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Gingival diseases

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Modern understanding of the pathogenesis and treatment of gingivitis is relatively young in comparison to other disciplines in dentistry.
Whereas nowadays the fact that the most common types of gingivitis can mostly be triggered by the presence of plaque is part of basic understanding of dentistry, during the 1960s this link had hardly been examined and not proven clearly.
The Harald Löe et al. working group is particularly important as in 1965 they were able to show in an experimental study that with healthy test persons cessation of all hygiene measures led to a rapid increase in plaque and, consequently, to gingivitis. The study showed that the time required for gingivitis to set in varies from ten to 21 days depending on the person and is fully reversible once oral hygiene measures are resumed (Löe et al. 1965).
As described in the article “Classification of periodontal diseases“ we differentiate between the common plaque-induced and less common non-plaque-induced gingival diseases which often occur in connection with systemic diseases.
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The following characteristics apply for all gingival diseases:
  1. Clinical signs and symptoms are limited to the gingiva.
  2. The presence of dental plaque triggers the disease and/or increases the severity of the disease
  3. Clinical signs of inflammation (enlarged gingiva due to edema or fibrosis, change in color from red to red-blue, increased sulcus temperature, bleeding on stimulation, increased gingival exudate)
  4. Clinical signs and symptoms occur when there is a stable attachment level without bone loss or on stably reduced periodontium
    Signs of disease disappear when the causes are eliminated
  5. Possible precursor of loss of attachment around the teeth
(Mariotti 1999; Carranza et al. 2006)

The following aims at describing the above-mentioned clinical signs and observing the basic pathomechanisms.

Gingivitis can be acute, chronic or recurrent and occur either locally or in general. Gingivitis may follow a course which is painless or, in severely pronounced forms, very painful at times.

Gingivitis is divided into four stages.

1) Initial lesion
2) Early lesion
3) Established lesion
4) Advanced lesion

The cell physiological details can be reviewed here.

Different clinical signs appear between occurrence of the initial and advanced lesions (Carranza et al. 2006, 356–360).

General clinical signs of gingivitis

Symptoms of gingival lesions

Initial lesion
  • Increased bleeding
  • Reddening
Early lesion
  • Begins approx. one week following plaque accumulation
  • Erythema
  • Bleeding on probing possible
  • Increased crevicular fluid flow rate
Established lesion
  • Gingival oxygen deficiency
  • Bluish/dark red gingiva
  • Moderately to severely inflamed gingiva
Advanced lesion
  • Beginning of periodontal destruction
  • Pocket formation
Above all, gingivitis exhibits two early clinical parameters:
  • Increased crevicular fluid flow rate
  • Bleeding on probing
Further signs of inflammation are:
  • Reddening
  • Swelling
  • Bleeding on provocation
  • Changes in the contours
  • Presence of calculus or plaque
  • No loss of bone

Visible defense mechanisms of the gingiva (Carranza et al. 2006)

The gingival crevicular fluid

An increase in the gingival crevicular fluid flow rate is a dependable indicator of the presence of gingivitis.
Gingival crevicular fluid is an inflammable exudate which does not occur with healthy gingiva.
Fluid flow in the gingival sulcus is typical for an infection and may arise several days prior to other clinical signs being observed. It is generally accepted that the presence or absence of gingival crevicular fluid is linked with the presence or absence of inflammation. However, the exact connection remains to be clarified (Del Fabbro et al. 2001). In some cases the crevicular fluid flow rate is proportional to the degree of severity of the disease.
Crevicular fluid consists of numerous cellular elements such as leucocytes, scaled off skin cells and fragments of bacteria, electrolytes such as potassium, sodium and calcium, as well as other organic components like carbohydrates and proteins. To date, however, it is not possible to estimate the degree of the disease based on the composition of the crevicular fluid.
Crevicular fluid contains numerous immunologically active enzymes of bacterial origin.

Bleeding on probing


Bleeding on probing is a very important indicator for acute gingivitis and is triggered just 2 days after plaque infestation. Usually the patient is not aware of the gingivitis until bleeding occurs. The bleeding is not only due to oedematous swelling of the tissue, but also particularly to dilatation and stoppage of the surface capillaries which may rupture under minimal force. Signs of bleeding normally disappear 7-10 days after complete plaque removal.

During gingivitis therapy bleeding on probing may enable evaluation of the patient’s home plaque control.

Various indices are available for diagnosis of gingival bleeding. Whereas it is possible to determine if a tooth suffers from bleeding on probing using a dichotomous score (yes/no), specific indices may be used for estimating the degree of severity of the gingivitis. For example, the papillary bleeding index acc. to Saxer and Mühlemann provides for differentiation of 5 grades.

The papillary bleeding index acc. to Saxer and Mühlemann (1975)
Degree Type of bleeding following careful sulcus probing
0 No bleeding
1 Bleeding point
2 several isolated bleeding points or a small area of bleeding
3 the interdental triangle fills with blood
4 profuse bleeding

Leucocytes in the dentogingival zone

Leucocytes are a major factor in preventing plaque extending into the gingival sulcus. They are present in both healthy and inflamed gingiva. The majority of leucocytes is capable of phagocytosis and can kill bacteria cells.


Saliva has a major impact on the formation, maturation and metabolic process of plaque. It not only influences formation of caries and periodontal diseases but, in time, also wound healing.
Saliva contains proteolytic enzymes and antibodies which interact with bacteria. Glycoproteins in the saliva bond to bacteria and inhibit plaque formation.
A pathologically reduced amount of saliva is referred to as xerostomia and can lead to rapid deterioration in oral health.

Bacterial causes

When classifying periodontal diseases, three commonly occurring species of bacteria are mentioned which may lead to non-plaque-induced gingivitis (Holmstrup 1999).
  • Neisseria gonorrhea
  • Treponema pallidum
  • Streptococcae
The gingival lesions triggered by the above mentioned bacteria may occur in the form of conflagrant red oedematous painful ulcerations, asymptomatic ulcers or papules as well as being involved in atypical non-ulcerated, severely inflamed gingiva. Oral lesions may occur with or without manifestations on other areas of the body.


Gingivitis therapy comprises consistent removal of all bacterial plaque as a part of professional scaling and polishing as well as training the patient in systematic home oral care.

Professional scaling andpolishing

Professional scaling and polishing involves removing hard and soft plaque and polishing the teeth. It is also advisable to correct impeding restoration margins. Plaque and bleeding indices reveal whether the home oral care is satisfactory.

The required instruments:
  • Periodontal probe, 3A or other hooked probe
  • Mouth mirror
  • Hand or ultrasonic scaler
  • Prophy cup and polishing paste, Airflow if applicable
  • Instruments for adjusting fillings such as diamond-coated finishers, Sof-Lex-discs, rubber polishers, etc.
  • Fluoride gel
  • Irrigation solutions (e.g. CHX)
Professional scaling and polishing can be delegated to specially trained staff.

Home oral hygiene

Home oral hygiene should be matched to the patient’s specific needs.

The required dental care products
  • (own) toothbrush
    • manual toothbrush
    • powered toothbrush
      • oscillating-rotating
      • sonic toothbrush
    • fluoridated toothpaste
      • stannous, if applicable
    • dental floss or interdental brushes
    • mouthwashes
      • may contain ethereal oils
      • may contain antimicrobial substances (e.g. CHX)
      • may contain alcohol
      • may contain fluorides

Plaque-induced gingival diseases


Gingivitis associated with plaque accumulation is the most common form compared with other forms. Gingivitis has specific clinical signs of inflammation such as erythema, swelling, warmth and pain; it may develop with teeth where loss of attachment due to periodontitis has not yet occurred and also with teeth previously treated for periodontitis, where loss of attachment occurred in the past. The presence of gingivitis does not indicate initially whether further bone loss will take place. Close clinical surveillance is needed, however, to detect any changes promptly.

Summary of the characteristics of plaque-induced gingivitis:
  • Plaque present at the gingival margin
  • The disease begins at the gingival margin
  • Change in color
  • Change in contour
  • Change in sulcus temperature
  • Increase in gingival exudate
  • Bleeds when irritated
  • Absence of attachment loss (Mariotti 1999)
Characteristics of plaque-induced gingivitis after periodontitis:
  • Treated periodontitis, so attachment or bone loss may already be present
  • Plaque present at the gingival margin
  • The disease begins at the gingival margin
  • Change in color
  • Change in contour
  • Change in sulcus temperature
  • Increase in gingival exudate
  • Bleeds when irritated
  • No attachment loss
  • No bone loss
  • Histological changes
  • Reversible by plaque removal (Mariotti 1999)

Non-plaque-induced gingival diseases

(Holmstrup 1999, Carranza et al. 2006)

Non-plaque-associated gingivitis can develop for different reasons. Even if the cause cannot be found in bacterial plaque, good oral hygiene is nevertheless desirable in order to limit the severity of the disease.

The following are known causes of non-plaque-associated gingivitis:
  • Specific bacterial diseases
    • Neisseria gonorrhea
    • Treponema pallidum,
    • Streptococci,
    • Or other
  • Viral diseases
    • Herpes simplex 1 and 2
    • Varicella zoster
  • Fungal infections
  • Histoplasmosis
Special skin diseases are further causes of gingival lesions.
  • Lichen planus
  • Pemphigoid
  • Pemphigus vulgaris
  • Erythema multiforme
  • Lupus erythematosus
Allergic reactions can be the cause of non-plaque-associated gingivitis:
  • Against dental restoration materials
  • Against toothpaste or mouthwash
  • Against foods
Other reasons:
  • Toxic reactions
  • Foreign body reactions
  • Mechanical trauma
  • Thermal trauma
  • Not further specified

Hormonally influenced gingivitis

Characteristics of plaque-induced pubertal gingivitis:
  1. Plaque present at the gingival margin
  2. Increased gingival inflammatory response
  3. Only at Tanner stage 2 or later (estradiol in girls ≥ 26 pmol/L; testosterone in boys ≥ 8.7 nmol/L)
  4. Change in color
  5. Change in contour with possible increase in size
  6. Increase in gingival exudate
  7. Bleeds when irritated
  8. No attachment loss
  9. No bone loss
  10. Reversible after puberty (Mariotti 1999)
Characteristics of plaque-induced gingivitis associated with menstruation:
  1. Plaque present at the gingival margin
  2. Slightly increased gingival inflammatory response shortly before ovulation
  3. Only with LH rise shortly before ovulation (LH > 25 mlU/ml and/or estradiol > 200 pg/ml)
  4. Increase in gingival exudate by at least 20 % during ovulation
  5. No attachment loss
  6. No bone loss
  7. Reversible after ovulation (Mariotti 1999)
Characteristics of plaque-induced gingivitis in pregnancy:
  1. Plaque present at the gingival margin
  2. Increased gingival inflammatory response
  3. Onset in pregnant women in the second or third trimester
  4. Change in color
  5. Change in contour
  6. Increase in gingival exudate
  7. Bleeds when irritated
  8. No attachment loss
  9. No bone loss
  10. Reversible after delivery (Mariotti 1999)
Characteristics of pyogenic granuloma in pregnancy:
  1. Plaque present at the gingival margin
  2. Increased inflammatory response in the gingiva
  3. Can occur at any time during pregnancy
  4. More common in upper jaw
  5. More common approximally
  6. Solid or pedicled growth
  7. Not a neoplasm
  8. Disappears after delivery (Mariotti 1999)

Drug-associated gingivitis

Characteristics of drug-modified gingival enlargement.
  1. Differences both in the same patient and in different patients
  2. Site of predilection is the anterior gingiva
  3. Higher prevalence in children
  4. Onset within 3 months
  5. Change in contour leading to a change in size
  6. Enlargement initially in the interdental papillae
  7. Change in color
  8. Increase in gingival exudate
  9. Bleeding on provocation
  10. Occurs both with and without bone loss but is not associated with loss of attachment
  11. Increased gingival inflammatory response relative to the amount of plaque
  12. Plaque reduction can limit the extent of the lesion
  13. Occurs with phenytoin, ciclosporin A or special calcium channel blockers. The plasma concentration necessary to produce the disease has not yet been determined in humans (Mariotti 1999).
Characteristics of contraceptive-associated gingivitis
  1. Plaque present at the gingival margin
  2. Increased inflammatory response in the gingiva
  3. Change in color
  4. Change in contour leading to a change in size
  5. Increase in gingival exudate
  6. Bleeding on provocation
  7. Reversible on discontinuation of the oral contraceptive (Mariotti 1999)

Gingivitis modified by systemic diseases:

Characteristics of diabetes mellitus-associated gingivitis:
  1. Plaque present at the gingival margin
  2. Increased gingival inflammatory response
  3. Change in color
  4. Change in contour
  5. Increase in gingival exudate
  6. Bleeds when irritated
  7. Most common in children with poorly controlled type I diabetes
  8. No attachment loss
  9. No bone loss
  10. Reversible after diabetes is controlled
  11. Plaque reduction can improve the extent of the disease (Mariotti 1999)
Characteristics of leukemia-associated gingivitis:
  1. Increased gingival inflammatory response depending on the amount of plaque present; however, plaque does not have to be present.
  2. Lesions mainly with acute leukemia
  3. Change in color
  4. Change in contour with a possible change in size
  5. Enlargement first of the interdental papillae
  6. Bleeds when irritated (one of the initial signs of disease)
  7. Plaque reduction can limit the extent of the disease (Mariotti 1999)


  • Carranza, Fermin A.; Newman, Michael G.; Takei, Henry H.; Klokkevold, Perry R. (2006): Carranza's clinical periodontology. 10th ed. St. Louis, Mo.: Saunders Elsevier
  • Del Fabbro, M.; Francetti, L.; Bulfamante, G.; Cribiù, M.; Miserocchi, G.; Weinstein, R. L. (2001): Fluid dynamics of gingival tissues in transition from physiological condition to inflammation. In: Journal of periodontology 72 (1), S. 65–73. DOI: 10.1902/jop.2001.72.1.65. Pubmed-ID: 11210075
  • Holmstrup, P. (1999): Non-plaque-induced gingival lesions. In: Ann. Periodontol. 4 (1), S. 20–31. DOI: 10.1902/annals.1999.4.1.20
  • Löe, Harald; Theilade, Else; Jensen, S. Börglum (1965): Experimental gingivitis in man. In: The Journal of periodontology 36, S. 177–187. DOI: 10.1902/jop.1965.36.3.177. Pubmed-ID: 14296927
  • Mariotti, A. (1999): Dental plaque-induced gingival diseases. In: Ann. Periodontol. 4 (1), S. 7–19. DOI: 10.1902/annals.1999.4.1.7
  • Saxer, U. P.; Mühlemann, H. R. (1975): Motivation und Aufklärung. In: Schweizerische Monatsschrift für Zahnheilkunde = Revue mensuelle suisse d'odonto-stomatologie / SSO 85 (9), 905–919