Gingivitis presentation

All about gingivitis
*definition
*classification
*Signs and Symptoms: Increased GCF, Gingival Bleeding, Color change, Consistency, Surface texture (STIPPLING), Position of Gingiva, Gingival Contour, Size.
Treatment consisits of scaling and root planing. The more inflamed a gingival unit appears clinically, the better the chances of therapeutic measures resulting in a return to normal gingival health
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1. GINGIVITIS

2. Perio Files

3. Index Definition Etiology Types of Gingivitis (a) Depending on course and duration (b) Depending on Distribution (c) Classification of Gingivitis (Page and S chroeder 1976) (Histological Evaluation) Initial , Early , Established, Advanced .

4. Index 4. Clinical Features Increased GCF Gingival Bleeding Color change Consistency Surface texture (STIPPLING) Position of Gingiva Gingival Contour Size

5. GINGIVITIS Genco 1990- ‘Gingivitis is inflammation of the gingiva in which the junctional epithelium remains attached to the tooth at its original level.’ This definition infers that gingivitis does not exist if the tooth has periodontitis

6. GINGIVITIS VERSUS PERIODONTITIS Gingivitis is inflammation of the gingiva in which the junctional epithelium remains attached to the tooth at its original level. Periodontitis is inflammation of the gingiva in which the junctional epithelium shifts apically leading to clinical attachment loss.

7. ETIOLOGY

8. In recent classification of periodontal diseases (2017) Gingivitis has been classified under ‘Periodontal health, Gingival diseases and conditions’ 1. Periodontal health and gingival health (a. Clinical gingival health on an intact periodontium ; b. Clinical gingival health on a reduced periodontium ) 2 .Gingivitis : dental biofilm induced ( a. Associated with dental biofilm alone; b. Mediated by systemic or local risk factors; c. Drug-influenced gingival enlargement) 3 . Gingival diseases: non-dental biofilm-induced (1. Genetic or developmental disorder; 2. Specific infections; 3. Inflammatory and immune conditions; 4. Reactive processes; 5. Neoplasms; 6. Endocrine, nutritional and metabolic diseases; 7. Traumatic lesions; 8.Gingival Pigmentation)

9. Gingivitis : dental biofilm induced a. Associated with dental biofilm alone b. Mediated by systemic or local risk factors i ) Systemic risk factors a. Smoking b. Hyperglycemia c. Nutritional factors d. Pharmacological (prescription, non prescription) e. Sex Steroid hormones (Puberty, pregnancy, Menstrual cycle, oral contraceptives) f. Hematological agents ii) Local risk factors a. Oral dryness b. Dental plaque biofilm retention factors ( prominent restoration margins) c. Drug -influenced gingival enlargement

10. GINGIVAL DISEASES: NON-DENTAL BIOFILM- INDUCED (8 categories) 1. Genetic or developmental disorder 1.1 Hereditary Gingival fibromatosis 2. Specific infections 2.1 Bacterial infections a) Necrotizing Periodontal disease b) Neisseria Gonorrhoeae (gonorrhea) c) Treponema pallidum ( syphlis ) d) Mycobacterium tuberculosis (tuberculosis) e) Streptococcal gingivitis (strains of streptococcus)

11. b.2 Viral origin- a) Coxsachie virus (Hand foot and mouth disease b) Herpes simplex virus; HSV1,2 (primary or recurrent) c) Varicella zoster virus (chicken pox) d) Molluscum contagiosum e) Human papilloma virus b.3 Fungal- a) Candidiasis b) Other mycosis (eg. Histoplasmosis, aspergillosis)

12. 3 . Inflammatory and immune conditions 3.1 Hypersensitivity reaction- a) Contact allergy b) Plasma cell gingivitis c) Erythema multiforme 3.2 Auto immune diseases of skin and mucous membrane- a) Pemphigus vulgaris b) Pemphigoid c) Lichen Planus d) Lupus erythematosis

13. 3.3 Granulomatous inflammatory condition- a) Crohn’s disease b) Sarcoidosis 4. Reactive processes 4.1 Epulidus a) Fibrous epulis b) Calcifying fibroblastic granuloma c) Pyogenic granuloma d) Peripheral giant cell granuloma (or central)

14. 5. Neoplasms 5.1 Premalignant a) Leukoplakia b) Erythroplakia 5.2 Malignant a) Squamous cell carcinoma b) Leukemia c) Lymphoma

15. 6. Endocrine, nutritional and metabolic diseases 6.1 Vitamin deficiency a) Vitamin C deficiency (Scurvy) 7. Traumatic lesions 7.1 Physical and mechanical insults a) Frictional Keratosis b) Tooth brushing induced gingival abrasions c) Factitious injury (self harm)

16. 7.2 Chemical insults a) Etching b) Chlorhexidine c) Acetyl salicylic acid d) Cocaine e) Hydrogen peroxide f) Dentifrice detergent g) Paraformaldehyde/ calcium hydroxide 7.3 Thermal insults a) Burn of mucosa

17. 8. Gingival pigmentation a) Melanoplakia b) Smoker’s melanosis c) Drug induced pigmentation (antimalarial; minocycline) d) Amalgam tattoo

18. TYPES OF GINGIVITIS

19. Depending on course and duration Acute gingivitis Subacute gingivitis Chronic gingivitis Recurrent gingivitis

20. DEPENDING ON COURSE AND DURATION Acute gingivitis : S udden onset, short duration and can be painful. Subacute : Less severe phase of acute condition. Recurrent gingivitis: R eappears after treatment or after disappearing spontaneously. Chronic gingivitis: Slow onset, long duration, usually painless. The most commonly occurring gingival condition.

21. Depending on D istribution Localized gingivitis - Localized papillary gingivitis - Localized marginal gingivitis - Localized diffuse gingivitis ii) Generalized gingivitis - Generalized marginal gingivitis - Generalized diffuse gingivitis

22. DEPENDING ON THE DISTRIBUTION If g ingivitis is involving a single tooth or group of teeth it is called localized g ingivitis , while generalized g ingivitis involves entire mouth. According to distribution, g ingivitis can be marginal, papillary or diffuse Papillary , marginal and diffuse gingivitis can occur as localized or generalized conditions.

23. Depending on Distribution Marginal gingivitis: that involves the gingival margin. Papillary gingivitis: involves interdental papilla extending into gingival margin. Diffuse gingivitis: involves interdental papilla, gingival margin and attached gingiva. Normally it occurs in patients having some systemic diseases.

24. THE DIAGNOSIS OF GINGIVITIS SHOULD BE: L ocalized marginal/papillary/diffuse chronic/acute g ingivitis G eneralized marginal/papillary/diffuse chronic/acute g ingivitis

25. CLASSIFICATION OF GINGIVITIS ( PAGE AND SCHROEDER 1976)

26. HISTOLOGIC DEVELOPMENT OF THE GINGIVAL LESION The pathogenesis of human periodontitis was first documented in detail by Page and Schroeder in 1976 Initial , Early , Established , Advanced

27. CLINICAL CONDITION HISTOPATHOLOGIC CONDITION Pristine gingiva Histologic perfection Normal health gingiva Initial lesion of Page & Schroeder (PMNs) Early gingivitis Early lesion of Page & Schroeder (mainly T lymphocytes) Established gingivitis Established lesion with no bone loss and epithelial migration ( plasma cell density between 10% and 30% of leukocyte infiltrate) Periodontics Advanced lesion with bone loss and epithelial migration from the cementoenamel junction ( plasma cell density > 50%)

28. HEALTHY GINGIVA Super healthy or ‘‘pristine’’ state- histologically has little or no inflammatory infiltrate. It occurs in ideal conditions. ‘‘Clinically healthy’’ gingiva- looks similar clinically, but histologically has features of some inflammatory infiltrate . It is the healthy gingiva we see clinically in everyday situations. (Initial Lesion)

29. STAGE I :THE INITIAL LESION First manifestations are vascular changes: ‘vasodilatation, increased blood flow, increased vascular permeability’ Clinically not apparent: subclinical gingivitis

30. MICROSCOPICALLY - Widening of small capillaries or venules , adherence of neutrophils (PMNs) to vessel walls ( margination ) occur within 1 week and sometimes as early as 2 days after plaque accumulation PMNs leave the capillaries by migrating through the walls. From the connective tissue , they move through the junctional epithelium to the gingival sulcus to kill microbes

31. Increased vascular permeability causes the exudation of fluid (plasma) from the gingival sulcus. This leads to increased Gingival crevicular fluid (GCF) flow Increased GCF flow is the first sign of gingivitis, though it is not visible as its amount is very less.

32. STAGE II : THE EARLY LESION Clinical signs of erythema (redness) appear owing to proliferation of capillaries and increased formation of capillary loops. Bleeding on probing evident. It is the second sign of gingivitis but first objective (visible by patient) sign.

33. MICROSCOPICALLY Microscopic examination of the gingiva reveals a leukocyte infiltration in connective tissue below the epithelium, consisting of mainly lymphocytes (75%, with majority of them T cells ) and less of neutrophils , macrophages, plasma cells and mast cells. All the changes seen in initial lesion continue to intensify.

34. The junctional epithelium becomes densely infiltrated with neutrophils, as does the gingival sulcus. The junctional epithelium may begin to show development of rete pegs and ridges to increase the surface area of attachment.

35. Increased amount of collagen destruction (>70%) Circular and dento -gingival groups of gingival fibers are most severely affected Fibroblast show reduced collagen production

36. STAGE III : THE ESTABLISHED LESION It is a chronic stage of gingivitis. Blood vessels become engorged and congested, venous return is impaired and blood flow becomes sluggish . Stasis of blood leads to breakdown of hemoglobin leading to bluish hue

37. Microscopically Plasma cells (10-30%) are the predominant inflammatory cell type The junctional epithelium reveals widened intercellular spaces filled with granular cellular debris, including lysosomes derived from disrupted PMNs, lymphocytes and monocytes. The lysosomes contain acid hydrolases that can destroy its tissue components. The junctional epithelium develops rete pegs or ridges that protrude into the connective tissue and the basal lamina is destroyed in some areas.

38. Collagen fibers are destroyed around the infiltrate of inflammatory cells(disrupted plasma cells, PMNs , lymphocytes, monocytes and mast cells) Upto this stage, gingivitis is reversible

39. STAGE IV : THE ADVANCED LESION Extension of the lesion into alveolar bone Phase of periodontal breakdown Gingivitis will progress to this stage (periodontitis) only in individuals who are susceptible.

40. STAGE IV : THE ADVANCED LESION Irreversible stage Predominance of plasma cells > 50% Junctional epithelium infiltrated by increasing number of PMNs, unable to hold itself as lysosomes derived from disrupted PMNs contain acid hydrolases that can destroy its tissue component attachments to tooth, leading to its apical movement causing clinical attachment loss (Periodontitis)

41. Stage Time (days) Blood vessels Junctional/ sulcular epithelium Predominant Immune cells collagen Clinical findings I. Initial lesion 2-4 Vascular dilation vasculitis Infiltrated by PMNs PMNs Perivascular loss Gingival fluid flow II. Early lesion 4-7 Vascular proliferation Same as stage I Rete peg formation Atrophic areas lymphocytes Increased loss around infiltrate Erythema Bleeding on probing

42. Stage Time (days) Blood vessels Junctional/ sulcular epithelium Predominant immune cells collagen Clinical findings III. Established lesion 14-21 Same as stage II, plus blood stasis Same as stage II but more advanced Plasma cells Continued loss Changes in color, size, texture, etc.

43. BIOCHEMICAL CHANGES

44. BIOCHEMICAL CHANGES IN CHRONIC GINGIVITIS acid and alkaline phosphatase, ß-glucuronidase , ß - glucosidase , ß-galactosidase , esterases , aminopeptidase and cytochrome oxidase. Neutral mucopolysaccharide levels are decreased, presumably as a result of degradation of the ground substance.

45. CLINICAL FEATURES

46. CLINICAL CHARACTERISTICS 5 cardinal signs of inflammation: redness (rubor) swelling (tumor) heat (calor) pain (dolor) loss of function (functio laesa).

47. CLINICAL CHARACTERISTICS There are 3 other signs with potential diagnostic value: bleeding on probing suppuration gingival exudate (increase in GCF) and ulceration. All cases of gingivitis must have one or more of these 9 clinical signs of inflammation.

48. CLINICAL FINDINGS Normal gingiva Gingivitis Color Pale pink ( melanin pigmentation common in certain groups) Reddish / Bluish red Size Papillary gingiva fills interdental spaces ; marginal gingiva forms knife edge with tooth surface ; sulcus depth < 3mm Swelling both coronally and buccolingually ; false pocket formation

49. CLINICAL FINDINGS Normal gingiva Gingivitis Shape Surface Texture Scalloped - troughs in marginal areas rise to peaks in interdental areas Stippling present Edema which blunts the marginal and papillary tissues leads to loss of knife edge margins Stippling absent Consistency Firm, Resilient Soft; pressure induced pitting due to edema Tendency to bleed No bleeding on probing Bleeding on probing

50. 1. INCREASED GCF Increase in GCF is first clinical sign of gingivitis but is not visible by naked eye, so not a objective sign Increased vascular permeability causes the exudation of fluid (plasma) from the gingival sulcus. This leads to increased Gingival crevicular fluid (GCF) flow Observed in ‘Initial Lesion’ as discussed

51. 2. GINGIVAL BLEEDING Gingival Bleeding on Probing is the second sign of gingivitis , but it is the first visual sign of gingivitis Observed in ‘Early Lesion’ as discussed

52. GINGIVAL BLEEDING SIGNIFICANCE Earliest visual sign of inflammation A ppear earlier than color change or any other visual signs of inflammation. More objective sign (seen by patient) The severity and ease with which bleeding can be provoked indicates the intensity of the inflammation. Also its presence indicates that disease is active at that site

53. GINGIVAL BLEEDING Can occur in three conditions 1. Chronic inflammation ( eg . Accumulation of plaque) (CHRONIC BLEEDING) 2. Acute conditions (ACUTE BLEEDING) 3. Due to systemic diseases (GINGIVAL BLEEDING DUE TO SYSTEMIC CONDITIONS)

54. 1. Chronic and Recurrent Bleeding Lang et al demonstrated that any force greater than 0.25 N may evoke bleeding in an healthy sites with an intact periodontium . Thus the probing force should be ≤0.25N

55. 2. Acute Bleeding O ccur spontaneously by injury or in acute gingival disease like acute necrotizing ulcerative gingivitis Laceration of the gingiva by toothbrush bristles during aggressive tooth brushing or by sharp pieces of hard food. Gingival burns from hot foods or chemicals

56. 3. In some systemic disorders, gingival bleeding occurs spontaneously or after irritation and is excessive and difficult to control.

57. HISTOLOGIC FINDINGS In the epithelium: Thinning and micro-ulcerations of the sulcular epithelium. Thinning of the epithelium occurs due to the toxic substances released by plaque bacteria that destroys the inter­cellular junctions. Micro-ulcerations are due to bacteria trying to gain entry into the connective tissue by breaking through the epithelium and/or in response to inflammation. The neutrophils from the connective tissue cross the epithelial barrier to reach the site of infection, in doing so they also cause ulceration in sulcular epithelium

58. HISTOLOGIC FINDINGS In the connective tissue Dilation, and engorgement of the capillaries C apillaries are engorged and closer to the sulcular epithelium which is already thinned and less protective, stimuli that are otherwise innocuous can cause rupture of the capillaries which may result in gingival bleeding

59. 3. COLOR CHANGES THIRD SIGN OF GINGIVITIS Color Changes in Chronic Gingivitis. R ed or bluish red color due to vascular proliferation and decreased keratinization or thinning of epithelium V enous stasis (that occur due to chronicity ie . long duration of infection) contribute to bluish hue. The changes start in the interdental papillae spread to gingival margin and then to the attached gingiva.

60. COLOR CHANGES THIRD SIGN OF GINGIVITIS Color Changes in Acute Gingivitis.  Marginal , diffuse or patch like depending on the underlying acute condition. In i nitial stage: Red erythema. If the condition does not worsen, it reverts to normal. In severe acute inflammation: Red color gradually becomes dull , whitish gray due to tissue necrosis

61. COLOR CHANGES Color Changes Associated with Systemic Factors Endogenous Factors: melanin, bilirubin, or iron. I ncrease melanin pigmentation in: Addison's disease, Peutz-jeghers syndrome, Albright‘s syndrome Exogenous factors: atmospheric irritants such as coal/metal dust and coloring agents in food/ lozenges. Tobacco causes hyperkeratosis of the gingiva and increase in melanin pigmentation of oral mucosa. Localized bluish black areas of pigment due to amalgam implanted in the mucosa during restoration (amalgam tatoo )

62. COLOR CHANGES Metallic Pigmentation Occurs in patients working in metal industry as they contain metal in their blood. (It is not toxicity and normal condition) Occur only in inflamed gingiva and disappears after scaling and root planing . In inflammation due to increase in vascular permeability, plasma comes out along with metal in it. These metals form metallic sulphides in peri vascular areas giving color to gingiva

63. Metallic Pigmentation When inflammation subsides, vascular permeability decreases and the discoloration disappears. So treatment in these patients is only scaling and root planing This is different from tattooing produced by the accidental embedding of amalgam or other metal fragments.

64. 4. CONSISTENCY Normal : Firm & resilient. Resiliency is the property in which when we press the gingiva, it comes back to its original position. Gingivitis : Soft & edematous with necrosis in acute gingivitis Firm & leathery in chronic mainly in smokers because of vasoconstriction caused by nicotine. Normal Finding: C hronic inflammation (fibrosis) with overlying acute inflammation (e dematous/swollen gingiva) due to plaque accumulation

65. CHANGES IN THE CONSISTENCY OF GINGIVA Clinical changes Chronic gingivitis 1. Soggy puffiness that pits o n pressure 2. Marked softness and friability , with ready fragmentation and pinpoint surfaces of redness with probe and desquamation. 3. Firm , leathery consistency . Loss of resiliency. Underlying microscopic features 1. Infiltration of connective tissue by fluid (due to increased vascular permeability) and cells of inflammatory exudates. 2. Degeneration of connective tissue and epithelium by microbial infiltration, toxins and inflammatory exudates; Engorged edematous connective tissue, thinning of epithelium, leucocyte invasion, epithelial rete pegs are elongated to connective tissue. Fibrosis and epithelial proliferation due to long standing chronic inflammation .

66. CHANGES IN THE CONSISTENCY OF GINGIVA Clinical changes Acute gingivitis 1. Diffuse puffiness and softening. 2. Sloughing of grayish, flake like particles of debris adhering to eroded surface. 3. Vesicle formation Underlying microscopic features 1. Diffuse edema by acute inflammatory cells 2. Necrosis by formation of pseudo membrane (consisting of bacteria, polymorphonuclear leucocytes, and degenerated epithelial cells) in fibrous meshwork. 3. Intercellular and intracellular edema with degeneration of nucleus, cytoplasm and rupture of cell wall.

67. 5. CHANGES IN SURFACE TEXTURE OF GINGIVA Loss of surface stippling - early sign of gingivitis In inflammation - Surface is either smooth and shiny (in edematous gingiva) (Acute) or firm and nodular (in fibrotic gingiva) (Chronic) In C hronic D esquamative gingivitis - Peeling of the surface occurs Hyperkeratosis - Leathery texture, D rug-induced gingival overgrowth - Nodular surface.

68. STIPPLING ALSO CALLED AS ‘ORANGE PEEL APPEARANCE’ Microscopically it is seen as elevations and depressions of gingiva due to connective tissue papilla and epithelial rete pegs at interface of epithelium and connective tissue. EXAMINATION It is seen clearly with naked eye after drying the gingiva with cotton to minimize refraction of light caused by salivary layer. And its better to visualize in sunlight than in dental chair light.

69. STIPPLING I n inflammation, due to increased vascular permeability, plasma comes out of blood vessels and gets collected in connective tissue. The resulting edema in connective tissue flattens the junction (epithelium and connective tissue) leading to disappearance of stippling.

70. STIPPLING Presence of stippling is more important than its absence. Its presence always means healthy gingiva But its absence does not always means inflammation. Because it is absent in children below five years and disappears in old age

71. 6. CHANGES IN THE POSITION OF GINGIVA R ecession is the change in position of gingiva . I t is exposure of the root surface by an apical shift in the position of the gingiva. Position of the gingiva can be actual or apparent. Actual position is the level of epithelial attachment ( junctional epithelium) on the tooth i.e., from the cemento -enamel junction to the probable depth of the pocket. A pparent position is the level of crest of the gingival margin i.e., from the cemento -enamel junction to the gingival margin.

72. CLINICAL SIGNIFICANCE Exposed root surfaces are susceptible to Caries. Abrasion or erosion causing increased sensitivity Hyperemia of the pulp (Pulpitis) P laque accumulation.

73. 7. CHANGES IN GINGIVAL CONTOUR Normal : Marginal gingiva: scalloped and knife edged , Interdental papilla in anterior region: pyramidal; posteriorly: tent- shaped Factors affecting contour: - Shape of teeth - Alignment in the arch - Location & size of proximal contact Disease : M arginal gingiva: rounded or rolled I nterdental papilla: blunt and flat.

74. S calloped and knife edged margin makes the gingiva self cleansing as during chewing, food gets deflected away from the margins of gingiva and keep it plaque free R ounded or rolled margins cause plaque accumulation into the margins, causing gingivitis

75. Other changes in gingival contour Stillman's clefts and McCall festoons (life preserver- shaped enlargement of the margin).

76. Stillman's clefts: It is apostrophe (triangular) shaped indentations extending from and into the gingival margins. Occurs on facial surface of one or two teeth. It causes gingival recession exposing the cementum of root surface. When it reaches the mucogingival junction, the apical end becomes inflamed due to difficulty in maintaining plaque control. Gingival margin is blunt instead of knife edge Etiology : First described by Stillman to be caused by trauma from occlusion. But later Box described it as pathologic pockets in which ulcerative process has extended to the facial surface of gingiva. Treatment include G ingivoplasty or Gingivectomy if it is shallow and narrow. But if it is wide then Lateral pedicle or Connective tissue graft is required to cover the recession defect.

77. McCall festoons are life preserver- shaped enlargement of the margin of gingiva. Occurs mainly on buccal surface of incisors and premolars. Described by John Oppie McCall in1922. Thought to be due to trauma from occlusion. But now it is considered to be associated with inflammation of marginal gingiva due to accumulation of plaque.

78. 8 . SIZE Sum total of cellular & intercellular elements. Increases during gingival inflammation.

79. Scoring of gingival enlargement (increased size) Grade 0 : No signs of gingival enlargement Grade I : Enlargement confined to interdental papilla Grade II : Enlargement involves papilla and marginal gingiva. Grade III : Enlargement covers three quarters or more of the crown

80. COMPONENTS OF GINGIVAL INFLAMMATION Thus the two components are the acute inflammatory component, with vasodilation, edema, and polymorphonuclear (PMNs) infiltration Long standing inflammation leads to chronic inflammatory component, with B and T lymphocytes and capillary proliferation with fibrosis.

81. The more inflamed a gingival unit appears clinically, the better the chances of therapeutic measures resulting in a return to normal gingival health