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  3. 3. • An increase in size of the gingiva is a common feature of gingival disease. The accepted current terms for this condition are gingival enlargement and gingival overgrowth. • These are strictly clinical descriptive terms, and they avoid the erroneous pathologic connotations of terms used in the past, such as hypertrophic gingivitis and gingival hyperplasia. • Accroding to Glossary of Periodontal Terms: • “An overgrowth or increase in size of the gingiva”.
  4. 4. The many types of gingival enlargement can be classified according to etiologic factors and pathologic changes as follows: I. Inflammatory enlargement A. Chronic B. Acute II. Drug-induced enlargement A. Anticonvulsants B. Immunosuppressants C. Calcium channel blockers
  5. 5. III. Enlargements associated with systemic diseases or conditions A. Conditioned enlargement 1. Pregnancy 2. Puberty 3. Vitamin C deficiency 4. Plasma cell gingivitis 5. Nonspecific conditioned enlargement (pyogenic granuloma) B. Systemic diseases that cause gingival enlargement 1. Leukemia 2.Granulomatous diseases (e.g., Wegener’s granulomatosis, sarcoidosis) IV. Neoplastic enlargement (gingival tumors) A. Benign tumors B. Malignant tumors V. False enlargement
  6. 6. With the use of the criteria of location and distribution, gingival enlargement is designated as follows: Localized: Limited to the gingiva adjacent to a single tooth or group of teeth Generalized: Involving the gingiva throughout the mouth Marginal: Confined to the marginal gingiva Papillary: Confined to the interdental papilla Diffuse: Involving the marginal and attached gingiva and papillae Discrete: An isolated sessile or a pedunculated, tumor-like enlargement
  7. 7. Angelopoulos and Goaz (1972) described an index for measuring the vertical component of gingiva. Three grades based on the enlargement covering the clinical crown were described as: Grade 0: None. Grade I: Not more than 1/3rd of the clinical crown covered. Grade II: Any part of the middle third of the crown covered. Grade III: Greater than 2/3rd of the crown covered.
  8. 8. Miller and Damm (1992) modified the original Angelopoulos and Goaz index for enhanced assessment of gingival overgrowth. Vertical component Horizontal component The vertical gingival overgrowth index is described as: Grade 0: Normal gingival, no alteration Grade 1: Minimal overgrowth, ≤ 2mm, gingiva covering the cervical third or less of the anatomic crown. Grade 2: Moderate overgrowth: 2 to 4 mm, gingival covering the middle third of the anatomic crown. Grade 3: Severe overgrowth: ≥4mm, nodular growth, gingival covering more than two thirds of the dental crown. The horizontal gingival overgrowth index is described as: Grade 0: < 1mm Grade 1: 1 to 2 mm Grade 2: > 2 mm
  9. 9. Bokenkamp A and Bohnhorst B (1994) categorized gingival overgrowth dimensions into the following grades: Grade 0: No signs of gingival overgrowth Grade I: Gingival hyperplasia confined to interdental papilla Grade II: Hyperplasia of interdental papilla and marginal gingival Grade III: Gingival hyperplasia covering at least three- quarters of tooth crowns
  10. 10. Eva and Ingles (1999) introduced a new index for measuring gingival overgrowth caused due to drugs. In this index for standardization, the buccal and lingual papillae were scored separately. The criteria by which scores were divided are as mentioned below: Grade 0:  No overgrowth, firm adaptation of the attached gingiva to the underlying alveolar bone.  There is slight stippling; there is no granular appearance.  A knife-edged papilla is present toward the occlusal surface and no increase in density or size of the gingiva. 
  11. 11. Grade 1: Early overgrowth, as evidenced by an increase in density of the gingiva with marked stippling and granular appearance. The tip of the papilla is rounded and the probing depth is less than or equal to 3mm.
  12. 12. Grade 2: Moderate overgrowth, manifested by an increase in the size of the papilla and/ or rolled gingival margins. The contour of the margin is still concave or straight. Also the enlargement has a bucco-lingual dimension of up to 2mm, measured from the tip of the papilla outward. The probing depth is equal to or less than 6 mm and the papilla is somewhat retractable.
  13. 13. Grade 3: Marked overgrowth, represented by encroachment of the gingiva onto the clinical crown. Contour of the margin is convex rather than concave. The enlargement has a bucco-lingual dimension of approximately 3 mm or more, measured from the tip of the papilla outward. The probing depth is greater than 6mm and the papilla is clearly retractable.
  14. 14. Grade 4: • Severe overgrowth, characterized by a profound thickening of the gingiva. • A large percentage of the clinical crown is covered. • The papilla is retractable, the probing depth is greater than 6 mm and the buccolingual dimension is approximately 3 mm.
  15. 15. • Inflammatory enlargements are usually a secondary complication of any of the other types of enlargement, thereby creating a combined gingival enlargement. • In these cases, it is important to understand the double etiology and to treat both causes adequately. Chronic Inflammatory Enlargement Etiology • Prolonged exposure to dental plaque. • Poor oral hygiene, • Irritation by anatomic abnormalities, • Improper restorative and orthodontic appliances.
  16. 16. Clinical Features  Slight ballooning of the interdental papilla and marginal gingiva.  In the early stages, it produces a life-preserver – shaped bulge around the involved teeth. This bulge can increase in size until it covers part of the crowns  Discrete sessile or pedunculated mass that resembles a tumor.  It may be interproximal or on the marginal or attached gingiva.  The lesions are slow-growing masses, and they are usually painless.
  17. 17. Histopathology • Chronic inflammatory gingival enlargements show the exudative and proliferative features of chronic inflammation. • They also have a preponderance of inflammatory cells and fluid, with vascular engorgement, new capillary formation, and associated degenerative changes. • Lesions that are relatively firm, resilient, and pink have a greater fibrotic component with an abundance of fibroblasts and collagen fibers.
  18. 18. Gingival Changes Associated with Mouth Breathing. • The gingiva appears red and edematous, with a diffuse surface shininess of the exposed area. • The maxillary anterior region is the common site of such involvement. • In many cases, the altered gingiva is clearly demarcated from the adjacent unexposed normal gingiva.
  19. 19. GINGIVAL ABCESS Etiology. • Bacteria carried deep into the tissues when a foreign substance (e.g., toothbrush bristle, piece of apple core, lobster shell fragment) is forcefully embedded into the gingiva. • The lesion is confined to the gingiva and should not be confused with periodontal or lateral abscesses. CLINICAL FEATURE: • A gingival abscess is a localized, painful, rapidly expanding lesion that usually has a sudden onset. • It is generally limited to the marginal gingiva or the interdental papilla.
  20. 20. • In its early stages, it appears as a red swelling with a smooth, shiny surface. Within 24 to 48 hours, the lesion usually becomes fluctuant and pointed, with a surface orifice from which a purulent exudate may be expressed. • The adjacent teeth are often sensitive to percussion. If permitted to progress, the lesion generally ruptures spontaneously.
  21. 21. Histopathology. • The gingival abscess consists of a purulent focus in the connective tissue surrounded by a diffuse infiltration of polymorphonuclear leukocytes, edematous tissue, and vascular engorgement. • The surface epithelium has varying degrees of intracellular and extracellular edema, invasion by leukocytes, and sometimes ulceration.
  22. 22. Drug-induced gingival overgrowth was first reported in 1939 (Kimball 1939) Clinically and histologically, gingival overgrowth induced by different drugs, are virtually indistinguishable (Wysocki et al, 1983. Tyldesley & Rotter 1984) However, the prevalence of this unwanted effect does show differences between the agents, with approximately 50% of patients medicated with phenytoin experiencing significant gingival changes (Angeiopoulous & Goaz 1972), whilst the figures for cyclosporin and nifedipine are closer to 30% and 20% respectively (Seymour et al, 1987, Barclay ct ai, 1992).
  23. 23. Anticonvulsants: Hydantoins Ethotonin Mephenytoin Phenytoin Succinimide Ethosuximide Methsuximide Phensuximide Valproic acid Valproic acid Immunosuppressants: Cylcosporine A Calcium channel blockers: Dehydropyridine derivatives Amlodipine Felodipine Nicardipine Verapamil Diltiazem
  24. 24. Clinical Features: The growth starts as a painless, beadlike enlargement of the interdental papilla that then extends to the facial and lingual gingival margins. As the condition progresses, the marginal and papillary enlargements unite, and they may develop into a massive tissue fold that covers a considerable portion of the crowns; this may interfere with occlusion. When uncomplicated by inflammation, the lesion is mulberry shaped, firm, pale pink, and resilient, with a minutely lobulated surface and no tendency to bleed.
  25. 25. The enlargement characteristically appears to project from beneath the gingival margin, from which it is separated by a linear groove. However, the presence of the enlargement makes plaque control difficult, often resulting in a secondary inflammatory process that complicates the gingival overgrowth caused by the drug.
  26. 26. The resultant enlargement then becomes a combination of the increase in size caused by the drug and the complicating inflammation caused by bacteria. Secondary inflammatory changes not only add to the size of the lesion caused by the drug but also produce a red or bluish-red discoloration, obliterate the lobulated surface demarcations, and increase bleeding tendency.
  27. 27. • The enlargement is usually generalized throughout the mouth, but it is more severe in the maxillary and mandibular anterior regions. • It occurs in areas in which teeth are present (not in edentulous spaces), and the enlargement disappears in areas from which teeth have been extracted. • Hyperplasia of the mucosa in edentulous mouths has been reported but is rare. • Drug-induced enlargement may occur in mouths with little or no plaque, and it may be absent in mouths with abundant deposits.
  28. 28. • Hassell and colleagues have hypothesized that, in noninflammed gingiva, fibroblasts are less active or even quiescent and do not respond to circulating phenytoin, whereas fibroblasts within inflamed tissue are in an active state as a result of the inflammatory mediators and the endogenous growth factors that are present. • The enlargement is chronic, and it slowly increases in size. Even if it is surgically removed, it recurs. Spontaneous disappearance occurs within a few months after the discontinuation of the drug.
  29. 29. Histopathological feature: • Drug-induced gingival enlargement consists of a pronounced hyperplasia of the connective tissue and epithelium. • There is acanthosis of the epithelium, and elongated rete pegs extend deep into the connective tissue, which exhibits densely arranged collagen bundles with an increase in the number of fibroblasts and new blood vessels. • An abundance of amorphous ground substance has also been reported. • Structural changes in the outer epithelial cell surface have been reported with cyclosporine-induced
  30. 30. • The enlargement begins as a hyperplasia of the connective tissue core of the marginal gingiva and increases by its proliferation and expansion beyond the crest of the gingival margin. An inflammatory infiltrate may be found at the bottom of the sulcus or pocket. • Cyclosporine enlargements usually involve more highly vascularized connective tissue, with foci of chronic inflammatory cells (particularly plasma cells). • The “mature” phenytoin enlargement has a fibroblast-to- collagen ratio that is equal to that of normal gingiva from normal individuals, which suggests that, at some point in the development of the lesion, fibroblastic proliferation must have been abnormally high.
  31. 31. • The multifactorial nature of drug-induced gingival overgrowth, with particular reference to the following factors: Age; Genetic predisposition; Pharmacokinetic variables; Drug-induced alterations in gingival Connective tissue homeostasis; Histopathology, ultrastructural factors & inflammatory changes; Drug-induced action on growth factors
  32. 32. • Clinical studies suggest that children and adolescents appear more susceptible to drug-induced gingival overgrowth than adults (Esterberg & White 1945, Hefti et al. 1994). • Fibroblasts obtained from both cyclosporin and phenytoin-induced gingival overgrowth cases failed to show an age-dependent decrease in protein synthesis and collagen production (Sobhani et al. 1989,Johnson et a!. 1990). • The failure of these cell culture investigations to confirm the clinical findings may be related to a unique fibroblast phenotype or the influence of androgen metabolism
  33. 33. • A drug-related increase in gingival fibroblast androgen metabolism could be a significant factor in the pathogenesis of drug-induced gingival overgrowth. • The active androgen metabolites could "target" sub- populations of gingival fibroblasts and cause either an increase in collagen synthesis and/or a decrease in collagenase activity. • Such changes in androgen metabolism may account for the increased propensity of this unwanted effect in children and adolescents.
  34. 34. • It is now widely recognized that gingival fibroblasts exhibit functional heterogeneity in response to various stimuli (Hassell et al. 1976). • From this finding, it was shown subsequently that phenytoin (and its major metabolite pHPPH) could react with a phenotypically distinct subpopulation of gingival fibroblasts and cause an increase in protein synthesis and cell proliferation rate (Hassell & Gilbert 1983) • Comparable results have also been shown for cyclosporin (Hassell et al. 1988) and its major metabolite OL- 17 (Jacobs et al. 1990)
  35. 35. • Cell cultural studies from monozygous and dizygous twins have confirmed the functional heterogeneity of gingival fibroblasts (Cockey et al. 1989). • Paired cultures from dizygotic twins showed significantly greater (P<0.01) within pair division rates when compared with paired gingival fibroblast from monozygotic twins. • A marked heterogeneity of response of gingival fibroblasts to cyclosporin or calcium channel blockers, had also been reported.
  36. 36. • Fibroblast heterogeneity has also been investigated with respect to the collagenolytic response to cyclosporine (Tipton et al. 1991). • Collagenase, and tissue inhibitor of metalloproteinase (TIMP), activity were determined in each cell population both at baseline and after challenge with cyclosporine (0.1-0.75 ug/ml) • As with phenytoin, the heterogeneity of the collagenolytic response of different gingival fibroblast strains and their subpopulations to cyclosporine treatment may partly explain the variable gingival response noted in patients taking this drug. It is clear that overgrowth-inducing drugs are capable of altering the metabolism of human gingival fibroblasts.
  37. 37. • The 3 drug groups that are known to induce gingival overgrowth are each metabolised by members of the cytochrome P450 enzyme family. The dihydropyridines and cyclosporine are metabolised by the glucocorticoid inducible enzyme CYP3A4 (Guengerich et al. 1985, Kronbach et al. 1988) whereas phenytoin is metabolised mainly by CYP2C9 (Veronese et al. 1993). • Further evidence that genetic factors may relate to the expression of drug-induced gingival overgrowth has come from investigation of human lymphocyte antigen (HLA) expression (Pernu et al. 1994). • The group of patients with moderate or severe overgrowth had significantly lower frequency of HLA- DRI+ and higher frequency of HLA-DR2+ expression, when compared to those with little or no overgrowth.
  38. 38. • Patients who expressed HLA-DR1+ appeared to be afforded a degree of protection against the development of this unwanted effect, whilst those exhibiting HLA-DR2 + showed an increased risk for drug-induced gingival overgrowth. Whether there is any link between HLA expression, and gingival fibroblast phenotype, remains to be elucidated. • These include gingival fibroblast functional heterogeneity, collagenolytic activity (as expressed by collagenase and TIMP production), drug receptor binding, drug metabolism, collagen synthesis and many more factors. HLA expression may prove to be a useful genetic marker for the identification of patients a risk of developing drug- induced gingival overgrowth.
  39. 39. • A direct relationship between the degree of salivary phenytoin and gingival overgrowth has been demonstrated in institutionalised epileptic patients (Babcock & Nelson 1964). • Cyclosporine concentration in stimulated saliva and the extent of the gingival overgrowth (McGaw et al. 1987, Hefti et al. 1994). • By contrast, a lack of correlation between unstimulated salivary cyclosporine levels and gingival overgrowth has been reported (King et al. 1993).
  40. 40. • The possibility that the dental plaque may act as a reservoir for cyclosporine, which is released by the actions of developing stimulated saliva flow, may well explain the conflicting findings reported (McGaw et al. 1987, King et al. 1993). • A role for dental plaque as a reservoir for phenytoin in drug-induced gingival overgrowth has also been proposed. (Steinberg 1980) • It has been reported that the oral mucosal exposure to cyclosporine was approximately 130 times greater when the drug was administered as a mixture as opposed to capsule form. (Modeeret al. 1992)
  41. 41. • It has been shown that both nifedipine and amlodipine can be detected in GCF and significant sequestration of the drug occurs in patients exhibiting gingival overgrowth (Ellis et al. 1992, Seymour et al. 1994)
  42. 42. • Collagen production from gingival fibroblasts is controlled by the co-ordination of transcripted and post-transplation collagen regulatory mechanisms, including intracelluiar degradation. The latter is controlled by synthesis and release of metalloproteinase and tissue inhibitors of metalloproteinase (TIMPs). • Exposure of gingival fibroblasts to phenytoin increases the level of translatable collagen RNA. (Benveniste & Bitar 1980). • Overproduction of collagen by gingival Fibroblasts in phenytoin-induced gingival enlargement involves an increased steady state level of collagen mRNA and not a decrease in collagen degradation (Narayanan et al. 1988). Such fibroblasts may be selected during the development of overgrowth.
  43. 43. • Gingival fibroblasts from healthy volunteers were incubated with varying concentrations of nifedipine (100 and 200 ng/ml) and phenytoin (5-10 /ug/ml) (Salo et al. 1990). After 7 days, both drugs reduced total protein and collagen synthesis in the cultures. • In addition, the level of mRNA for type I collagen was also decreased, whereas the level of type 1 collagenase mRNA was unaffected. • By contrast, a more recent controlled study investigated the expression of type IV collagen genes and type IV collagen distribution in tissue and cell lines obtained from patients with either nifedipine or phenytoin- induced gingival overgrowth.
  44. 44. • Immunohistochemistry and Northern blot analysis showed an increased deposition of type IV collagen and an enhanced expression of type IV collagen genes. • Such increase may be important in the expression of either phenytoin or nifedipine- induced gingival overgrowth (Shikata et al. 1993). • The findings from these 2 studies imply that both phenytoin and nifedipine could alter differentially the expression of both type I and type IV collagen genes. Since type IV collagen appears resistant to both bacterial collagenase and various matrix metalloproteinase. it would remain in the tissue in the presence of plaque- induced gingival inflammation (Romanos et al. 1993)
  45. 45. • cyclosporin causes a significant increase in collagen synthesis in cultured gingival fibroblast. but not DNA synthesis (Schincaglia et al. 1992). • In particular, the cyclosporine-induced changes were related to a rise in the level of type I procollagen. The effects of the drug on the fibroblasts correlated well with an increase in type I procollagen mRNA indicating increased synthesis with increased secretion.
  46. 46. • Non-collagenous matrix comprise 20% of the dry weight in gingival tissue from phenytoin patients and only 7% in normal tissue (Ballard & Butler J974). • Patients on prolonged phenytoin therapy have significantly raised levels of hexosamine, uronic acid and total protein per wet weight of tissue when compared with controls (Goultschin et al. 1983) • Overgrowth has a significantly higher volume density of the non-collagenous matrix than of the collagenous matrix (Dahllof et al. 1984)
  47. 47. • It is uncertain whether the increased amount of glycosaminoglycans in phenytoin-induced gingival overgrowth is due to increased synthesis or reduced degradation. • The effect of cyclosporin and nifedipine on non- collagenous matrix has been investigated with respect to 3H glucosamine utilization (Zebrowski et al. 1994).
  48. 48. • Phenytoin-induced gingival overgrowth may be more related to a lack of collagen breakdown as opposed to an increase in collagen production (goultchin & shoskan 1980). • This finding was further supported by evidence that fibroblasts from patients with phenytoin- induced gingival overgrowth produce an inactive collagenase thus favoring collagen deposition. • Collagenase activity, as measured by the degradation of c14-collagen, was increased by nifedipine. Decreased by phenytoin and unaffected by cyclosporine. • A drug-induced increase in the synthesis of TIMP was perhaps more significant than a decrease in collagenase activity,
  49. 49. • Gingival fibroblasts in cyclosporine-induced overgrowth show characteristics of active protein synthesis and secretion, with reduced cytotoxic or degenerative changes. • An increased proportion of cells containing microfilament bands with semi periodic dense nodes, nuclear indentations, and basal lamina associated cell to stromal junctions has also been found (Yamasaki et al. 1987). • Cyclosporin induced gingival overgrowth is a consequence of individual hypersensitivity to the drug (Deliliers et al. 1986, Mariani et al, 1993)
  50. 50. • It can be argued that plaque-induced inflammatory changes within the gingival tissues enhance the interaction between the drug and gingival fibroblasts. • Cyclosporin has generated renewed interest in this area because of its selective immunosuppressive properties, and ability to inhibit production of interieukins. The latter cytokines are potent stimulators of collagenase production from fibroblasts (Postlethwaite et al. 1983) • A patient's susceptibility to cyclosporin-induced gingival overgrowth may be related to genetically determined populations of both lymphocytes and fibrobiasts which are sensitive to the drug.
  51. 51. • The selective infiltration of T-lymphocytes would support a T-cell mediated immunological mechanism which may play a role in the pathogenesis of gingival overgrowth. • The number of Langerhans cells also increase in gingival epithelium in patients with phenytoin-induced gingival overgrowth (Kinane et al. 1990). • The relationship between such an increase in Langerhans cell and gingival overgrowth remains speculative, it has been shown that an increase in interleukin-I is related to an increase m Langerhans ceils in chronically inflamed gingiva (Walsh et al, 1988)
  52. 52. • Interieukin-1 can stimulate fibroblast proliferation in the presence of primary growth factors, thus phenytoin- induced gingival overgrowth and the increase in Langerhans cells may be mediated via interleukin-1/ growth factor interaction. • Immunohistochemical analysis of the gingival tissues showed significantly higher numbers of monocyte/macrophage (CD68) subsets, plasmacytoid ceils, and total T-lymphocytes (CD3) in the cyclosporin treated patients than in gingival tissues obtained from healthy controls. • Differences were also found in the helper/inducer T- lymphocytes tCD4) and cytotoxic/ suppressor T- lymphocytes (CDS). Similarly, the CD4/CD8 ratio was higher in the cyclosporin treated patients than in control.
  53. 53. • The degree of gingival overgrowth appeared to be related to an in increase in CD4+ and CD68+ leucocyte subsets, together with an increase in CD45+, the common leucocyte antigen. • These findings suggest that local populations of leucocyte subsets may play a pathogenic role in the development of gingival overgrowth. • The immune response appears to be suppressed in the epithelial layer of the gingiva the gingiva through a decrease in Leu- 6+epithelial dendritic cells, HLADR+ epithelial dendritic cells and T-cell infiltration due to cyclosporin in plaque.
  54. 54. • Tissue from cyclosporine and phenytoin-induced gingival overgrowth tissues exhibited less DNA polymerase a in the basal keratinocytes than control tissues. • These findings suggest that the epithelial acanthosis seen in both cyclosporine and phenytoin-induced gingival overgrowth may be due to an enhanced keratinocyte life span, rather than an increase of keratinocyte proliferation (Niimi et al. 1990). • Phenytoin therapy results in an up regulation of prostaglandin formation in gingival fibroblasts. Such an up regulation could cause an increase in glycosaminoglycan synthesis which would affect the extracellular gingival matrix (Karlinsky & Goldstein 1989)
  55. 55. • The direct effect of bacterial lipopolysaccharide on tissue culture models has been investigated, Lipopolysaccharide is an important component of the bacterial ceil wall which is known to be cytotoxic for fibroblast cell lines (Horiba et al, 1989), • Cyclosporine, in the presence of lipopolysaccharide at a concentration that would normally inhibit fibroblast proliferation, has been shown to negate the inhibitory effect of the lipopolysaccharide and maintain the ability of the drug to stimulate fibroblast proliferation (Bartold 1989),
  56. 56. • Studies to date have focused on the drug phenytoin and its interaction with epidermal growth factor (EGF) and platelet derived growth factor (PDGF) • Fibroblasts from the 2 patients showed no difference in the affinity of the receptor for EGF, However, the responder patients showed an increase in both internalization of EGF receptor-ligand and steady state level of EGF receptor mRNA after phenytoin therapy, whereas in the non-responder a decrease was observed in both factors. • These findings suggest that phenytoin causes a down regulation of EGF receptor metabolism in responder patients, whilst in non-responders there is an up regulation.
  57. 57. • Thus phenytoin can cause an increase in the number of cell surface EGF-receptors. which in turn may cause an alteration in gingival connective tissue homeostasis. This effect may be mediated by the action of the drug on intracellular Ca+2 accumulation (Brunius & Modeer 1989) • Phenytoin induced increased in PDGF secretion from macrophages could be an important factor in the expression of gingival overgrowth. Macrophages play a fundamental role in orchestrating the plaque induced inflammatory changes in the gingival tissues. There is considerable evidence that such inflammatory changes exacerbate phenytoin-induced gingival overgrowth (Hassell et al. 1983)
  58. 58. • Brown et al (1991a) further enlarged upon this mechanism discussion regarding a biochemical pathway hypothesis which included the following: • The research evidence regarding an anabolic hypothesis for causation for DIGO was consistently contradictory and at best confusing, and without any unifying conceptual basis (Brown et al (1991a) and McCulloch and Bordin (1991) • All of the inducing drugs are known to effect cation (Na+ and Ca++)channels (Antman et al (1980), DeLorenzo (1980), Colombani et al (1985), Jones and Wimbish (1985), Messing et al (1985), Dretchen et al (1986) and Fugii and Kobayashi (1990)
  59. 59. • DIGO appears to be the result of a defect in catabolism due to increased amounts sulfated glycosaminoglycan (GAGs/connective tissue) within DIGO gingival tissues. (Hassell (1982), Kantor and Hassell (1983), Dahllof et al (1986), Deliliers et al (1986) and Bowman et al (1988) • Topical folate demonstrated clinical efficacy in the treatment of DIGO (and systemic folate was not as efficacious) (Drew et al (1987), Backman et al (1989), Brown et al (1991b) and Poppell et al (1991) • Folate cellular uptake is due to both a cation regulated channel, and by passive diffusion (Ariel et al (1978, 1982), Rose et al (1978), Eilam et al (1981), Rosenberg et al (1985), Zimmerman et al (1986) and Zimmerman (1990)
  60. 60. • Folate is necessary for protein synthesis and the conversion of DNA base-pairs necessary for DNA synthesis (Burka and Marks (1967) and Taheri et al (1982) • Plaque control decreases the incidence, recurrence, and severity of DIGO (Nuki and Cooper (1972), Russell and Bay (1978), Staple et al (1978), O’Neil and Figures (1982), Daley and Wysocki (1984), Dahllof et al (1986), Dahllof and Modeer (1986), Modeer et al (1986), Modeer and Dahllof (1987), Fitchie et al (1989) and Francetti et al (1991)
  61. 61. • Collagenase is necessary for the tissue degradation of gingival connective tissue and is an inactive enzyme which requires activation with a matrix Metalloproteinases (Murphy et al (1982, 1986, 1987), Moy et al (1985) and Meikle et al (1989) • Gingival sulcular epithelium has a relatively high turnover rate which requires protein synthesis (Beagrie and Skougaard (1962) and Engler et al (1965)
  62. 62. • This hypothesis purports that the biochemical pathway for DIGO is influenced by bacterial plaque which causes gingival inflammation which increases the buildup of gingival connective tissue (glycosaminoglycans—GAGs). The inducing drugs (anti-convulsants, CCBAs, and calcineurin inhibitor/immunosuppressive drugs) decrease folate cellular uptake in gingival fibroblast cells. The secondary effect of decreased cellular folate is that the synthesis and/or activation of a particular MMP (or MMPs) is/are decreased and as that (a) particular MMP(s) is/are necessary to convert inactive collagenase to active collagenase within the gingiva; therefore, there is an insufficient amount of active collagenase necessary to breakdown excess gingival connective tissues (built up secondary to inflammation) resulting in the side effect of DIGO (Brown et al, 1991a).
  63. 63. • Chronic Inflammatory Enlargement: • Of the inflammatory type of gingival enlargement, treatment consists of the establishment of excellent oral hygiene, the elimination of all local predisposing factors and proper home care by the patient. • In patients with extensive gingival enlargement, the affected tissues must be removed surgically and the remaining tissues properly contoured. • All local irritative factors such as calculus, the margins of cervical cavities, or areas of food impaction should be corrected.
  64. 64. • The purpose of treatment of an acute abscess is to alleviate pain, control the spread of infection and establish drainage. • After the cause is diagnosed, the patients general systemic response should be evaluated and his or her temperature taken. • Drainage can be established through the pocket or by means of an incision from the outer surface; the former is preferable, • After application of a topical anesthetic, a flat instrument or a probe is introduced into the pocket in an attempt to
  65. 65. • With a Bard-Parker no. 11 blade, a vertical incision is made through the most fluctuant part of the lesion, extending from the mucogingival fold to the gingival margin. If the swelling is on the lingual surface, the incision is started just apical to the swelling and extended through the gingival margin. • After the initial extravasation of pus, irrigate the area with warm water and gently spread the incision to facilitate drainage.. • If the tooth is extruded, it should be ground slightly to avoid contact with its agonists. • In addition to the rinses, penicillin or other antibiotics can be prescribed patients. • If the residual size of the lesion is too great (chronic
  66. 66. • After topical anesthesia is applied, the fluctuant area of the lesion is incised with a Bard-Parker blade, and the incision is gently widened to permit drainage. The area is cleansed with warm water and covered with a gauze pad.
  67. 67. • The treatment should be particularly concerned with cases where there is evidence of gingival enlargement of patients taking one or more of these drugs because : • Poses a plaque control problem • It may affect mastication • It may alter tooth eruption • It may interfere with speech • It may cause aesthetic concerns.
  68. 68. • The clinician should also emphasize plaque control as the first step in the treatment of drug induced gingival enlargement. • Although the exact role played by bacterial plaque in drug induced gingival enlargement is unclear, there is evidence that good oral hygiene and frequent professional removal of plaque decreases the degree of the gingival enlargement present and improves overall gingival health.
  69. 69. • It has been suggested that folic acid is taken up primarily in a Na++ coupled, Na-- dependent active transport mechanism and secondarily through passive diffusion. • The sulcular gingival epithelium has one of the highest cellular turnover rate increases the need for intracellular folate. • The favorable results of topical application and the negative results of systemic administration of folic acid in the treatment of human support of the concept of an end organ deficiency. • The topical administration of folic acid would be more likely than systemic administration to produce an increased extracellular concentration of folic acid necessary to override the decreased active transport uptake with increased passive diffusion.
  70. 70. • It is well established that phenytoin interferes with folic acid metabolism (Klipstein 1964, Flexner and Hartmann 1363, Jensen and Olsen 1963:). • The incidence of folic acid deficiency in patients treated by anticonvulsants has been reported in various studies as ranging from 37%. to 90%. (Klipstein 1964. Malpas et al 1966, reynolds et al 1966, Jensen and 0lsen;1969) .
  71. 71. • The mechanism of this deficiency is still not well understood. • It has been postulated that phenytoin acts as a weak folic acid antagonist, thus interfering with its metabolism in tissues. • This may be explained by the close structural resemblance of phenytoin to folic acid. Since phenytoin inhibits the utilization of folic acid at the cellular level, • Folic acid deficiency has been associated with increased gingival inflammation
  72. 72. • The results of several clinical studies have indicated that supplementation with folic acid, either systemically or by topical application, is associated with a decrease in the plaque-induced inflammatory response. • A controlled clinical trial of topical folate rinse (1mg/ml) vs. systemic folate (4mg daily) in patients treated with phenytoin for a minimum of 3 months, also demonstrated some reduction in overgrowth and mean periodontal probing depth without any reduction in plaque or gingival indices (Drew HJ et al 1987).
  73. 73. • Alternative meditations to phenytoin include carbamazepine and valproic acid and both of which have been reported to have a lesser impact in inducing gingival enlargement. • For patienls on nifedipine, with prevalence of gingival enlargement has up to 44%, other calcium channel blockers such as diltiazem and verapamil may be viable alternatives, since the prevalence is 20% and 4%, respectively. • Also, consideration may be given to the use of another class of antihypertensive medications
  74. 74. • Drug substitution options for cyclosporin are more limited due to the fact that few of these options exist. • Recently, it has been shown that cyclosporin induced gingival enlargement can spontaneously resolve if the drug is substituted by tracolimus. • There is also preliminary evidence that the antibiotic azithromycin may aid in decreasing the severity of cyclosporin induced gingival enlargement. • If any drug substitution is attempted, it is important to allow for 6-12 months to elapse between discontinuation of the offending drug and the possible resolution of gingival enlargement before a decision to implement
  75. 75. • Gingival enlargement may persist, despite drug substitution attempts and good plaque control. • These cases need to be treated by periodontal surgery, either gingivectomy or the periodontal flap. • Gingivectomy presents with the advantages of technique simplicity and quickness but, unlike the periodontal flap, will not allow for osseous recontouring and may sacrifice keratinized tissue.
  76. 76. • Also, gingivectomy results in healing by secondary intention, which causes discomfort and an increased chance of post operative bleeding. • Small areas (up to six teeth) presenting with drug induced gingival enlargement where there is no evidence of attachment loss can be effectively treated with the gingivectomy technique
  77. 77. • An important aspect is the amount of keratinized tissue present. • It is recommended that at least 3 mm of keratinized tissue in the apicocoronal direction remain after the surgical procedure is concluded. • Therefore, if the initial gingivectomy incision needs to be placed in close proximity to or at the mucogingival junction, this technique is contraindicated.
  78. 78. The gingivectomy technique used in the treatment of drug- induced gingival enlargement is as follows. • Following administration of local anesthesia, the deepest point in each pocket is marked on the external gingival wall using a pocket marker or a probe. The series of bleeding points obtained with pocket marking works as a guideline for the initial scalloped external bevel incision. • This incision is accomplished with the Kirkland knife or a # 15 blade if angulation permits. • A sulcular incision follows the initial external bevel incision and the release of the interproximal tissue can be achieved with an Orban knife following excision of most of the enlarged tissue with curettes.
  79. 79. • Gingivoplasty is performed. The goal of gingivoplasty is to restore the physiological contour observed in healthy gingiva and the recreation of gingival festooning. • Gingivoplasty is performed with surgical scissor, tissue nippers and high-speed diamonds of various shapes and sizes under adequate refrigeration. • Meticulous scaling and root planning should be performed before application of periodontal dressing to the surgical area. • Gingivectomy or gingivoplasty can also be performed by electrosurgery or by a laser device
  80. 80. • Advantages: Electrosurgery permits adequate contouring of the tissue and controls hemorrhage. • Disadvantages: Electrosurgery cannot be used in patients who have a noncompatible or a poorly shielded cardiac pacemaker. The treatment causes an unpleasant odor. • The heat generated by injudicious use can cause tissue damage and loss of periodontal support when the electrode is used close to bone. • When the electrode touches the roots, areas of cementum burn are produced. • Therefore, the use of electrosurgery should be limited to superficial procedures such as removal of gingival
  81. 81. • It should not be used for procedures that involve proximity to the bone, such as flap operations or mucogingival surgery. • Technique: • The removal of gingival enlargements and gingivoplasty is performed with the needle electrode, supplemented by the small ovoid loop or the diamond- shaped electrodes for festooning. • A blended cutting and coagulating (fully rectified) current is used. In all reshaping procedures "shaving" motion.
  82. 82. • Larger areas of gingival enlargement (more than six teeth) or areas where attachment loss combined with osseous defects is present should be treated with the periodontal flap. • Also, any situation in which the gingivectomy technique may result in the elimination of all keratinized tissue and consequent creation of mucogingival problems should be treated with the periodontal flap.
  83. 83. • The initial scalloped internal bevel incision is made with a # 15 blade at least 3 mm coronal to the mucogingival junction, including the creation of new interdental papillae. • It is then used to thin the gingival tissues in the buccolingual direction; this thinning process should be carried out in the mucogingival junction. • At the mucogingival junction level, a full or split thickness flap is elevated. • The gingival tissue collar, which attached to the bone and teeth, is removed with the use of large and small curettes. • Following debridement and osseous recontouring when necessary; flap are positioned right on top of the alveolar crest and sutures are placed
  84. 84. • Another situation in which the periodontal flap is used in the treatment of DIGO is in assisting tooth eruption in younger patients. • The result of the process may be the soft tissue impaction of the tooth apical to or as its normal occluding position. • If the gingivectomy technique were to be applied in that situation, it would result in the complete elimination of all keratinized tissue and the creation of a mucogingival problem. • The flap technique follows for the complete exposure of the impacted tooth or teeth by apically positioning the thinned flap without, compromising the mucogingival status of the area.
  85. 85. • Idiopathic gingival enlargement is a rare condition of undetermined cause. It has been designated by such terms as gingivostomatosis, elephantiasis, idiopathic fibromatosis, hereditary gingival hyperplasia, and congenital familial fibromatosis. • Syndrome associated with IGF: • Zimmerman – Laband syndrome • Murray-Puretic Drescher syndrome • Rutherford syndrome • Cowden syndrome • Cross syndrome
  86. 86. Classification • Isolated HGF • isolated IGF • GF with hypertrichosis • GF with hypertrichosis and mental retardation or epilepsy. • GF with mental retardation or epilepsy. • GF associated with other disease as part of a syndrome.
  87. 87. Clinical Features • The enlargement affects the attached gingiva as well as the gingival margin and the interdental papillae. • The facial and lingual surfaces of the mandible and maxilla are generally affected, but the involvement may be limited to either jaw.
  88. 88. • The enlarged gingiva is pink, firm, and almost a leathery in consistency, and it has a characteristic minutely pebbled surface. • In severe cases, the teeth are almost completely covered, and the enlargement projects into the oral vestibule. The jaws appear distorted as a result of the bulbous enlargement of the gingiva. • Secondary inflammatory changes are common at the gingival margin.
  89. 89. Histopathology • Idiopathic gingival enlargement shows a bulbous increase in the amount of connective tissue that is relatively avascular and that consists of densely arranged collagen bundles and numerous fibroblasts. • The surface epithelium is thickened and acanthotic, with elongated rete pegs.
  90. 90. • The magnification of an existing inflammation initiated by dental plaque. This group of diseases, which are discussed in the Conditioned Enlargements section, includes some hormonal conditions (e.g., pregnancy, puberty), some nutritional diseases (e.g., vitamin C deficiency), and some cases in which the systemic influence is not identified (i.e., nonspecific conditioned enlargement). • The manifestation of the systemic disease independently of the inflammatory status of the gingiva. These mechanisms are described in the Systemic Diseases that Cause Gingival Enlargement section and the Neoplastic Enlargement (Gingival Tumors) section.
  91. 91. Conditioned Enlargements • Conditioned enlargements occur when the systemic condition of the patient exaggerates or distorts the usual gingival response to dental plaque. • Bacterial plaque is necessary for the initiation of this type of enlargement. • The three types of conditioned gingival enlargement : • Hormonal (pregnancy, puberty), • Nutritional (associated with vitamin c deficiency), • Allergic.
  92. 92. • These hormonal changes induce changes in vascular permeability, which leads to gingival edema and an increased inflammatory response to dental plaque. • The sub gingival microbiota may also undergo changes, including an increase in Prevotella intermedia. Marginal Enlargement. • The enlargement is usually generalized, and it tends to be more prominent interproximal than on the facial and lingual surfaces. • The enlarged gingiva is bright red or magenta, soft, and friable, and it has a smooth, shiny surface. Bleeding occurs spontaneously or on slight provocation.
  93. 93. Tumor like Gingival Enlargement. • The so-called pregnancy tumor is not a neoplasm; it is an inflammatory response to bacterial plaque, and it is modified by the patient’s condition. • It usually appears after the third month of pregnancy. • The lesion appears as a discrete, mushroom like, flattened spherical mass that protrudes from the gingival margin or more often from the interproximal space, and it is attached by a sessile or pedunculated base.
  94. 94. • It tends to expand laterally, and pressure from the tongue and the cheek perpetuates its flattened appearance. • It is generally dusky red or magenta in color; it has a smooth, glistening surface that often exhibits numerous deep-red, pinpoint markings. • It is a superficial lesion that usually does not invade the underlying bone. • It is usually painless.
  95. 95. Histopathology. • Gingival enlargement in pregnancy is called angiogranuloma. • Both marginal and tumor like enlargements consist of a central mass of connective tissue, with numerous diffusely arranged, newly formed, and engorged capillaries lined by cuboid endothelial cells as well as a moderately fibrous stroma with varying degrees of edema and chronic inflammatory infiltrate. • The stratified squamous epithelium is thickened, with prominent rete pegs and some degree of intracellular and extracellular edema, prominent intercellular bridges, and leukocytic infiltration.
  96. 96. TREATMENT • Treatment requires the elimination of all local irritants that may be responsible for precipitating the gingival changes that occur during pregnancy. • The elimination of local irritants early in pregnancy is preventive measure against gingival disease, which is preferable to the treatment of gingival enlargement after it occurs. • Marginal and interdental gingival inflammation and enlargement are treated by scaling and curettage.
  97. 97. • The treatment of tumor like gingival enlargements consists of surgical excision as well as the scaling and planing of the tooth surface. • The enlargement recurs unless all irritants are removed. Food impaction is frequently an inciting factor. Timing of Treatment and Indications • Gingival lesions during pregnancy should be treated as soon as they are detected, although not necessarily by surgical means. • Scaling and root planing procedures and adequate oral hygiene measures may reduce the size of the enlargement.
  98. 98. • Gingival enlargements do shrink after pregnancy, but they usually do not disappear. • Lesions should be removed surgically during pregnancy only if they interfere with mastication or produce an aesthetic disfigurement that the patient wants removed.
  99. 99. • It is marginal and interdental, and it is characterized by prominent bulbous interproximal papillae. • Often, only the facial gingivae are enlarged, and the lingual surfaces are relatively unaltered; the mechanical action of the tongue and the excursion of food prevent a heavy accumulation of local irritants on the lingual surface. • After puberty, the enlargement undergoes spontaneous reduction, but does not disappear completely until the plaque and calculus are removed.
  100. 100. • A longitudinal study of the subgingival microbiota of children between the ages of 11 and 14 years and their association with clinical parameters implicated Capnocytophaga species in the initiation of pubertal gingivitis. • Other studies have reported that hormonal changes coincide with an increase in the proportion of Prevotella intermedia and Prevotella nigrescens.
  101. 101. TREATMENT • Gingival enlargement during puberty is treated by performing scaling and curettage, removing all sources of irritation, and controlling plaque. • Surgical removal may be required in severe cases. • The main problem in these patients is recurrence, which is caused by poor oral hygiene.
  102. 102. • Acute vitamin C deficiency itself does not cause gingival inflammation, but it does cause haemorrhage, collagen degeneration, and edema of the gingival connective tissue. • These changes modify the response of the gingiva to plaque to the extent that the normal defensive delimiting reaction is inhibited and the extent of the inflammation is exaggerated, thereby resulting in the massive gingival enlargement seen in patients with scurvy.
  103. 103. • Gingival enlargement with vitamin C deficiency is marginal; the gingiva is bluish red, soft, and friable, and it has a smooth, shiny surface. • Hemorrhage that occurs either spontaneously or on slight provocation as well as surface necrosis with pseudo membrane formation are common features.
  104. 104. • Plasma cell gingivitis consists of a mild marginal gingival enlargement that extends to the attached gingiva. • The gingiva appears red, friable, and sometimes granular, and it bleeds easily; usually it does not induce a loss of attachment. • This lesion is located in the oral aspect of the attached gingiva and therefore differs from plaque-induced gingivitis.
  105. 105. • Pyogenic granuloma is a tumor like gingival enlargement that is considered an exaggerated conditioned response to minor trauma. • Pyogenic granuloma is similar in clinical and microscopic appearance to the conditioned gingival enlargement seen during pregnancy. The differential diagnosis is based on the patient’s history.
  106. 106. Leukemia. • Leukemic gingival enlargement may be diffuse or marginal and localized or generalized. • It may appear as a diffuse enlargement of the gingival mucosa, an oversized extension of the marginal gingiva, or a discrete tumor like interproximal mass.
  107. 107. Clinical Features. • In patients with leukemic enlargement, the gingiva is generally bluish red, and it has a shiny surface. The consistency is moderately firm, but there is a tendency toward friability and hemorrhage that occur either spontaneously or with slight irritation. • Acute painful necrotizing ulcerative inflammatory involvement may occur in the crevice formed at the junction of the enlarged gingiva and the contiguous tooth surfaces.
  108. 108. TREATMENT • After acute symptoms subside, attention is directed to the correction of the gingival enlargement. • The enlargement is treated by scaling and root planing, which are carried out in stages after the patient has received topical anesthesia. • The initial treatment consists of gently removing all loose accumulations with cotton pellets, performing superficial scaling, and instructing the patient in oral hygiene for plaque control; this hygiene should include, at least initially, the daily use of chlorhexidine mouthwashes.
  109. 109. Granulomatous Diseases. Wegener’s Granulomatosis. • The initial manifestations of Wegener’s granulomatosis may involve the oro-facial region and include oral mucosal ulceration, gingival enlargement, abnormal tooth mobility, exfoliation of teeth, and delayed healing response. • The granulomatous papillary enlargement is reddish purple and bleeds easily on stimulation.
  110. 110. Sarcoidosis. • Sarcoidosis is a granulomatous disease of unknown etiology. It starts in individuals during their twenties or thirties, it predominantly affects blacks, and it can involve almost any organ, including the gingiva, in which a red, smooth, painless enlargement may appear. Neoplastic Enlargement (Gingival Tumors) Benign Tumors of the Gingiva • Epulis is a generic term that is used clinically to designate all discrete tumors and tumorlike masses of the gingiva. •
  111. 111. Fibroma. • Fibromas of the gingiva arise from the gingival connective tissue or from the periodontal ligament. They are slow growing spherical tumors that tend to be firm and nodular but that may be soft and vascular. Fibromas are usually pedunculated. • Hard fibromas of the gingiva are rare; most of the lesions that are diagnosed clinically as “fibromas” are inflammatory enlargements.
  112. 112. Papilloma. • Papilloma are benign proliferations of surface epithelium that are, in many (but not all) cases, associated with the human papillomavirus (HPV). • Gingival papilloma appear as solitary wartlike or cauliflower-like protuberances. • They may be small and discrete, or they may be broad, hard elevations with minutely irregular surfaces.
  113. 113. Peripheral Giant Cell Granuloma. • Giant cell lesions of the gingiva arise interdentally or from the gingival margin; they occur most frequently on the labial surface, and they may be sessile or pedunculated. • They vary in appearance from smooth, regularly outlined masses to irregularly shaped, multilobulated. protuberances with surface indentations.
  114. 114. • The ulceration of the margin is occasionally seen. The lesions are painless, they vary in size, and they may cover several teeth. • They may be firm or spongy, and their color varies from pink to deep red or purplish blue.
  115. 115. Central Giant Cell Granuloma. • Giant cell lesions arise within the jaws and produce central cavitation. They occasionally create a deformity of the jaw that makes the gingiva appear enlarged. Leukoplakia. • Leukoplakia is a strictly clinical term defined by the World Health Organization as a white patch or plaque that does not rub off and that cannot be diagnosed as any other disease. • Leukoplakia of the gingiva varies in appearance from a greyish white, flattened, scaly lesion to a thick, irregularly shaped, keratinous plaque.
  116. 116. Gingival Cyst. • Localized enlargements that may involve the marginal and attached gingiva. • The cysts occur in the mandibular canine and premolar areas, most often on the lingual surface. • They are painless, but, with expansion, they may cause erosion of the surface of the alveolar bone. • The gingival cyst should be differentiated from the lateral periodontal cyst. • Gingival cysts develop from odontogenic epithelium or from surface or sulcular epithelium traumatically implanted in the area. •
  117. 117. Carcinoma • Squamous cell carcinoma is the most common malignant tumour of the gingiva. It may be exophytic, presenting as an irregular outgrowth, or ulcerative, appearing as flat, erosive lesions. • It is often symptom free, going unnoticed until complicated by inflammatory changes that may mask the neoplasm but cause pain; sometimes it becomes evident after tooth extraction.
  118. 118. Malignant Melanoma. • Malignant melanoma is a rare oral tumour that tends to occur in the hard palate and maxillary gingiva of older persons. • It is usually darkly pigmented, and it is often preceded by localized pigmentation. It may be flat or nodular, and it is characterized by rapid growth and early metastasis.
  119. 119. • False enlargements are not true enlargements of the gingival tissues, but they may appear as such as a result of increases in the size of the underlying osseous or dental tissues. • The gingiva usually presents with no abnormal clinical features except the massive increase in the size of the area. Underlying Osseous Lesions • Enlargement of the bone subjacent to the gingival area occurs most often with tori and exostoses, but it can also occur with Paget’s disease, fibrous dysplasia, cherubism, central giant cell granuloma, ameloblastoma, osteoma, and osteosarcoma.
  120. 120. Underlying Dental Tissues • During the various stages of eruption, particularly of the primary dentition, the labial gingiva may show a bulbous marginal distortion caused by the superimposition of the bulk of the gingiva on the normal prominence of the enamel in the gingival half of the crown. • This enlargement has been called developmental enlargement, and often persists until the junctional epithelium has migrated from the enamel to the cementoenamel junction.
  121. 121. • Gingival enlargement can be caused by a wide variety of etiologies • The clinician can often diagnose the cause by a careful history (e.g., drug-induced or pregnancy-induced enlargement), by location (e.g., mouth-breathing enlargement), or by the clinical presentation (e.g., generalized enlargement with gingival hematoma formation seen in leukemia). • Plaque-induced inflammation can be the sole cause of gingival enlargement or can be a secondary cause, so in all patients, therapy to control gingival inflammation is essential. • Thus Correct diagnosis & treatment planning form the most essential part of the treatment of gingival enlargement to achieve proper functional and esthetic harmony.
  122. 122. • Newman, Takei, Klollevold, Carranza. Carranza’s clinical periodontology. 11th edition. • Eva Ingles. New clinical index for drug-induced gingivai Overgrowth. Quintessence Int 1999;30:467-73 • RS Brown, PR Arany. Mechanism of drug-induced gingival overgrowth revisited: a unifying hypothesis. Oral Diseases 2014 • Seymour RA, ThomasonJM, Ellis JS: The palhogenesis of drug-induced gingival overgrowth. J Clin Periodontol 1996: 23: 165-75.

Notas del editor

  • The vertical component is measured from cemento-enamel junction to the free gingival margin.
    Horizontal component from the enamel surface at the point of contact to the external margin of the interdental papilla.
  • They may undergo a spontaneous reduction in size that is followed by exacerbation and continued enlargement.
    Painful ulceration sometimes occurs in the fold between the mass and the adjacent gingiva.

  • They also have a preponderance of inflammatory cells and fluid, with vascular engorgement, new capillary formation, and associated degenerative changes.
  • Recurring phenytoin enlargements appear as granulation tissue composed of numerous young capillaries and fibroblasts and irregularly arranged collagen fibrils with occasional lymphocytes