Clinical features and stages of gingivitis

Described here are the clinical features of gingiva, the various stages of gingivitis and the clinical features associated with them. The microscopic features have been described on a different slide presentation.

1. DR.NEHA PRITAM 1 ST YEAR MDS PGT DEPARTMENT OF PERIODONTICS HIDSAR CLINICAL FEATURES AND STAGES OF GINGIVITIS

2. CLINICAL FEATURES OF GINGIVA COLOR PHYSIOLOGIC PIGMENTATION(MELANIN) SIZE CONTOUR SHAPE CONSISTENCY SURFACE TEXTURE POSITION STAGES OF GINGIVITIS STAGE I STAGE II STAGE III STAGE IV CLINICAL FEATURES OF GINGIVITIS CONTENTS

3. The gingiva is the part of the oral mucosa that covers the alveolar processes of the jaws and surrounds the necks of the teeth . In an adult, normal gingiva covers the alveolar bone and tooth root to a level just coronal to the cementoenamel junction . GINGIVA

4. The gingiva is divided anatomically into marginal, attached, and interdental areas .

5. MARGINAL GINGIVA The marginal, or unattached gingiva is the terminal edge or border of the gingiva surrounding the teeth in collarlike fashion. In about 50% of cases, it is demarcated from the adjacent attached gingiva by a shallow linear depression, the free gingival groove. Usually about 1 mm wide, the marginal gingiva forms the soft tissue wall of the gingival sulcus. It may be separated from the tooth surface with a periodontal probe.

6. In clinically healthy human gingiva, a sulcus of some depth can be found. The depth of this sulcus, as determined in histologic sections, has been reported as 1.8 mm, with variations from 0 to 6 mm

7. ATTACHED GINGIVA The attached gingiva is continuous with the marginal gingiva. It is firm, resilient, and tightly bound to the underlying periosteum of alveolar bone. The facial aspect of the attached gingiva extends to the relatively loose and movable alveolar mucosa and is demarcated by the mucogingival junction .

8. 000 The width of the attached gingiva on the facial aspect differs in different areas of the mouth. It is generally greatest in the incisor region (3.5 to 4.5 mm in maxilla, 3.3 to 3.9 mm in mandible), and narrower in the posterior segments (1.9 mm in maxillary and 1.8 mm in mandibular first premolars ).

9. INTERDENTAL GINGIVA The interdental gingiva occupies the gingival embrasure, which is the interproximal space beneath the area of tooth contact. The interdental gingiva can be pyramidal or can have a “col” shape. In the former the tip of one papilla is located immediately beneath the contact point; the latter presents a valleylike depression that connects a facial and lingual papilla and conforms to the shape of the interproximal contact.

10. In the premolar/molar regions of the dentition, the teeth have approximal contact surfaces rather than contact points. Since the interdental papilla has a shape in conformity with the outline of the interdental contact surfaces, a concavity —a col — is established in the premolar and molar regions.Thus , the interdental papillae in these areas often have one vestibular (VP) and one lingual/ palatal portion (LP) separated by the col region.

11. CLINICAL FEATURES OF GINGIVA

12. COLOR PHYSIOLOGIC PIGMENTATION(MELANIN) SIZE CONTOUR SHAPE CONSISTENCY SURFACE TEXTURE POSITION CLINICAL FEATURES OF GINGIVA

13. The color of the attached and marginal gingiva is generally described as “coral pink” . The alveolar mucosa is red, smooth, and shiny rather than pink and stippled . COLOR

14. H emoglobin -derived brown pigment. R esponsible for the normal pigmentation of the skin, gingiva, and remainder of the oral mucous membrane . Melanin pigmentation in the oral cavity is prominent in black individuals. Ascorbic acid directly downregulates melanin pigmentation in gingival tissues. PHYSIOLOGIC PIGMENTATION MELANIN

15. The size of the gingiva corresponds with the sum total of the bulk of cellular and intercellular elements and their vascular supply. Alteration in size is a common feature of gingival disease . CONTOUR The contour or shape of the gingiva varies considerably and depends on the shape of the teeth and their alignment in the arch, the location and size of the area of proximal contact, and the dimensions of the facial and lingual gingival embrasures. SIZE

16. The marginal gingiva envelops the teeth in collarlike fashion and follows a scalloped outline on the facial and lingual surfaces. On teeth in lingual version, the gingiva is horizontal and thickened .

17. The shape of the interdental gingiva is governed by the contour of the proximal tooth surfaces and the location and shape of gingival embrasures . When the proximal surfaces of the crowns are relatively flat faciolingually , the roots are close together, the interdental bone is thin mesiodistally , and the gingival embrasures and interdental gingiva are narrow mesiodistally . SHAPE

18. Conversely, with proximal surfaces that flare away from the area of contact, the mesiodistal diameter of the interdental gingiva is broad . The height of the interdental gingiva varies with the location of the proximal contact. Thus, in the anterior region of the dentition, the interdental papilla is pyramidal in form, whereas the papilla is more flattened in a buccolingual direction in the molar region.

19. The gingiva is firm and resilient and with the exception of the movable free margin, tightly bound to the underlying bone. The collagenous nature of the lamina propria and its contiguity with the mucoperiosteum of the alveolar bone determine the firmness of the attached gingiva. The gingival fibers contribute to the firmness of the gingival margin. CONSISTENCY

20. SURFACE TEXTURE The gingiva presents a textured surface similar to an orange peel and is referred to as being stippled . Stippling is best viewed by drying the gingiva. The attached gingiva is stippled; the marginal gingiva is not . The central portion of the interdental papillae is usually stippled, but the marginal borders are smooth. The pattern and extent of stippling vary among individuals and different areas of the same mouth.

21. Stippling is less prominent on lingual than facial surfaces and may be absent in some persons . Stippling varies with age. It is absent in infancy, appears in some children at about 5 years of age, increases until adulthood, and frequently begins to disappear in old age . Microscopically, stippling is produced by alternate rounded protuberances and depressions in the gingival surface. The papillary layer of the connective tissue projects into the elevations, and the elevated and depressed areas are covered by stratified squamous epithelium . The degree of keratinization and the prominence of stippling appear to be related STIPPLING

22. Stippling is a form of adaptive specialization or reinforcement for function. It is a feature of healthy gingiva, and reduction or loss of stippling is a common sign of gingival disease. When the gingiva is restored to health after treatment, the stippled appearance returns . The surface texture of the gingiva is also related to the presence and degree of epithelial keratinization. Keratinization is considered a protective adaptation to function. It increases when the gingiva is stimulated by toothbrushing . However, research on free gingival grafts has shown that when connective tissue is transplanted from a keratinized area to a nonkeratinized area, it becomes covered by a keratinized epithelium.

23. Gingival biopsy of patient demonstrating alternate elevations and depressions(arrows) in the attached gingiva responsible for stippled appearance.

24. When the tooth erupts into the oral cavity, the margin and sulcus are at the tip of the crown; as eruption progresses, they are seen closer to the root. During this eruption process, as described earlier, the junctional epithelium, oral epithelium , and reduced enamel epithelium undergo extensive alterations and remodeling while maintaining the shallow physiologic depth of the sulcus. Without this remodeling of the epithe- lia , an abnormal anatomic relationship between the gingiva and the tooth would result. POSITION

25. Pathologic changes in gingivitis are associated with the presence of oral microorganisms attached to the tooth and perhaps in or near the gingival sulcus . The sequence of events cumulating in clinically apparent gingivitis is categorized into initial, early, and established stages, with periodontitis designated as the advanced stage . GINGIVAL INFLAMMATION

26. STAGES OF GINGIVITIS

27. The first manifestations of gingival inflammation are vascular changes consisting of dilated capillaries and increased blood flow . These initial inflammatory changes occur in response to microbial activation of resident leukocytes and the subsequent stimulation of endothelial cells. Clinically, this initial response of the gingiva to bacterial plaque (subclinical gingivitis) is not apparent . Subtle changes can also be detected in the junctional epithelium and perivascular connective tissue at this early stage. For example, the perivascular connective tissue matrix becomes altered, and there is exudation and deposition of fibrin in the affected area.Also , lymphocytes soon begin to accumulate. STAGE I GINGIVITIS: THE INITIAL LESION

28. Classic features of acute inflammation can be seen in the connective tissue beneath the junctional epithelium. Changes in blood vessel morphologic features (e.g., widening of small capillaries or venules ) and adherence of neutrophils to vessel walls ( margination ) occur within 1 week and sometimes as early as 2 days after plaque has been allowed to accumulate. Leukocytes, mainly polymorphonuclear neutrophils (PMNs), leave the capillaries by migrating through the walls ( diapedesis , emigration ). They can be seen in increased quantities in the connective tissue, the junctional epithelium, and the gingival sulcus. Exudation of fluid from the gingival sulcus and extravascular proteins are present. MICROSCOPICALLY

29. Human biopsy sample ,experimental gingivitis. After 4days of plaque accumulation,the blood vessels immediately adjacent to the junctional epithelium are distended and contains polymorphonuclear leukocytes( PMNs,neutrophils ). Neutrophils have also migrated between the cells of the junctional epithelium(JE). OSE,Oral sulcular epithelium.

30. The early lesion evolves from the initial lesion within about 1 week after the beginning of plaque accumulation . Clinical signs of erythema may appear, mainly because of the proliferation of capillaries and increased formation of capillary loops between rete pegs or ridges. Bleeding on probing may also be evident. Gingival fluid flow and the numbers of transmigrating leukocytes reach their maximum between 6 and 12 days after the onset of clinical gingivitis. STAGE II GINGIVITIS: THE EARLY LESION Marginal gingivitis and irregular gingival contour .

31. The amount of collagen destruction increases; 70% of the collagen is destroyed around the cellular infiltrate . Main fiber groups affected- circular and dentogingival fiber assemblies . Alterations in blood vessel morphologic features and vascular bed patterns have also been described.

32. PMNs that have left the blood vessels in response to chemotactic stimuli from plaque components travel to the epithelium, cross the basement lamina, and are found in the epithelium, emerging in the pocket area .PMNs are attracted to bacteria and engulf them in the process of phagocytosis . PMNs release their lysosomes in association with the ingestion of bacteria. Fibroblasts show cytotoxic alterations, with a decreased capacity for collagen . Meanwhile, on the opposite side of molecular events, collagen degradation is related to matrix metalloproteins (MMPs). Different MMPs are responsible for extracellular matrix remodeling within 7 days of inflammation, which is directly related to MMP-2 and MMP-9 production and activation.

33. Examination of the gingiva reveals a leukocyte infiltration in the connective tissue beneath the junctional epithelium, consisting mainly of lymphocytes (75%, with the majority T cells) but also composed of some migrating neutrophils, as well as macrophages, plasma cells, and mast cells. All the changes seen in the initial lesion continue to intensify with the early lesion.The junctional epithelium becomes densely infiltrated with neutrophils, as does the gingival sulcus, and the junctional epithelium may begin to show development of rete pegs or ridges. MICROSCOPICALLY

34. Human biopsy, experimental gingivitis. A , Control biopsy specimen from a patient with good oral hygiene and no detectable plaque accumulation. The junctional epithelium is at the left. The connective tissue ( CT) shows few cells other than fibroblasts, blood vessels, and a dense background of collagen fibers . (×500.) B, Biopsy specimen taken after 8 days of plaque accumulation. The connective tissue is infiltrated with inflammatory cells, which displace the collagen fibers . A distended blood vessel (V) is seen in the center . (×500.) C, After 8 days of plaque accumulation, the connective tissue next to the junctional epithelium at the base of the sulcus shows a mononuclear cell infiltrate and evidence of collagen degeneration (clear spaces around cellular infiltrate). (×500.). D, The inflammatory cell infiltrate at higher magnification. After 8 days of plaque accumulation, numerous small (SL) and medium-sized (ML) lymphocytes are seen within the connective tissue. Most of the collagen fibers around these cells have disappeared, presumably as a result of enzymatic digestion.

35. Over time, the established lesion evolves, characterized by a predominance of plasma cells and B lymphocytes and probably in conjunction with the creation of a small gingival pocket lined with a pocket epithelium. The B cells found in the established lesion are predominantly of the immunoglobulin G1 (IgG1) and G3 ( IgG3)subclasses. STAGE III GINGIVITIS: THE ESTABLISHED LESION

36. Extravasation of erythrocytes into the connective tissue and breakdown of hemoglobin into its component pigments can also deepen the color of the chronically inflamed gingiva. The established lesion can be described as moderately to severely inflamed gingiva.

37. In chronic gingivitis, which occurs 2 to 3 weeks after the beginning of plaque accumulation, the blood vessels become engorged and congested, venous return is impaired, and the blood flow becomes sluggish . The result is localized gingival anoxemia , which superimposes a somewhat bluish hue on the reddened gingiva. Marginal supragingival plaque and gingivitis

38. An intense, chronic inflammatory reaction is observed. Several detailed cytologic studies have been performed on chronically inflamed gingiva. A key feature that differentiates the established lesion is the increased number of plasma cells, which become the preponderant inflammatory cell type. Plasma cells invade the connective tissue not only immediately below the junctional epithelium but also deep into the connective tissue, around blood vessels, and between bundles of collagen fibers . MICROSCOPICALLY

39. The junctional epithelium reveals widened intercellular spaces filled with granular cellular debris, including lysosomes derived from disrupted neutrophils, lymphocytes, and monocytes . The lysosomes contain acid hydrolases that can destroy 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. In the connective tissue, collagen fibers are destroyed around the infiltrate of intact and disrupted plasma cells, neutrophils, lymphocytes, monocytes, and mast cells .

40. Extension of the lesion into alveolar bone characterizes a fourth stage known as the advanced lesion or phase of periodontal breakdown . Patients with experimental gingivitis showed significantly more plaque accumulation, higher IL-1 β, and lower IL-8 concentrations at 28 days . Gingivitis will progress to periodontitis only in individuals who are s usceptible. STAGE IV GINGIVITIS: THE ADVANCED LESION

41. There is fibrosis of the gingiva and widespread manifestations of inflammatory and immunopathologic tissue damage. At the advanced stage, plasma cell presence dominates connective tissue and neutrophils continue dominating the junctional epithelium. MICROSCOPICALLY

42. CLINICAL FEATURES OF GINGIVITIS

43. In general, clinical features of gingivitis may be characterized by the presence of any of the following clinical signs: redness and sponginess of the gingival tissue, bleeding on provocation, changes in contour, and presence of calculus or plaque with no radiographic evidence of crestal bone loss. Histologic examination of inflamed gingival tissue reveals ulcerated epithelium. The presence of inflammatory mediators negatively affects epithelial function as a protective barrier . Repair of this ulcerated epithelium depends on the proliferative or regenerative activity of the epithelial cells. Removal of the etiologic agents triggering the gingival breakdown is essential . CHANGES IN GINGIVAL CONTOUR

44. Gingivitis can occur with sudden onset and short duration and can be painful. A less severe phase of this condition can also occur. Recurrent gingivitis reappears after having been eliminated by treatment or disappeared spontaneously . Chronic gingivitis is slow in onset and of long duration. It is painless, unless complicated by acute or subacute exacerbations, and is the type most often encountered . Chronic gingivitis is a fluctuating disease in which inflammation persists or resolves and normal areas become inflamed. COURSE AND DURATION

45. Localized gingivitis is confined to the gingiva of a single tooth or group of teeth, whereas generalized gingivitis involves the entire mouth. Marginal gingivitis involves the gingival margin and may include a portion of the contiguous attached gingiva . DESCRIPTION

46. Papillary gingivitis involves the interdental papillae and often extends into the adjacent portion of the gingival margin. Diffuse gingivitis affects the gingival margin, the attached gingiva, and the interdental papillae. Papillae are involved more frequently than the gingival margin, and the earliest signs of gingivitis often occur in the papillae.

47. Gingival disease in individual cases is described by combining the preceding terms as follows: • Localized marginal gingivitis is confined to one or more areas of the marginal gingiva . • Localized diffuse gingivitis extends from the margin to the mucobuccal fold in a limited area . • Localized papillary gingivitis is confined to one or more interdental spaces in a limited area.

48. Generalized marginal gingivitis involves the gingival margins in relation to all the teeth. The interdental papillae are usually affected .

49. • Generalized diffuse gingivitis involves the entire gingiva. The alveolar mucosa and attached gingiva are affected, so the mucogingival junction is sometimes obliterated . Systemic conditions can be involved in the cause of generalized diffuse gingivitis and should be evaluated if suspected as an etiologic cofactor.

50. GINGIVAL BLEEDING ON PROBING The two earliest signs of gingival inflammation preceding established gingivitis are (1) increased gingival crevicular fluid production rate and (2) bleeding from the gingival sulcus on gentle probing . CLINICAL FINDINGS Bleeding on probing. A, Mild edematous gingivitis; a probe has been introduced to the bottom of the gingival sulcus. B, Bleeding appears after a few seconds.

51. Gingival bleeding varies in severity, duration, and ease of provocation. Bleeding on probing is easily detected clinically and therefore is of value for the early diagnosis and prevention of more advanced gingivitis. It has been shown that bleeding on probing appears earlier than a change in color or other visual signs of Inflammation . In general, gingival bleeding on probing indicates an inflammatory lesion both in the epithelium and in the connective tissue that exhibits specific histologic differences compared with healthy gingiva. Even though gingival bleeding on probing may not be a good diagnostic indicator for clinical attachment loss, its absence is an excellent negative predictor of future attachment loss. Therefore the absence of gingival bleeding on probing is desirable and implies a low risk of future clinical attachment loss.

52. Gingival Bleeding Caused By Local Factors Contributing factors to plaque retention that may lead to gingivitis include anatomic and developmental tooth variations, caries, frenum pull, iatrogenic factors, malpositioned teeth, mouth breathing, overhangs , partial dentures, lack of attached gingiva, and recession . In addition, orthodontic treatment and fixed retainers were associated with increased plaque retention and increased bleeding on probing.

53. CHRONIC AND RECURRENT BLEEDING The most common cause of abnormal gingival bleeding on probing is chronic inflammation . The bleeding is chronic or recurrent and is provoked by mechanical trauma (e.g., from toothbrushing , toothpicks, or food impaction) or by biting into solid foods such as apples . The severity of bleeding and the ease of its provocation depend on the intensity of the inflammation

54. Hemorrhagic disorders in which abnormal gingival bleeding is encountered include vascular abnormalities (vitamin C deficiency or allergy [e.g., Schönlein-Henoch purpura ]), platelet disorders (thrombocytopenic purpura ), hypoprothrombinemia (vitamin K deficiency ), other coagulation defects ( hemophilia , leukemia , Christmas disease), deficient platelet thromboplastic factor ( PF3) resulting from uremia , multiple myeloma and postrubella purpura . GINGIVAL BLEEDING ASSOCIATED WITH SYSTEMIC CHANGES

55. The effects of hormonal replacement therapy, oral contraceptives, pregnancy, and the menstrual cycle are also reported to affect gingival bleeding. In addition, in women, long-term depression-related stress exposure may increase concentrations of interleukin-6 (IL-6) in gingival crevicular fluid and may worsen periodontal conditions with elevated gingival inflammation and increased pocket depths.

56. F luctuating estrogen /progesterone levels on the periodontium , starting as early as puberty among adolescents . Among pathologic endocrine changes , diabetes is an endocrine condition with a well-characterized effect on gingivitis . Several medications have also been found to have adverse effects on the gingiva. For example, anticonvulsants, antihypertensive ,calcium channel blockers, and immunosuppressant drugs are known to cause gingival enlargement, which secondarily can cause gingival bleeding.

57. The American Heart Association has recommended over-the-counter aspirin as a therapeutic agent for cardiovascular disease, and aspirin is often prescribed for rheumatoid arthritis, osteoarthritis, rheumatic fever, and other inflammatory joint diseases. Thus it is important to consider aspirin’s effect on bleeding during a routine dental examination to avoid false-positive readings, which could result in an inaccurate patient diagnosis .

58. Change in color is an important clinical sign of gingival disease . The normal gingival color is “coral pink” and is produced by the tissue’s vascularity and modified by the overlying epithelial layers. For this reason, the gingiva becomes red when vascularization increases or the degree of epithelial keratinization is reduced or disappears. The color becomes pale when vascularization is reduced (in association with fibrosis of the corium) or epithelial keratinization increases . COLOR CHANGES IN GINGIVITIS

59. Thus chronic inflammation intensifies the red or bluish red color because of vascular proliferation and reduction of keratinization. Additionally, venous stasis will contribute a bluish hue . The gingival color changes with increasing chronicity of the inflammatory process. The changes start in the interdental papillae and gingival margin and spread to the attached gingiva

60. Color changes in acute gingival inflammation differ in both nature and distribution from those in chronic gingivitis. The color changes may be marginal, diffuse, or patchlike , depending on the underlying acute condition . In acute necrotizing ulcerative gingivitis , the involvement is marginal ; in herpetic gingivostomatitis , it is diffuse ; and in acute reactions to chemical irritation, it is patchlike or diffuse .

61. Heavy metals (bismuth, arsenic, mercury , lead, and silver) absorbed systemically from therapeutic use or occupational or household environments may discolor the gingiva and other areas of the oral mucosa. These changes are rare but still should be ruled out in suspected cases. Typically , metals produce a black or bluish line in the gingiva that follows the contour of the margin . The pigmentation may also appear as isolated black blotches involving the interdental, marginal and attached gingiva. This differs from the tattooing produced by the accidental embedding of amalgam or other metal fragments. METALLIC PIGMENTATION

62. Gingival pigmentation from systemically absorbed metals results from perivascular precipitation of metallic sulfides in the subepithelial connective tissue. Gingival pigmentation is not a result of systemic toxicity. It occurs only in areas of inflammation in which the increased permeability of irritated blood vessels permits seepage of the metal into the surrounding tissue . Pigmentation can be eliminated by treating the inflammatory changes without necessarily discontinuing the metal containing medication.

63. Endogenous oral pigmentations can be caused by melanin bilirubin iron . COLOR CHANGES ASSOCIATED WITH SYSTEMIC FACTORS

64. Melanin oral pigmentations can be normal physiologic pigmentations and are often found in highly pigmented ethnic groups . Diseases that increase melanin pigmentation include the following : • Addison’s disease is caused by adrenal dysfunction and produces isolated patches of discoloration varying from bluish black to brown . • Peutz-Jeghers syndrome produces intestinal polyposis and melanin pigmentation in the oral mucosa and lips . • Albright’s syndrome ( polyostotic fibrous dysplasia) and von Recklinghausen’s disease (neurofibromatosis) produce areas of melanin pigmentation

65. Skin and mucous membranes can be stained by bile pigments. Jaundice is best detected by examination of the sclera, but the oral mucosa may also acquire a yellowish color . The deposition of iron in hemochromatosis may produce a blue- gray pigmentation of the oral mucosa. Several endocrine and metabolic disturbances, including diabetes and pregnancy, may result in color changes. Blood dyscrasias , such as anemia , polycythemia , and leukemia , may also induce color changes.

66. Exogenous factors capable of producing color changes in the gingiva include atmospheric irritants, such as coal and metal dust, and coloring agents in food or lozenges. Tobacco causes hyperkeratosis of the gingiva and also may induce a significant increase in melanin pigmentation of the oral mucosa. Localized bluish black areas of pigment are often caused by amalgam implanted in the mucosa

67. Both chronic and acute inflammations produce changes in the normal firm and resilient consistency of the gingiva. As previously noted , in chronic gingivitis, both destructive ( edematous ) and reparative (fibrotic) changes coexist, and the consistency of the gingiva is determined by their relative predominance. CHANGES IN CONSISTENCY OF THE GINGIVA

68. Calcified microscopic masses may be found in the gingiva. They can occur alone or in groups and vary in size, location, shape, and structure. Such masses may be calcified material removed from the tooth and traumatically displaced into the gingiva during scaling,root remnants, cementum fragments , or cementicles . CALCIFIED MASSES IN THE GINGIVA FACTORS AFFECTING THE CONSISENCY OF GINGIVA

69. TOOTHBRUSHING Toothbrushing has various effects on the consistency of the gingiva such as promoting keratinization of the oral epithelium, enhancing capillary gingival circulation, and thickening alveolar bone. Toothbrushing causes an increased turnover rate and desquamation of the junctional epithelial surfaces. This process may repair small breaks in the junctional epithelium and prevent direct access to the underlying tissue by periodontal pathogens

70. The surface of normal gingiva usually exhibits numerous small depressions and elevations, giving the tissue an orange-peel appearance referred as stippling. Stippling is restricted to the attached gingiva and is predominantly localized to the subpapillary area, but it extends to a variable degree into the interdental papilla. Although the biologic significance of gingival stippling is not known , some investigators conclude that loss of stippling is an early sign of gingivitis. CHANGES IN SURFACE TEXTURE OF THE GINGIVA

71. In chronic inflammation the gingival surface is either smooth and shiny or firm and nodular, depending on whether the dominant changes are exudative or fibrotic. Smooth surface texture is also produced by epithelial atrophy in atrophic gingivitis, and peeling of the surface occurs in chronic desquamative gingivitis. Hyperkeratosis results in a leathery texture , and drug-induced gingival overgrowth produces a nodular surface.

72. Traumatic Lesions- One of the unique features of the most recent gingival disease classification is the recognition of non–plaque-induced traumatic gingival lesions as distinct gingival conditions. Traumatic lesions, whether chemical, physical, or thermal , are among the most common lesions in the mouth . CHANGES IN POSITION OF THE GINGIVA

73. Sources of chemical injuries include aspirin, hydrogen peroxide, silver nitrate, phenol, and endodontic materials . Physical injuries can include lip, oral, and tongue piercing, which can result in gingival recession. Thermal injuries can result from hot drinks and foods . In acute cases , the appearance of slough ( necrotizing epithelium), erosion, or ulceration and the accompanying erythema are common features . In chronic cases , permanent gingival defects are usually present in the form of gingival recession. Typically, the localized nature of the lesions and the lack of symptoms readily eliminate them from the differential diagnosis of systemic conditions that may be present with erosive or ulcerative oral lesions.

74. Gingival Recession- Gingival recession is a common finding. The prevalence, extent, and severity of gingival recession increase with age and are more prevalent in males . Positions of the Gingiva- By clinical definition, recession is exposure of the root surface by an apical shift in the position of the gingiva.

75. The actual position is the level of the coronal end of the epithelial attachment on the tooth, whereas the apparent position is the level of the crest of the gingival margin . The severity of recession is determined by the actual position of the gingiva, not its apparent position. For example, in periodontal disease, the inflamed pocket wall covers part of the denuded root; thus some of the recession is hidden and some may be visible. The total amount of recession is the sum of the two.

76. The following etiologic factors have been implicated in gingival recession : faulty tooth brushing technique (gingival abrasion), tooth malposition , friction from soft tissues (gingival ablation ), gingival inflammation , abnormal frenum attachment, and iatrogenic dentistry . Susceptibility to recession is also influenced by the position of teeth in the arch, the root-bone angle, and the mesiodistal curvature of the tooth surface . Trauma from occlusion has been suggested in the past, but its mechanism of action has never been demonstrated. For example, a deep overbite has been associated with gingival inflammation and recession . Excessive incisal overlap may result in a traumatic injury to the gingiva.

77. CLINICAL SIGNIFICANCE -several aspects of gingival recession make it clinically significant. Exposed root surfaces are susceptible to caries. Abration or erosion of cementum exposed by recession leaves an underline dentinal surface which can be sensitive. Hyperemia of the pulp and associated sympotms may also result from eccessive exposure of root surface. Interproximal recession creates oral hygiene problems and resulting plaque accumulation.

78. Changes in gingival contour are primarily associated with gingival enlargement. Of historical interest are the descriptions of indentations of the gingival margin referred to as Stillman’s clefts and the McCall festoons . The term “ Stillman’s clefts ” has been used to describe a specific type of gingival recession consisting of a narrow, triangular-shaped gingival recession. As the recession progresses apically, the cleft becomes broader, exposing the cementum of the root surface. When the lesion reaches the mucogingival junction, the apical border of oral mucosa is usually inflamed because of the difficulty in maintaining adequate plaque control at this site . CHANGES IN GINGIVAL CONTOUR

79. The term “McCall festoons” has been used to describe a rolled, thickened band of gingiva usually seen adjacent to the cuspids when recession approaches the mucogingival junction. Initially, Stillman’s clefts and McCall festoons were attributed to traumatic occlusion, and the recommended treatment was occlusal adjustment. McCall’s Festoons  (right).The attached gingiva consists of nothing more than a collar-like, fibrous thickening (arrow). This may be a tissue response to further recession beyond the mucogingival line.  Stillman Cleft (left) Cleft-like defect of traumatic etiology . Such clefts may spread laterally, creating an area of gingival recession. The exposed root surface may be extremely sensitive. Such clefts are often covered with plaque.

80. TREATMENT OF PLAQUE INDUCED GINGIVITIS The treatment of plaque induced gingivitis is primarily self-administered plaque control. Although mechanical plaque control remains the mainstay for plaque control, chemical control of plaque is an effective option for those individuals who, because of physical or mental disability, cannot effectively apply mechanical means. However , the presence of plaque retaining factors, such as dental calculus or inadequate restorations , may result in either method being ineffective . Professional intervention is needed to eliminate these as an adjunct to self-administered plaque control.

81. RECENT STUDIES

82. Wegener's granulomatosis (WG) is an immunologically mediated inflammatory disease characterized by granulomatous vasculitis of the upper and lower aerodigestive tracts together with glomerulonephritis. Correlation of histopathology with routine hematoxylin and eosin and special stains [ Grocott-Gomori methenamine -silver nitrate and Periodic Acid Schiff (PAS)], Mantoux test, peripheral blood smear and clinical presentation were established in diagnosing this rare entity. By the above-mentioned procedures and methodology, it was arrived at the diagnosis of Wegner's granulomatosis limited to the upper aerodigestive tract . Strawberry gingivitis: A diagnostic feature of gingival Wegener's granulomatosis . R.Heera et al. (2012) Dental R esearch Journal 2012 Dec; 9( Suppl 1): S123–S126.

83. This is the first reported case of WG manifesting as “strawberry gingivitis” in the Indian population. A rare case of gingival WG that presented with erythematous and painful generalized gingival enlargement. Therefore, the aim of reporting this case was to emphasize that, the dental surgeon often being the first person to examine the oral cavity, should be familiar with the typical appearance of gingival WG as “strawberry gingivitis,” its clinical course as well as diagnostic parameters and adequate management.

84. STRAWBERRY GINGIVITIS

85. The decrease in plasminogen level reduces natural fibrinolysis, which causes fibrin deposits on the membranes . This change leads to the formation of pseudomembranous lesions on mucous membranes which impairs normal tissue and its functions. Ligneous conjunctivitis is the most common clinical manifestation of congenital plasminogen deficiency ( CPD). If left untreated, progressive vision loss and even blindness can occur. Ligneous lesions can also be seen in other mucous membranes such as ears, nose, mouth (as gingivitis), cerebral vascular spaces, tonsils, respiratory, gastrointestinal and genitourinary tracts . Plasminogen  deficiency is a rare congenital condition that leads to pseudomembraneous lesions, such as ligneous  conjunctivitis  and ligneous  gingivitis . Because of its rarity, ligneous gingivitis is not a pathology one may easily suspect from its clinical symptoms. Ligneous gingivitis: Hard to diagnose and treat Tiraje Celkan (2019) Pediatric Hematology -Oncology, Cerrahpasa Medical Faculty, Istanbul University Cerrahpasa , Istanbul,Turkey .

86. Ligneous gingivitis

87. The efficacy of several variants of essential oil mouthrinses has been studied extensively. This was the first study to compare the anti-plaque and anti-gingivitis efficacy of two marketed essential oil mouthrinses : one is an alcohol containing mouthrinse and the other one is an alcohol-free mouthrinse . This examiner randomized subjects to three groups: 1) Mechanical Oral Hygiene (MOH) only; 2) MOH plus Alcohol-Containing essential oil Mouthrinse (ACM); 3) MOH plus Alcohol-Free essential oil Mouthrinse (AFM ). A total of 348 subjects completed the study. After six months, subjects using essential oil mouthrinses with or without alcohol showed significant reduction (p < 0.001) in gingivitis (28.2% and 26. 7%, respectively) and significant reduction (p < 0.001) in plaque (37.8% and 37.0%, respectively), compared to those performing MOH only. No statistically significant differences were observed for all measured indices between ACM and AFM groups at any time point. Both mouthrinses were well tolerated. Conclusions : No significant differences were observed in the efficacy of ACM and AFM to reduce plaque and gingivitis, when used in addition to MOH, over six months. The effects of essential oil mouthrinses with or without alcohol on plaque and gingivitis: a randomized controlled clinical study Michael C. Lynch et al. (2018) BMC Oral Health .  2018 Jan 10;18(1):6.

88. This study evaluated the distribution of dental plaque and gingivitis scores within the dental arches after prophylaxis. Enrolled subjects underwent oral examinations for dental plaque (PI) and gingivitis (GI) using the Turesky modification of the Quigley-Hein and the Lo¨e-Silness Index, respectively, at the baseline visit, followed by a whole mouth dental prophylaxis. Subjects were given fluoride toothpaste for twice daily oral hygiene for the next 30 days. Subjects were recalled on days 15 and 30 for PI and GI examinations identical to baseline. Results: Analyses indicated that mean scores for PI and GI on either arch and the whole mouth were higher than 2 and 1, respectively, during all examinations. Anterior surfaces consistently exhibited lower PI scores than posterior regions of either arch, or the entire dentition. Regional GI differences within the dentition were similar to PI scores, with lower scores on anterior than posterior teeth. Differences observed in PI and GI within the dentition have several practical implications: (a) there are advantages of whole mouth assessments for oral health (b) a need for oral hygiene formulations to reduce the larger deposits of dental plaque in the posterior region and resultant gingival inflammation, and (c) a requirement for ongoing oral hygiene education. Distribution of dental plaque and gingivitis within the dental arches. Prem K. Sreenivasan et al. (2017) Journal of International Medical Research

89. Individuals with altered passive eruption (APE) are assumed to be more susceptible to periodontal diseases. To date, this hypothesis has not been sufficiently supported by scientific evidence. The aim of this study, using an experimental gingivitis model, was to examine the development and resolution of gingival inflammation in patients with APE when compared to patients with normal gingival anatomy. Results : During the experimental gingivitis phase (days 0 – 21), the rate of change in gingival inflammation (GI) was dramatically different between the APE test group and the control group. On day 21, at the time of maximum plaque accumulation, the GI of the APE test group was a 109% greater than the GI of the test group (p≤ 0.001) despite similar plaque levels (p = 0.436). During the resolution of inflammation phase (days 22 – 42), the APE test group continued to exhibit statistically higher GI scores than the control group (p=0.029 ). Conclusion: In the presence of similar amounts of plaque deposits and plaque accumulation rates, APE patients exhibited differences in the development and resolution of plaque-induced gingival inflammation when compared to controls. Experimental Gingivitis in Patients with and without Altered Passive Eruption Rustam Aghazada et al. (2019) Section of Periodontics, Department of Oral and Maxillofacial Sciences, “ Sapienza ” University of Rome , Rome, Italy

90. 1.Clinical periodontology- newman,tokei,klokevold 11 th edition 2.Clinical periodontology and implatology-lindhe 4 th edition 3. Celkan T. Ligneous gingivitis: Hard to diagnose and treat. Haemophilia. 2020 Mar;26(2):e49-e50. doi : 10.1111/hae.13924. Epub 2019 Dec 30. PMID: 31886930 . 4. Kaczor-Urbanowicz KE, Trivedi HM, Lima PO, Camargo PM, Giannobile WV, Grogan TR, Gleber-Netto FO, Whiteman Y, Li F, Lee HJ, Dharia K, Aro K, Martin Carreras- Presas C, Amuthan S, Vartak M, Akin D, Al- Adbullah H, Bembey K, Klokkevold PR, Elashoff D, Barnes VM, Richter R, DeVizio W, Masters JG, Wong DTW. Salivary exRNA biomarkers to detect gingivitis and monitor disease regression. J Clin Periodontol . 2018 Jul;45(7):806-817. doi : 10.1111/jcpe.12930. Epub 2018 Jun 15. PMID: 29779262; PMCID: PMC6023773. REFERENCE

91. 5.Sreenivasan PK, Prasad KVV. Distribution of dental plaque and gingivitis within the dental arches. J Int Med Res. 2017 Oct;45(5):1585-1596. doi : 10.1177/0300060517705476. Epub 2017 Aug 10. PMID: 28795618; PMCID: PMC5718714 . 6. Aghazada R, Marini L, Zeza B, Trezza C, Vestri A, Mariotti A, Pilloni A. Experimental gingivitis in patients with and without altered passive eruption. J Periodontol . 2020 Jul;91(7):938-946. doi : 10.1002/JPER.19-0443. Epub 2019 Dec 29. PMID: 31833068 . 7. Lynch MC, Cortelli SC, McGuire JA, Zhang J, Ricci- Nittel D, Mordas CJ, Aquino DR, Cortelli JR. The effects of essential oil mouthrinses with or without alcohol on plaque and gingivitis: a randomized controlled clinical study. BMC Oral Health. 2018 Jan 10;18(1):6. doi : 10.1186/s12903-017-0454-6. PMID: 29321067; PMCID: PMC5763666 . 8. Msallem B, Bassetti S, Matter MS, Thieringer FM. Strawberry gingivitis: Challenges in the diagnosis of granulomatosis with polyangiitis on gingival specimens. Oral Surg Oral Med Oral Pathol Oral Radiol . 2019 Dec;128(6):e202-e207. doi : 10.1016/j.oooo.2019.07.015. Epub 2019 Aug 2. PMID: 31501032.