Gingivitis

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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]

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. It is initiated by substances derived from microbial plaque accumulating at or near the gingival sulcus; where, all other suspected local and systemic etiologic factors either enhance plaque accumulation or retention, or enhance the susceptibility of the gingival tissue to microbial attack. This 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 This thin cellular transudate is gradually superseded by a fluid consisting of serum plus leucocytes.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 sub-epithelial 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[1]

Periodontal Health
  1. Clinical health on an intact periodontium
  2. Clinical gingival health on a reduced periodontium
  • Stable periodontitis patient
  • Non-periodontitis patient
Gingivitis—Dental Plaque-induced
  1. Associated with biofilm alone
  2. Drug-influenced gingival enlargement
  3. 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
  1. Genetic and developmental disorders (e.g., hereditary gingival fibromatosis)
  2. Specific infections: Bacterial, viral, fungal
  3. Inflammatory and immune conditions: Hypersensitivity reactions, Autoimmune diseases of skin and mucous membranes, Granulomatous inflammatory lesions (e.g., orofacial granulomatosis)
  4. Reactive processes: Epulides
  5. Neoplasms: Premalignancy, Malignancy
  6. Endocrine, nutritional, and metabolic diseases (e.g., vitamin deficiencies)
  7. Traumatic lesions: Physical/mechanical trauma, Chemical (toxic) burn, Thermal insults
  8. 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.[2]

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. [3] [4]

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[5]

  • 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 [5]

  • 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 [5]

  • 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. [6] [7]

Hormonal gingivitis

  • This form of gingivitis occurs during pregnancy, puberty, or steroid therapy even without the presence of plaque.
  • Pregnancy: An increase in the circulating female sex hormones causes pregnancy gingivitis. [8]
  • Puberty: During adolescence, gingivitis observed to appear earlier in girls (eleven to thirteen years) in comparison to boys (thirteen to fourteen years). [9]

It has been found that the receptors in the cytoplasm of the gingival cells have a high affinity for both estrogens and testosterone. The receptors for estrogen are specifically present in the basal and spinous layers of the epithelium; whereas in the connective tissue, such receptors are found deeper in the fibroblasts and endothelial cells of small vessels. Hence, the gingiva is considered as an easy target organ for these steroid hormones resulting in gingivitis. [5] [9]

Drug induced gingivitis [5]

  • An ability of the drug metabolites to induce the proliferation of fibroblasts is held responsible for the gingival inflammation.
  • Additionally, 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 from local, systemic, genetic to behavioral factors giving synergistic effect in most cases. The most common cause is an inadequate oral hygiene that leads to dental plaque formation.

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

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

A B C D E
F G H I K
L M N O P
R S T V Z

Differentiating Gingivitis from other Diseases

Table 5: Enumerate the conditions mimicking the gingivitis[10]

Differentiating condition Differentiating sign and symptoms Differentiating diagnostic features
Oral Lichen planus
  • A chronic inflammatory mucocutaneous disease commonly manifesting on the gingiva as a red nonswollen gingivae with painful atrophic/ulcerative lesions.
  • White papular, reticular and plaque-type lesions may 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 measures.
  • It may also develop on oral mucosa (50%-70% of cases), other mucosal surfaces and on skin of extremities.
  • Oral lesions may present in the absence of skin lesions.[11]
  • Direct immunofluorescence (DIF) is positive for fibrinogen fluorescence outlining the basement membrane zone with irregular extensions into the superficial lamina propria giving shaggy appearance inspite of being negative for all other autoantibodies.[12]
  • Histopathology reveals a dense lymphocytic infiltrate with possible changes to the epithelium.
Pemphigoid
  • A chronic, mucocutaneous autoimmune disorders in which autoantibodies are directed toward components of the basement membrane, and characterized by bullae and blisters rupturing into superficial, painful, and persistent ulcerations.
  • It may occasionally leave scars, but the oral lesions usually do not result in scarring. [13]
  • Gingival involvement is characterized either by the clinical pattern known as desquamative gingivitis or by localized bullous formation quickly evolving into painful and persisting erosions.[11]
  • Linear band of IgG, C3, and fibrin seen at the basement membrane zone. [14]
  • Indirect immunofluorescence (IIF) is negative, but salt-split-skin IIF is positive in up to 50% of the cases.[15]
Pemphigus
  • An autoimmune diseases characterized by formation of intraepithelial bullae in both skin and mucous membranes.
  • The average age of onset is 50 years and rarely seen in children.
  • A positive Nikolsky sign is seen where the top layers of skin slide over the lower layers on rubbing.
  • The typical oral lesions are chronic, superficial, ragged irregular painful erosions which may appear earlier than skin lesions.
  • 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. [13]
  • DIF is positive for intercellular IgG and C3 between epithelial cells; no linear reactivity along basement membrane zone seen. [14]
  • IIF is positive.[14]
Lupus erythematosus
  • Oral mucosal lesions resemble erosive lichen planus either as erosions and striae or atrophy with fine white stippling.[13]
  • Gingival involvement in the form of desquamative gingivitis, gingival ulceration, and plaque-induced gingivitis secondary to Sjogren syndrome seen.
  • DIF is positive for IgM, IgG, and/or C3 in a shaggy or granular band at the basement membrane zone. [16]
  • Serum ANAs and antidouble-stranded DNA antibodies are found.
Desquamative gingivitis
  • A clinical reaction pattern produced by several disorders involving the gingiva which is characterized by an extensive desquamation and/or erosion of the affected gingival, particularly in the buccal aspect of anterior teeth.
  • Marginal gingival is unaffected in the absence of plaque accumulation which differentiates it from others. [13]
  • Biopsy: About 80% of cases confirms mucous membrane pemphigoid and oral lichen planus. Other less frequently includes pemphigus vulgaris, linear IgA disease, epidermolysis bullosa acquisita, systemic lupus erythematosus, chronic ulcerative stomatitis, and paraneoplastic pemphigus. [17]
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 shows a normal color with an enlargement ranging from focal to extensive areas impairing the mastication of food. However, it may be reddened, puffy, and painful in case of secondary inflammation caused by dental plaque.[18]
  • Diagnosis: Clinical oral exam and detailed history taking.
  • Treatment: Oral hygiene maintenance, gingival surgery, and rarely substituting an acceptable alternative drug. [18]
Primary herpetic gingivostomatitis
  • It has a bimodal age distribution of 2-3 years and >60 years. [13]
  • Clusters of small vesicles coalesce to form blisters that rupture to leave painful mucosal ulcerations.
  • The gingivae are enlarged, very erythematous, and painful in a form of necrotizing gingivitis without significant hemorrhage.
  • Other mucosal surfaces shows clusters of painful ruptured vesicles.
  • Fever, cervical lymphadenopathy and skin rashes can be seen.
  • No specific tests are needed. Cytologic smear may confirm viral inclusions.
  • It is self-limiting lasts up to 2 weeks in immunocompetent patients.
Allergic reactions
  • They usually occur after the use of mouthwashes, toothpastes, chewing gums, flavor additives (e.g., cinnamon) or preservatives, natural products, or lipsticks. [11]
  • It appears as a swollen red area with painful ulcerations or white striae in some cases.
  • 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. [13]
  • Withdrawal of suspected offending agent brings relief within 1 week. [19] [20]
  • Patch testing may be useful. [21]
Leukemia
  • It presents in the oral cavity with spontaneous hemorrhage, petechiae and possible pain. [13]
  • Gingival enlargement or manifestations are most likely seen with acute than chronic leukemia.
  • Ulcers are found on the gingival and the mucosal surfaces.
  • CBC and peripheral blood film usually establish the leukemic type.
Gingival candidosis
  • It is characterized by a distinct 2- to 3-mm linear band of pronounced erythema with a granular surface along the gingival margin directly adjacent to the teeth not responding to conventional oral hygiene procedures. [13] [22]
  • Some cases are associated with oral candidosis and positive HIV status.
  • Diagnosis: Culture, smear, and biopsy. [22]
Primary and metastatic carcinoma
  • Most gingival carcinomas, both primary and metastatic, present with localized exophytic masses rather than diffuse pseudoinflammatory changes seen 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
  • 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 and usually locates in the connective tissue deep to the sulcular epithelium. [13]
  • Diagnosis: History and clinical features.
  • Biopsy: A nonspecific pattern of chronic or subacute mucositis and a foreign body.
  • However, when granulomatous inflammation is microscopically found and a foreign body is not detected; search for signs and symptoms of granulomatous diseases such as Crohn disease, sarcoidosis, tuberculosis, orofacial granulomatosis.[13]
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. [11]
  • Biopsy: 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.
  • Multiple, painless, yellow-white lesions, vegetative mucosal folds, and microabscesses are found on both gingival and oral mucosa.[13]
  • Biopsy: An acantholytic appearance of the epithelium due to the presence of numerous eosinophils seen forming intraepithelial microabscesses.
  • DIF 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. [23]
  • Lesions affect the hard and soft palates, tonsillar pillars, buccal mucosa, tongue, and gingiva in the presence of skin lesions. [24]
  • DIF: Linear deposition of IgA along the dermoepidermal basement membrane zone seen. [13]
  • IIF: Circulating anti-basement membrane IgA detected in approximately 30% cases.
  • Differentiating feature: An exclusive oral lesions showing linear IgA staining at the basement membrane zone should be considered mucous membrane pemphigoid not linear IgA disease. [25]
Wegener granulomatosis
  • 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.[13]
  • Biopsy: 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.[13] [26]
  • Circulating perinuclear antineutrophil cytoplasmic antibody (p-ANCA) or cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA) may be detected.
  • 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. [27]
Erythema multiforme
  • Acute onset of symmetrically distributed cutaneous target lesions often accompanied by mucus membrane involvement. [13]
  • 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 immunization.
  • Diagnosis: It is based on clinical features and exclusion of other vesiculo-erosive disorders as histopathology is rarely helpful due to non specific features. [28]
Agranulocytosis
  • Gingiva appears as necrotizing gingivitis in patient with 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 suspected drug leading to resolution within 2 weeks may be diagnostic.
  • CBC shows granulocytopenia (<500 cells/mm^3) and normal erythrocytes and platelets.[13]
Histoplasmosis
  • Very rare. Oral lesions may occur with disseminated form of the disease in older or immunocompromised patients. [13]
  • They appear as chronic ulcers with firm rolled margins and may resemble oral carcinoma of the gingiva.
  • Biopsy: Granulomatous inflammation with periodic acid-Schiff and Gomori methenamine silver-positive fungi; and morphologically consistent with Histoplasma capsulatum infection. [29]
  • Nonculture methods include zymogen-based colorimetric assays to detect (13)-beta-D-glucan and molecular methods to detect fungal DNA.
Cyclic neutropenia
  • It 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. [13]
  • 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.[13]

Epidemiology and Demographics

Age

  • Gingivitis is the commonest periodontal disease seen in all age groups prevailing worldwide. [5]
  • Gingivitis occurs in half the population by the age of 4 or 5 years, and the incidence continues to increase with age.
  • The prevalence peaks at close to 100% at puberty; however it declines slightly after puberty and shows constant rate into adulthood. [30]

Gender predilection:

Gingivitis is more prevalent in males as compared to females as females been found to follow better oral care regimes and thus maintaining oral hygiene.

  • Women: Pregnant women develops more severe form of gingivitis as compared to non-pregnant women. [31]
  • Socioeconomic status: It is more commonly seen among low socioeconomic status as people with high social status tend to show a more positive attitude towards the maintenance of oral hygiene and have better access to health care.[5]

Risk Factors

  • Common risk factors in the development of gingivitis include

Table 6: List the risk factors for gingivitis[32] [33]

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

Acute Necrotizing Ulcerative Gingitivitis (ANUG or Trench mouth)

  • Chronic gingivitis can progress to ANUG if not treated timely, oral hygiene neglected by the patient or the immune system gets compromised.
  • The condition is commonly seen in developing countries where the living conditions are poor.
  • Risk factors: Smoking, debilitated patients under stress, poor oral hygiene, nutritional deficiencies, immunodeficiency (eg, HIV/AIDS, use of immunosuppressive drugs), and sleep deprivation.
  • Etiopathogenesis: An overgrowth of a particular type of pathogenic bacteria (fusiform-spirochete variety) which gets exacerbated in association with other risk factors.
  • Clincal features: It is a severe form of gingivitis associated with pain, ulceration, marked gingival edema, spontaneous bleeding, or bleeding in response to minimal local trauma. It may be associated with altered taste (metallic taste mostly), and halitosis. Ulcerations, which are pathognomonic, are present on the dental papillae and marginal gingiva. They have a characteristically punched-out appearance and are covered by a gray pseudomembrane. Swallowing and talking may be painful. Regional lymphadenopathy often is present.
  • Treatment: Debridement, rinses (eg, hydrogen peroxide, chlorhexidine) and improved oral hygiene. If debridement is delayed, 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. [34]

Prognosis

  • Gingivitis can easily be resolved in its early stages if identified and treated timely.
  • However, if left untreated; chronic cases can progress to periodontitis which thereby results in bone destruction and tooth loss.

Clinical presentation

  • The clinical manifestations are usually episodic phenomenal characterized by discontinuous bursts of acute inflammation which are mostly transient or persistent.
  • Onset: It can be acute or chronic, and can be either localized or generalized which is categorized as follows: [35]
    • Marginal gingivitis: An inflammation confined to the gingival margin.
    • Papillary gingivitis: It involves an inflammation of an interdental papillae.
    • Diffuse gingivitis: It has extensive 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 on gentle brushing and flossing
  • 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 [36] [37]

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, and bleeding on probing
  • Severe gingivitis: Overt redness, edema and bleeding on palpation rather on probing
Plaque-induced gingivitis Clinical signs on examination
Puberty
  • Bleeding on probing or tooth brushing associated with mild to moderate redness
Menstrual cycle
  • Mild redness and edema based on severity of inflammation seen during the menstrual cycle
Pregnancy
  • Deep gingival probing depths, bleeding on probing or toothbrushing, and elevated gingival crevicular fluid flow in pregnancy
Oral contraceptives
  • Mild redness and edema based on severity of inflammation seen after 1 to 3 months of drug use
Hyperglycemia
  • Signs of inflammation of gingivitis and high blood glucose levels
Leukemia
  • Cervical lymphadenopathy; petechiae and ulcers seen in the mucosa; bleeding on slight provocation; swollen, glazed and spongy gingiva; and 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, and mild edema seen in the area of restoration.
Hyposalivation
  • Dental caries, taste changes, halitosis, mucosal and gingival dryness, and gingival inflammation noted.
Drug-influenced gingival enlargements
  • An increase in gingival size after 3 months of drug intake seen commonly in anterior gingiva 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 review and physical examination (Table 7) should be performed.
  • Clinical evaluation: Finding erythematous and friable tissue at the gum margins confirm the diagnosis. To detect early gingival disease, the depth of the pocket around each tooth should be measured. Depths < 3 mm are normal; however, the deeper pockets are at high risk of gingivitis and periodontitis. [38]
  • 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. [5]

Treatment

  • Treatment approach: An interprofessional approach is required to identify the causes of gingivitis and to intervene at an early stage to stop the progression to periodontitis.
  • Aim: To restore the inflamed tissues to clinical health, and then to maintain clinically healthy gingivae, and subsequently preventing periodontitis.
  • Stepwise approach:[5] [35]
    • A dentist or dental hygienist will perform a thorough cleaning of the teeth and gums, and remove localized factors promoting 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 subsides by 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 identification of faulty prosthesis should be done and replaced.
    • In severe cases, patients can also be prescribed oral antibiotics.

Prevention

  • Oral hygiene: Maintaining a good oral hygiene can prevent the formation of plaque and gingivitis. Patients should be taught about the correct brushing technique, frequency of brushing (twice daily) and the use of floss.[5] [39]
    • Brushing: Brushing after meals including the tongue helps to remove food debris and plaque trapped between your teeth and gums.
    • Floss: Flossing at least once a day helps remove food particles and plaque between teeth and along the gum line that 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). [38]
  • Know your risk: Age, smoking, diet, drugs, and genetics can all increase the risk for gingival disease.

References

  1. ↑ Chapple, Iain L.C.; Mealey, Brian L.; Van Dyke, Thomas E.; Bartold, P. Mark; Dommisch, Henrik; Eickholz, Peter; Geisinger, Maria L.; Genco, Robert J.; Glogauer, Michael; Goldstein, Moshe; Griffin, Terrence J.; Holmstrup, Palle; Johnson, Georgia K.; Kapila, Yvonne; Lang, Niklaus P.; Meyle, Joerg; Murakami, Shinya; Plemons, Jacqueline; Romito, Giuseppe A.; Shapira, Lior; Tatakis, Dimitris N.; Teughels, Wim; Trombelli, Leonardo; Walter, Clemens; Wimmer, Gernot; Xenoudi, Pinelopi; Yoshie, Hiromasa (2018). "Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions". Journal of Periodontology. 89: S74–S84. doi:10.1002/JPER.17-0719. ISSN 0022-3492.
  2. ↑ Page RC, Schroeder HE (March 1976). "Pathogenesis of inflammatory periodontal disease. A summary of current work". Lab. Invest. 34 (3): 235–49. PMID 765622.
  3. ↑ Bosshardt DD, Selvig KA (February 1997). "Dental cementum: the dynamic tissue covering of the root". Periodontol. 2000. 13: 41–75. doi:10.1111/j.1600-0757.1997.tb00095.x. PMID 9567923.
  4. ↑ Syndergaard B, Al-Sabbagh M, Kryscio RJ, Xi J, Ding X, Ebersole JL, Miller CS (August 2014). "Salivary biomarkers associated with gingivitis and response to therapy". J. Periodontol. 85 (8): e295–303. doi:10.1902/jop.2014.130696. PMC 4390171. PMID 24502627.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 5.9 Rathee M, Jain P. Gingivitis. [Updated 2020 May 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557422/
  6. ↑ Bosma-den Boer MM, van Wetten ML, Pruimboom L (April 2012). "Chronic inflammatory diseases are stimulated by current lifestyle: how diet, stress levels and medication prevent our body from recovering". Nutr Metab (Lond). 9 (1): 32. doi:10.1186/1743-7075-9-32. PMC 3372428. PMID 22510431.
  7. ↑ Dickinson S, Hancock DP, Petocz P, Ceriello A, Brand-Miller J (May 2008). "High-glycemic index carbohydrate increases nuclear factor-kappaB activation in mononuclear cells of young, lean healthy subjects". Am. J. Clin. Nutr. 87 (5): 1188–93. doi:10.1093/ajcn/87.5.1188. PMID 18469238.
  8. ↑ Emmatty R, Mathew JJ, Kuruvilla J (January 2013). "Comparative evaluation of subgingival plaque microflora in pregnant and non-pregnant women: A clinical and microbiologic study". J Indian Soc Periodontol. 17 (1): 47–51. doi:10.4103/0972-124X.107474. PMC 3636944. PMID 23633772.
  9. ↑ 9.0 9.1 Nakagawa S, Fujii H, Machida Y, Okuda K (November 1994). "A longitudinal study from prepuberty to puberty of gingivitis. Correlation between the occurrence of Prevotella intermedia and sex hormones". J. Clin. Periodontol. 21 (10): 658–65. doi:10.1111/j.1600-051x.1994.tb00783.x. PMID 7852609.
  10. ↑ "Gingivitis Differential Diagnosis - Epocrates Online".
  11. ↑ 11.0 11.1 11.2 11.3 Laskaris, George, and Crispian Scully. Periodontal Manifestations of Local and Systemic Diseases : Colour Atlas and Text. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. Print.
  12. ↑ Jordan, Richard C.K.; Daniels, Troy E.; Greenspan, John S.; Regezi, Joseph A. (2002). "Advanced diagnostic methods in oral and maxillofacial pathology. Part II: Immunohistochemical and immunofluorescent methods". Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology. 93 (1): 56–74. doi:10.1067/moe.2002.119567. ISSN 1079-2104.
  13. ↑ 13.00 13.01 13.02 13.03 13.04 13.05 13.06 13.07 13.08 13.09 13.10 13.11 13.12 13.13 13.14 13.15 13.16 13.17 13.18 Neville BW, Damm D, Allen CM,et al. Oral and maxillofacial pathology. 3rd ed. St Louis, MO: Elsevier; 2009.
  14. ↑ 14.0 14.1 14.2 Rinaggio, Joseph; Crossland, David M.; Zeid, Mohamed Y. (2007). "A Determination of the Range of Oral Conditions Submitted for Microscopic and Direct Immunofluorescence Analysis". Journal of Periodontology. 78 (10): 1904–1910. doi:10.1902/jop.2007.070095. ISSN 0022-3492.
  15. ↑ Calabresi, Valentina; Carrozzo, Marco; Cozzani, Emanuele; Arduino, Paolo; Bertolusso, Giorgio; Tirone, Federico; Parodi, Aurora; Zambruno, Giovanna; Di Zenzo, Giovanni (2007). "Oral pemphigoid autoantibodies preferentially target BP180 ectodomain". Clinical Immunology. 122 (2): 207–213. doi:10.1016/j.clim.2006.10.007. ISSN 1521-6616.
  16. ↑ Fabbri, Paolo; Cardinali, Carla; Giomi, Barbara; Caproni, Marzia (2003). "Cutaneous Lupus Erythematosus". American Journal of Clinical Dermatology. 4 (7): 449–465. doi:10.2165/00128071-200304070-00002. ISSN 1175-0561.
  17. ↑ Lo Russo, Lucio; Fedele, Stefano; Guiglia, Rosario; Ciavarella, Domenico; Lo Muzio, Lorenzo; Gallo, Pio; Di Liberto, Chiara; Campisi, Giuseppina (2008). "Diagnostic Pathways and Clinical Significance of Desquamative Gingivitis". Journal of Periodontology. 79 (1): 4–24. doi:10.1902/jop.2008.070231. ISSN 0022-3492.
  18. ↑ 18.0 18.1 "Informational Paper:Drug-Associated Gingival Enlargement". Journal of Periodontology. 75 (10): 1424–1431. 2004. doi:10.1902/jop.2004.75.10.1424. ISSN 0022-3492.
  19. ↑ Bousquet, Philippe-Jean; Guillot, Bernard; Guilhou, Jean-Jacques; Raison-Peyron, Nadia (2005). "A Stomatitis Due to Artificial Cinnamon-Flavored Chewing Gum". Archives of Dermatology. 141 (11). doi:10.1001/archderm.141.11.1466-c. ISSN 0003-987X.
  20. ↑ Sainio, Eeva-Liisa; Kanerva, Lasse (1995). "Contact allergens in toothpastes and a review of their hypersensitivity". Contact Dermatitis. 33 (2): 100–105. doi:10.1111/j.1600-0536.1995.tb00509.x. ISSN 0105-1873.
  21. ↑ Torgerson, Rochelle R.; Davis, Mark D.P.; Bruce, Alison J.; Farmer, Sara A.; Rogers, Roy S. (2007). "Contact allergy in oral disease". Journal of the American Academy of Dermatology. 57 (2): 315–321. doi:10.1016/j.jaad.2007.04.017. ISSN 0190-9622.
  22. ↑ 22.0 22.1 Holmstrup, Palle; Plemons, Jacqueline; Meyle, Joerg (2018). "Non-plaque-induced gingival diseases". Journal of Periodontology. 89: S28–S45. doi:10.1002/JPER.17-0163. ISSN 0022-3492.
  23. ↑ Leao, JC; Ingafou, M; Khan, A; Scully, C; Porter, S (2008). "Desquamative gingivitis: retrospective analysis of disease associations of a large cohort". Oral Diseases. 14 (6): 556–560. doi:10.1111/j.1601-0825.2007.01420.x. ISSN 1354-523X.
  24. ↑ Torchia, D; Caproni, M; Fabbri, P (2008). "Linear IgA disease and desquamative gingivitis: time for inclusion in mucous membrane pemphigoid". Oral Diseases. 14 (8): 768–769. doi:10.1111/j.1601-0825.2008.01485.x. ISSN 1354-523X.
  25. ↑ Chan, Lawrence S.; Ahmed, A. Razzaque; Anhalt, Grant J.; Bernauer, Wolfgang; Cooper, Kevin D.; Elder, Mark J.; Fine, Jo-David; Foster, C. Stephen; Ghohestani, Reza; Hashimoto, Takashi; Hoang-Xuan, Thanh; Kirtschig, Gudula; Korman, Neil J.; Lightman, Susan; Lozada-Nur, Francina; Marinkovich, M. Peter; Mondino, Bartly J.; Prost-Squarcioni, Catherine; Rogers III, Roy S.; Setterfield, Jane F.; West, Dennis P.; Wojnarowska, Fenella; Woodley, David T.; Yancey, Kim B.; Zillikens, Detlef; Zone, John J. (2002). "The First International Consensus on Mucous Membrane Pemphigoid". Archives of Dermatology. 138 (3). doi:10.1001/archderm.138.3.370. ISSN 0003-987X.
  26. ↑ Comfere, Nneka I.; Macaron, Nada C.; Gibson, Lawrence E. (2007). "Cutaneous manifestations of Wegener?s granulomatosis: a clinicopathologic study of 17 patients and correlation to antineutrophil cytoplasmic antibody status". Journal of Cutaneous Pathology. 34 (10): 739–747. doi:10.1111/j.1600-0560.2006.00699.x. ISSN 0303-6987.
  27. ↑ KAWAKAMI, Tamihiro (2010). "New algorithm (KAWAKAMI algorithm) to diagnose primary cutaneous vasculitis". The Journal of Dermatology. 37 (2): 113–124. doi:10.1111/j.1346-8138.2009.00761.x. ISSN 0385-2407.
  28. ↑ Wiedemeyer, K; Enk, A; Jappe, U (2007). "Erythema Multiforme Following Allergic Contact Dermatitis: Case Report and Literature Review". Acta Dermato-Venereologica. 87 (6): 559–561. doi:10.2340/00015555-0316. ISSN 0001-5555.
  29. ↑ Wheat, L. Joseph (2008). "Nonculture diagnostic methods for invasive fungal infections". Current Infectious Disease Reports. 9 (6): 465–471. doi:10.1007/s11908-007-0071-7. ISSN 1523-3847.
  30. ↑ Stenberg WV. Periodontal problems in children and adolescents. In: Nowak, AJ, Christensen JR, Mabry TR,Townsend JA, Wells MH, eds. Pediatric Dentistry-Infancy through Adolescence, 6th ed. St. Louis, Mo.: Elsevier/Saunders; 2017:371-8.
  31. ↑ Patil, Prashant; Kashetty, Meena; Kumbhar, Sagar; Patil, Smita (2018). "Oral hygiene status, gingival status, periodontal status, and treatment needs among pregnant and nonpregnant women: A comparative study". Journal of Indian Society of Periodontology. 22 (2): 164. doi:10.4103/jisp.jisp_319_17. ISSN 0972-124X.
  32. ↑ AlJehani, Yousef A. (2014). "Risk Factors of Periodontal Disease: Review of the Literature". International Journal of Dentistry. 2014: 1–9. doi:10.1155/2014/182513. ISSN 1687-8728.
  33. ↑ Risk factors associated with periodontal diseases and their clinical considerations,” Int J Contemp Dent Med Rev, Vol. 2015, Article ID: 040115, 2015. doi: 10.15713/ins.ijcdmr.31
  34. ↑ "Acute Necrotizing Ulcerative Gingivitis (ANUG) - Dental Disorders - MSD Manual Professional Edition".
  35. ↑ 35.0 35.1 Neville, Brad W.; Damm, Douglas D.; Allen, Carl M.; Chi, Angela C. (2019). "Periodontal Pathology": 93–107. doi:10.1016/B978-0-323-55225-7.00004-X.
  36. ↑ Newman, Michael G., et al. Newman and Carranza's clinical periodontology. Philadelphia, PA: Elsevier, 2019. Print.
  37. ↑ Murakami, Shinya; Mealey, Brian L.; Mariotti, Angelo; Chapple, Iain L.C. (2018). "Dental plaque-induced gingival conditions". Journal of Clinical Periodontology. 45: S17–S27. doi:10.1111/jcpe.12937. ISSN 0303-6979.
  38. ↑ 38.0 38.1 "Gingivitis - Dental Disorders - MSD Manual Professional Edition".
  39. ↑ "PREVENTING PERIODONTAL DISEASE | Perio.org".

External links

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