherwise known as "trench mouth." 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. This results in the breath being extremely bad-smelling, and the gums feeling considerable pain and degeration of the periodontium rapidly occurs. Fortunately, this can be cured with a 1-week course of Metronidazole antibiotic, followed by a deep cleaning of the gums by a dental hygienist or dentist and reduction of risk factors such as stress.

When the teeth are not cleaned properly by regular brushing and flossing, bacterial plaque accumulates, and becomes mineralized by calcium and other minerals in the saliva transforming it into a hard material called calculus (tartar) which harbors bacteria and irritates the gingiva (gums). Also, as the bacterial plaque biofilm becomes thicker this creates an anoxygenic environment which allows more pathogenic bacteria to flourish and release toxins and cause gingival inflammation. Alternatively, excessive injury to the gums caused by very vigorous brushing may lead to recession, inflammation and infection. Pregnancy, uncontrolled diabetes mellitus and the onset of puberty increase the risk of gingivitis, due to hormonal changes that may increase the susceptibility of the gums or alter the composition of the dentogingival microflora. The risk of gingivitis is increased by misaligned teeth, the rough edges of fillings, and ill fitting or unclean dentures, bridges, and crowns. This is due to their plaque retentive properties. The drug phenytoin, birth control pills, and ingestion of heavy metals such as lead and bismuth may also cause gingivitis.

The sudden onset of gingivitis in a normal, healthy person should be considered an alert to the possibility of an underlying viral aetiology, although most systemically healthy individuals have gingivitis in some area of their mouth, usually due to inadequate brushing and flossing.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

• Inadequate oral hygiene
• Dental plaque

Causes by Organ System

Cardiovascular	Arteriosclerosis
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
Drug Side Effect	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
Environmental	No underlying causes
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
Iatrogenic	No underlying causes
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
Neurologic	No underlying causes
Nutritional/Metabolic	Malnutrition, vitamin C deficiency
Obstetric/Gynecologic	Pregnancy
Oncologic	Langerhans cell histiocytosis, leukemia, pancreatic cancer
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
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
Sexual	Puberty
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	No underlying causes

Causes in Alphabetical Order

A	B	C	D	E	F	G	H	I	K
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)	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	R	S	T	V	Z
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	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

• 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)
• 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
• 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
• 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

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	Example	Example
Gingival candidosis	Example	Example
Primary and metastatic carcinoma	Example	Example
Foreign body gingivitis	Example	Example
Orofacial granulomatosis	Example	Example
Pyostomatitis vegetans	Example	Example
Linear IgA disease	Example	Example
Wegener granulomatosis	Example	Example
Erythema multiforme	Example	Example
Agranulocytosis	Example	Example
Histoplasmosis	Example	Example
Cyclic neutropenia	Example	Example

Natural History, Complications and Prognosis

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

Clinical presentation

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

Diagnosis

It is recommended that a dental hygienist or dentist be seen after the signs of gingivitis appear. A dental hygienist or dentist will check for the symptoms of gingivitis, and may also examine the amount of plaque in the oral cavity. A dental hygienist or dentist should also test for periodontitis using X-rays or gingival probing as well as other methods.

Treatment

A dentist or dental hygienist will perform a thorough cleaning of the teeth and gums; following this, persistent oral hygiene is necessary. The removal of plaque is usually not painful, and the inflammation of the gums should be gone between one and two weeks. A gargling of Brine Water also helps. Oral hygiene including proper brushing and flossing is required to prevent the recurrence of gingivitis. Anti-bacterial rinses or mouthwash, in particular Chlorhexidine digluconate 0.2% solution, may reduce the swelling and local mouth gels which are usually antiseptic and anaesthetic can also help.

Prevention

Gingivitis can be prevented through regular oral hygiene that includes daily brushing and flossing.

Researchers analyzed government data on calcium consumption and periodontal disease indicators in nearly 13,000 people representing U.S. adults. They found that men and women who had calcium intakes of fewer than 500 milligrams, or about half the recommended dietary allowance, were almost twice as likely to have gum disease, as measured by the loss of attachment of the gums from the teeth. The association was particularly evident for people in their 20s and 30s.

Research says the relationship between calcium and gum disease is likely due to calcium’s role in building density in the alveolar bone that supports the teeth.

External links

• Gingivitis - Medline plus

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