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Gingival enlargment and its treatment

Gingival Enlargement, concepts, types, classification, Aetiology, Treatment modalities

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Gingival enlargment and its treatment

  1. 1. Presented by: Surbhi Kapoor MDS 2nd year
  2. 2.  Gingival enlargement is the proliferation and intensification of the gingiva which is a prevailing character of the diseased gingival tissues.  Thus, increase in size of the gingiva is a common feature of gingival disease.  Accepted current terminology for this condition is GINGIVAL ENLARGEMENT OR GINGIVAL OVERGROWTH.  However “Hypertrophic Gingivitis”, “Gingival Hypertrophy” and “Gingival Hyperplasia” were the former histopathological loculations which are not applicable these days considering that it is unable to differentiate clinically in the increase in the number of cells or in the size of the cells.
  3. 3. I. Inflammatory enlargement A. Chronic B. Acute II. Drug-induced enlargement 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 (granuloma pyogenicum) B. Systemic diseases causing gingival enlargement 1. Leukemia 2. Granulomatous disease (Wegener’s granulomatosis, sarcoidosis) IV. Neoplastic enlargement (gingival tumors) A. Benign tumors B. Malignant tumors V. False enlargement Classification ( Acc. to etiological factors & pathological changes)
  4. 4. 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 gingivae and papillae Discrete: An isolated sessile or pedunculated, tumor like enlargement Using the criteria of location & distribution, gingival enlargement is designated as follows:
  5. 5. The degree of gingival enlargement can be scored as follows: 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. Seymour et al 1985 0 = No encroachment of the interdental papilla onto the tooth surface 1 = Mild encroachment of the interdental papilla, producing a blunted appearance to papilla tip 2 = Moderate encroachment, involving lateral spread of papilla across buccal tooth surface of less than one quarter of tooth width 3 = Marked encroachment of papilla, i.e. more than 1/4th tooth width. Loss of normal papilla form
  6. 6. Miller and Damm (1992) enlargement was divided into a vertical and a horizontal component and abbreviated as GOI index. Vertical component is measured from CEJ to the free gingival margin and the horizontal component from the enamel surface at the point of contact to the external margin of the interdental papilla. 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. horizontal gingival overgrowth index is described as: Grade 0: < 1mm Grade 1: 1 to 2 mm Grade 2: >2mm Bokenkamp A and Bohnhorst B (1994) Grade 0: No signs of gingival overgrowth Grade I: Gingival hyperplasia confined to interdental papilla c. Grade II: Hyperplasia of interdental papilla and marginal gingiva Grade III: Gingival hyperplasia covering at least three-quarters of tooth crowns
  7. 7. 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. 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. 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. The probing depth is equal to or less than 6mm and the papilla is somewhat retractable. Grade 3: Marked overgrowth, represented by encroachment of the gingiva onto the clinical crown. Contour of the margin is convex rather than concave. The probing depth is greater than 6mm and the papilla is clearly retractable. 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.
  8. 8. Miranda and Brunet index (2001) described an index in which horizontal measurement of the enlargement is possible. This index is also termed as nodullary papilla index. In this index the measurement is carried out with the help of a periodontal probe from the enamel surface of the interdental contact point to the outer papillary area. The scores of this index is as mentioned below: Score 0: Papilla thickness < 1 mm Score 1: Papilla thickness 1- 2 mm Score 2: Papilla thickness > 2 mm
  9. 9. Gingival enlargement may result from chronic or acute inflammatory changes; chronic changes are much more common. In addition, inflammatory enlargements usually are a secondary complication to any of the other types of enlargement, creating a combined gingival enlargement. A) Chronic Inflammatory Enlargement Etiology •Prolonged exposure to dental plaque. Factors that favor plaque accumulation and retention include -poor oral hygiene. -irritation by anatomic abnormalities. -Improper restorative and orthodontic appliances. -Mouth breathing INFLAMMATORY ENLARGEMENT
  10. 10. CLINICAL FEATURES • Originates as Slight ballooning of the interdental papilla and/or the marginal gingiva. • Produces a life preserver-shaped bulge around the involved teeth in early stages. • May be localized or generalized and progresses slowly & painlessly, unless it is complicated by acute infection or trauma. Chronic inflammatory gingival enlargement localized to anterior region
  11. 11. Discrete sessile or pedunculated mass •Occasionally, occurs as a discrete sessile or pedunculated mass resembling a tumor. • May be interproximal or on the marginal or attached gingiva. •Lesions are slow-growing masses and usually painless. •They may undergo spontaneous reduction in size, followed by exacerbation and continued enlargement. • Painful ulceration sometimes occurs in the fold between the mass and the adjacent gingiva. Gingival Changes Associated with Mouth Breathing • Gingiva appears red and edematous with a diffuse surface shininess of the exposed area. •maxillary anterior region -common site • Harmful effect is attributed to irritation from surface dehydration.
  12. 12. Histopathology •Show the exudative and proliferative features of chronic inflammation. •Lesions that are clinically deep red or bluish red are soft and friable with a smooth, shiny surface, and they bleed easily. • 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. Demarcation between exposed gingiva and unexposed gingiva
  13. 13. B) Acute Inflammatory Enlargement GINGIVALABSCESS •localized, painful, rapidly expanding lesion •usually of sudden onset. • Generally limited to marginal gingiva or interdental papilla. •In its early stages –appears as red swelling with a smooth, shiny surface. •Within 24 to 48 hours, -fluctuant and pointed with a surface orifice from which a purulent exudate may be expressed. Adjacent teeth are sensitive to percussion. Etiology Acute inflammatory gingival enlargement results from bacteria carried deep into the tissues when foreign substances such as a toothbrush bristle, a piece of apple core, or a lobster shell fragment is forcefully embedded into the gingiva. (Lesion is confined to gingiva).
  14. 14. Histopathology 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 intra- and extracellular edema, invasion by leukocytes, and sometimes ulceration. Periodontal (Lateral) Abscess It is a localized purulent inflammation in the periodontal tissues. Also known as Lateral or Parietal abscess.  It involves the supporting periodontal tissues causing enlargement of gingiva.
  15. 15. Periodontal abscess formation may occur in the following ways: 1. Extension of infection from a periodontal pocket deeply into the supporting periodontal tissues and localization of the suppurative inflammatory process along the lateral aspect of the root. 2. Lateral extension of inflammation from the inner surface of a periodontal pocket into the connective tissue of the pocket wall. Localization of the abscess results when drainage into the pocket space is impaired . 3. In a pocket that describes a tortuous course around the root, a periodontal abscess may form in the cul -de- sac, the deep end of which is shut off from the surface. 4. Incomplete removal of calculus during treatment of a periodontal pocket. In this instance, the gingival wall shrinks, occluding the pocket orifice, and a periodontal abscess occurs in the sealed-off portion of the pocket. 5. A periodontal abscess may occur in the absence of periodontal disease after trauma to the tooth or perforation of the lateral wall of the root in endodontic therapy.
  16. 16. Periodontal abscesses are classified acc. to location: 1. Abscess in the supporting periodontal tissues along the lateral aspect of the root.- SINUS FORMATION occur in the bone that extends laterally from the abscess to external surface. 2. Abscess in the soft tissue wall of a deep periodontal pocket. Histopathology -localized accumulation of viable & non viable PMNs within the periodontal pocket wall. -The PMNs liberate enzymes that digest the cells & other structures forming the liquid product known as pus, which constitutes the center of abscess. -An acute inflammatory reaction surrounds the purulent area & overlying epithelium exhibits intracellular & extracellular edema and invasion of leukocytes. -The localized acute abscess becomes a chronic abscess when its purulent content drains through a fistula into the outer gingival surface or into the periodontal pocket and the infection causing the abscess is not resolved
  17. 17. Gingival enlargement is a well-known consequence of the administration of some anticonvulsants, immunosuppressants, and calcium channel blockers and may create speech, mastication, tooth eruption, and aesthetic problems. Clinical Features •Growth starts as a painless, bead-like enlargement of the interdental papilla and extends to the facial and lingual gingival margins. •As the condition progresses, the marginal and papillary enlargements unite and may develop into a massive tissue fold covering a considerable portion of the crowns; they may interfere with occlusion Case of phenytoin induced gingival enlargement DRUG INDUCED GINGIVAL ENLARGEMENT
  18. 18. •usually generalized throughout the mouth but 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 are extracted. •Hyperplasia of the mucosa in edentulous mouths has been reported but is rare •The enlargement is chronic and slowly increases in size •When surgically removed, it recurs. •Spontaneous disappearance occurs within a few months after discontinuation of the drug. •When UNCOMPLICATED BY INFLAMMATION- lesion is mulberry shaped, firm, pale pink, and resilient, with a minutely lobulated surface and no tendency to bleed.
  19. 19. •The presence of the enlargement makes plaque control difficult resulting in a secondary inflammatory process that complicates the gingival overgrowth caused by the drug. • 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 add to the size of the lesion caused by the drug and produce a red or bluish red discoloration, obliterate the lobulated surface demarcations, and increase bleeding tendency •Drug-induced enlargement may occur in mouths with little or no plaque and may be absent in mouths with abundant deposits. •Some investigators believe that inflammation is a prerequisite for development of the enlargement, which therefore could be prevented by plaque removal and fastidious oral hygiene (Ciancio and Yaffe J periodontol 1972)
  20. 20.  Hassell et al (1982) have hypothesized that in noninflamed 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 present.  Barclay S et al (J Clin Periodontol 1992) evaluated the incidence and severity of nifedipine-induced gingival overgrowth and concluded that nifedipine therapy results in significant gingival changes, an effect which may be mediated by the drug's action on calcium transport.  Thomason JM et al ( J Clin Periodontol 1993) studied the prevalence and severity of cyclosporin and nifedipine induced gingival overgrowth and concluded that patients taking cyclosporin or cyclosporin and nifedipine experience gingival overgrowth and that the severity of the overgrowth is greater in patients taking the combined therapy.
  21. 21. Histopathology •Pronounced hyperplasia of the connective tissue and epithelium. •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 as well as marked plasma cell; infiltration has also been reported (Mariani et al 1993). •Cyclosporine enlargements usually have a more highly vascularized connective tissue with foci of chronic inflammatory cells, particularly plasma cells. • The “mature” phenytoin enlargement has a fibroblast/collagen ratio equal to that of normal gingiva from normal individuals, suggesting that at some point in the development of the lesion, fibroblastic proliferation must have been abnormally high. • Recurring phenytoin enlargements appear as granulation tissue composed of numerous young capillaries and fibroblasts and irregularly arranged collagen fibrils with occasional lymphocytes.
  22. 22. ANTICONVULSANTS •The first drug-induced gingival enlargements reported were those produced by phenytoin (Dilantin). •Other hydantoins known to induce gingival enlargement are ethotoin (Peganone) and mephenytoin (Mesantoin). •Other anticonvulsants that have the same side effect are the succinimides (ethosuximide [Zarontin], methsuximide [Celontin]), and valproic acid [Depakene]). (Hallmon et al 1999) Prevalence Gingival overgrowth becomes clinically noticeable within 2 to 3 months after initial administration of phenytoin and reaches its maximal severity at 12 to 18 months. (Livingston S 1990)  occurs in 50% of patients receiving the drug, (Taicher S et al1991) Range is 3% to 84.5%. (Goaz PW,1972; Glickman 1941) It occurs more often in younger patients . Its occurrence and severity are not necessarily related to the dosage after a threshold level has been exceeded.
  23. 23. Pathogenesis A direct stimulating action on gingival fibroblasts or mast-cells with secondary fibroblastic involvement have been suggested. (Shafer et al 1960) It has also been proposed that susceptibility or resistance to pharmacologically induced gingival overgrowth may be governed by the existence of differential proportions of fibroblast subsets in each individual which exhibit a fibrogenic response to these medications. (JISP 2013) It has been hypothesized that only few subsets of patients on phenytoin develop enlargement. These individuals have fibroblasts with abnormal susceptibility to drug. Also fibroblasts from overgrown gingiva in phenytoin treated patients are characterized by elevated levels of proteins, esp. Collagen. (J Periodontol 2004) Tissue culture experiments by Shafer in 1960 indicate that phenytoin stimulates proliferation of fibroblast-like cells and epithelium. Two analogues of phenytoin (l-allyl-5-phenylhydantoinate and 5-methyl-5- phenylhydantoinate) have a similar effect on fibroblast-like cells.
  24. 24. Fibroblasts from a phenytoin-induced gingival overgrowth show increased synthesis of sulfated glycosaminoglycans in vitro. (Hassel TM 1983) Other proposed mechanisms include: -the production of inactive fibroblastic collagenase causing a decrease in collagen turnover Phenytoin may induce a decrease in collagen degradation as a result of the production of an inactive fibroblastic collagenase. (Hassell 1982) -phenytoin-induced folic acid deficiency that can cause degenerative changes in the sulcular epithelium and exacerbate the inflammatory response - phenytoin-induced increase in the synthesis of testosterone metabolites by gingival fibroblasts with resultant overgrowth. (Butler RT 1987, Brown RS 1991) Genetic predisposition is a suspected factor in determining whether a person treated with phenytoin will develop enlargement or not. Hassell et al (1994) hypothesized that gingival enlargement may result from the genetically determined ability or inability of the host to deal effectively with prolonged administration of phenytoin. In conclusion, the pathogenesis of gingival enlargement induced by phenytoin is not known, but some evidence links it to a direct effect on specific, genetically predetermined subpopulations of fibroblasts, inactivation of collagenase, and plaque-induced inflammation.
  25. 25. IMMUNOSUPPRESSANTS •Cyclosporine is a potent immunosuppressive agent used to prevent organ transplant rejection and to treat several diseases of autoimmune origin. •Mechanism of action- not well known, but it appears to selectively and reversibly inhibit helper T cells, which play a role in cellular and humoral immune responses. •Cyclosporin A (Sandimmune, Neoral) is administered intravenously or by mouth, and dosages greater than 500 mg/day have been reported to induce gingival overgrowth.(Daley TD 1986) •Cyclosporine-induced gingival enlargement is more vascularized than phenytoin enlargement . • Occurrence varies from 25% to 70% (Romito GA 2004) •Affects children more frequently, and its magnitude appears to be related more to the plasma concentration than to the patient’s periodontal status.
  26. 26. •Gingival enlargement is greater in patients who are medicated with both cyclosporine and calcium channel blockers. (Taylor J 1987) •The microscopic finding of many plasma cells plus the presence of an abundant amorphous extracellular substance has suggested that the enlargement is a hypersensitivity response to the cyclosporine. (Mariani G et al 1993) •In addition to gingival enlargement, cyclosporine induces other major side effects such as –nephrotoxicity - hypertension -hypertrichosis. •Another immunosuppressive drug, TACROLIMUS, has been used effectively and is also nephrotoxic, but it results in much less severe hypertension, hypertrichosis, and gingival overgrowth. (Bader G 1988)
  27. 27. CALCIUM CHANNEL BLOCKERS •Drugs developed for the treatment of cardiovascular conditions such as hypertension, angina pectoris, coronary artery spasms, and cardiac arrythmias. •They inhibit calcium ion influx across the cell membrane of heart and smooth muscle cells, blocking intracellular mobilization of calcium. This induces direct dilation of the coronary arteries and arterioles, improving oxygen supply to the heart muscle; it also reduces hypertension by dilating the peripheral vasculature. •These drugs are: -DIHYDROPYRIDINE DERIVATIVES (amlodipine [Lotrel, Norvasc], felodipine [Plendil], nicardipine [Cardene], nifedipine [Adalat, Procardia]) - BENZOTHIAZINE DERIVATIVES (diltiazem [Cardizem, Dilacor XR, Tiazac]) -PHENYLALKYLAMINE DERIVATIVES (verapamil [Calan, Isoptin, Verelan, Covera HS]). Nifedipine, one of the most often used,induces gingival enlargement in 20% of patients. (Lucas RM 1985)
  28. 28. It has been postulated that the drug may stimulate cell proliferation and synthesis indirectly by one of three mechanisms: oNifedipine is also used with cyclosporine in kidney transplant recipients, and the combined use of both drugs induces larger overgrowths. (Bokenkamp A 1994) oNifedipine gingival enlargement has been induced experimentally in rats, where it appears to be dose dependent; in humans, however, this dose dependency is not clear. oOne report indicates that nifedipine increases the risk of periodontal destruction in patients with diabetes mellitus type 2. (Wang X et al 2008) (3)by causing a calcium- dependent inhibitory effect on T cells that would increase gingival susceptibility to bacterial infection through immunosuppression. (Seymour RA 1991) (2)by stimulating the production of either interleukin 2 by T cells or metabolites of testosterone by gingival fibroblasts that in turn would promote cellular proliferation and synthesis (Nishikawa S 1991) (1) by giving rise to the formation of a more potent metabolic byproduct.
  29. 29. oDiltiazem, felodipine, nitrendipine, and verapamil also induce gingival enlargement. (Brown RS 1990) oThe dihydropyridine derivative, isradipine, can replace nifedipine in some cases and does not induce gingival overgrowth. (Carlson M et al 1997) oLars Heijl et al (J Periodontol, 1988) assessed the development of gingival overgrowth in dogs given nitrendipine, a new antihypertensive dihydropyridine. The results demonstrated that nitrendipine administered to Beagle dogs during a 20- week period causes marked overgrowth of gingival tissue of apparently normal composition. oLucas R M et al (1984) compared the nifedipine- and phenytoin-induced gingival hyperplasia at the light microscopic level and concluded that the nifedipine induced gingival hyperplasia is not only similar to phenytoin-induced gingival hyperplasia in its histopathologic morphology, but also in its response to treatment.
  30. 30. oIdiopathic gingival enlargement is a rare condition of undetermined cause. oIt has been designated by terms like Gingivomatosis, elephantiasis, idiopathic fibromatosis, hereditary gingival hyperplasia, and congenital familial fibromatosis. Etiology •The cause is unknown and thus designated as idiopathic. •Some cases- Hereditary basis but the genetic mechanisms are not well understood. •Mode of inheritance is found to be autosomal recessive in some cases and autosomal dominant in others. (Cocker et al 1974) •Recently a locus for autosomal dominant HGF has been mapped to a region on chromosome 2 (Hart et al. 1998, Xiao et al. 2000) •In some families the gingival enlargement may be linked to impairment of physical development. (Collan Y et al 1978) •The enlargement usually begins with the eruption of the primary or secondary dentition and may regress after extraction, suggesting that the teeth (or the plaque attached to them) may be initiating factors. The presence of bacterial plaque is a complicating factor. IDIOPATHIC GINGIVAL ENLARGEMENT
  31. 31. Described in tuberous sclerosis, which is an inherited condition characterized by a triad of epilepsy, mental deficiency, and cutaneous angiofibromas . (Thomas D, 1992) HGF may be an isolated disease entity or part of a syndrome associated with other clinical manifestations, such as hypertrichosis, mental retardation ,epilepsy, hearing loss , growth retardation and abnormalities of extremities. Studies have suggested that an important pathogenic mechanism may be enhanced production of transforming growth factor (TGF-beta 1) reducing the proteolytic activities of HGF fibroblasts, which again favor the accumulation of extracellular matrix (Coletta et al. 1999).
  32. 32. Clinical Features •Affects the attached gingiva, as well as the gingival margin and interdental papillae •The facial and lingual surfaces of the mandible and maxilla are generally affected, but the involvement may be limited to either jaw. •Enlarged gingiva is pink, firm, and almost leathery in consistency and has a characteristic minutely pebbled surface. •Severe cases- teeth are almost completely covered & enlargement projects into the oral vestibule. •The jaws appear distorted because of the bulbous enlargement of the gingiva.
  33. 33. ENLARGEMENTS ASSOCIATED WITH SYSTEMIC DISEASES Many systemic diseases can develop oral manifestations that may include gingival enlargement. These diseases and conditions can affect the periodontium by two different mechanisms, as follows: 1. Magnification of an existing inflammation initiated by dental plaque.  This group of diseases (Conditioned Enlargements) includes:  hormonal conditions (e.g., pregnancy and puberty)  nutritional diseases such as vitamin C deficiency  some cases in which the systemic influence is not identified (nonspecific conditioned enlargement). 2. Manifestation of the systemic disease independently of the inflammatory status of the gingiva. This group involves Systemic Diseases Causing Gingival Enlargement and Neoplastic Enlargement (Gingival Tumors).
  34. 34. Conditioned Enlargements •Conditioned enlargement occurs when the systemic condition of the patient exaggerates or distorts the usual gingival response to dental plaque. • The specific manner in which the clinical picture of conditioned gingival enlargement differs from that of chronic gingivitis depends on the nature of the modifying systemic influence. •Bacterial plaque is necessary for the initiation of this type of enlargement. However, plaque is not the sole determinant of the nature of the clinical features. •The three types of conditioned gingival enlargement are:  Hormonal (pregnancy, puberty), Nutritional (associated with vitamin C deficiency),  Allergic.
  35. 35. A) Enlargement in Pregnancy Pregnancy gingival enlargement may be marginal and generalized or may occur as single or multiple tumor-like masses . During pregnancy, there is an increase in levels of both progesterone and estrogen, which by the end of the third trimester reach levels 10 and 30 times the levels during the menstrual cycle, respectively. (Amar S 1994) These hormonal changes induce changes in vascular permeability leading to gingival edema and an increased inflammatory response to dental plaque. The subgingival microbiota may also undergo changes, including an increase in Prevotella intermedia. (Kornman KS 1980) A 55 fold increase in the proportion of P intermedia has been demonstrated in pregnant females as compared to non pregnant controls, implying a role for gestational hormones in causing a change in microbial ecology in the gingival pocket. (Jensen et al 1981)
  36. 36. Marginal gingival enlargement •Marginal gingival enlargement during pregnancy results from the aggravation of previous inflammation, •Incidence reported as 10% and 70%. •The enlargement is usually generalized and tends to be more prominent interproximally than on the facial and lingual surfaces. •The enlarged gingiva is bright red or magenta, soft, and friable and has a smooth, shiny surface. •Bleeding occurs spontaneously or on slight provocation. Tumorlike Gingival Enlargement. •The so-called pregnancy tumor is not a neoplasm; it is an inflammatory response to bacterial plaque and is modified by the patient’s condition. •Usually appears after the third month of pregnancy but may occur earlier. •The reported incidence is 1.8% to 5%. •Appears as a discrete, mushroomlike, flattened spherical mass that protrudes from the gingival margin or more often from the interproximal space and is attached by a sessile or pedunculated base.
  37. 37. •Generally dusky red or magenta, it has a smooth, glistening surface that often exhibits numerous deep-red, pinpoint markings. •Superficial lesion and usually does not invade the underlying bone. •Consistency varies; the mass is usually semifirm, but it may have various degrees of softness and friability. •Usually painless unless its size and shape foster accumulation of debris under its margin or interfere with occlusion, in which case, painful ulceration may occur. Histopathology •A central mass of connective tissue, with numerous diffusely arranged, newly formed, and engorged capillaries lined by cuboid endothelial cells and a moderately fibrous stroma. • The stratified squamous epithelium is thickened, with prominent rete pegs and some degree of intracellular and extracellular edema
  38. 38. B) Enlargement in Puberty Enlargement of the gingiva is sometimes seen during puberty and occurs in both male and female adolescents and appears in areas of plaque accumulation. The size of the gingival enlargement greatly exceeds that usually seen in association with comparable local factors. It is marginal and interdental 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.
  39. 39. Gingival enlargement during puberty has all the clinical features generally associated with chronic inflammatory gingival disease.  It is the degree of enlargement and its tendency to recur in the presence of relatively scant plaque deposits that distinguish pubertal gingival enlargement from uncomplicated chronic inflammatory gingival enlargement. After puberty the enlargement undergoes spontaneous reduction but does not disappear completely until plaque and calculus are removed. A longitudinal study of subgingival microbiota of children between ages 11 and 14 and their association with clinical parameters has implicated Capnocytophaga species in the initiation of pubertal gingivitis. (Mombelli A, Lang NP ,1990) Other studies have reported that hormonal changes coincide with an increase in the proportion of Prevotella intermedia and Prevotella nigrescens. (Fujii H, 1994) The microscopic appearance of gingival enlargement in puberty is chronic inflammation with prominent edema and associated degenerative changes
  40. 40. C) Enlargement in Vitamin C Deficiency  Enlargement of the gingiva is generally included in classic descriptions of scurvy. Acute vitamin C deficiency itself does not cause gingival inflammation, but it does cause hemorrhage, 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, resulting in the massive gingival enlargement seen in scurvy. Gingival enlargement in vitamin C deficiency is marginal; the gingiva is bluish red, soft, and friable and has a smooth, shiny surface.  Hemorrhage, occurring either spontaneously or on slight provocation, and surface necrosis with pseudomembrane formation are common features.
  41. 41. D) Plasma Cell Gingivitis  Consists of a mild marginal gingival enlargement that extends to the attached gingiva. Gingiva appears red, friable, and sometimes granular and bleeds easily; usually it does not induce a loss of attachment. Lesion is located in the oral aspect of the attached gingiva and therefore differs from plaque-induced gingivitis. An associated cheilitis and glossitis have been reported. Plasma cell gingivitis is thought to be allergic in origin, possibly related to components of chewing gum, dentifrices, or various diet components. Rare instances-marked inflammatory gingival enlargements with a predominance of plasma cells can appear; these are associated with rapidly progressive periodontitis.
  42. 42. E) Nonspecific Conditioned Enlargement (Pyogenic Granuloma): tumorlike gingival enlargement that may be conceived as an exaggerated reaction to minor trauma without it having been possible to demonstrate a definite infectious organism. more correctly called telangiectatic granuloma, since the lesion is highly vascular and usually is not purulent as the term pyogenic suggests. frequently ulcerated and the appearance of the fibrin-coated ulcer may resemble purulence. may occur in all areas of the oral mucosa, but is most frequently found on the marginal gingiva (Makek & Sailer 1985). may develop rapidly and the size varies considerably. reddish or bluish, sometimes lobulated, and may be sessile or pedunculated.  Bleeding from the ulcerated lesion is common, but typically it is not painful. Teeth may become separated due to interdental growth of the lesion.
  43. 43. A) Leukemia malignant neoplasms of WBC precursors characterized by: (1) Diffuse replacement of the bone marrow with proliferating leukemic cells; (2) Abnormal numbers and forms of immature WBCs in the circulating blood; (3) Widespread infiltrates in the liver, spleen, lymph nodes, and other sites throughout the body. According to the type of WBC involved, leukemias are classified as:  lymphocytic  myelocytic /myelogenous According to their evolution, leukemias can be acute, which is rapidly fatal  subacute chronic SYSTEMIC DISEASES CAUSING GINGIVAL ENLARGEMENT
  44. 44. Leukemic Infiltration of the Periodontium Leukemic cells can infiltrate the gingiva and, less frequently, the alveolar bone. Gingival infiltration often results in leukemic gingival enlargement Leukemic gingival enlargement consists of a basic infiltration of the gingival corium by leukemic cells that creates gingival pockets where bacterial plaque accumulates, initiating a secondary inflammatory lesion that contributes also to the enlargement of the gingiva.  It may be localized to the interdental papilla area or expand to include the mar- ginal gingiva and partially cover the crowns of the teeth Oral and periodontal manifestations of leukemia may include:  leukemic infiltration Bleeding  oral ulcerations and infections. The expression of these signs is more common in acute and subacute forms of leukemia than in chronic forms.
  45. 45. Clinically, the gingiva appears bluish red and cyanotic, with a rounding and tenseness of the gingival margin and has a shiny surface. Leukemic infiltration causing localized gingival swelling of the interdental papillae between the maxillary CI and LI The consistency is moderately firm, but there is a tendency towards friability and hemorrhage, occurring either spontaneously or on slight irritation. Enlargement may be diffuse or marginal, localized or generalized.
  46. 46. Appear as a diffuse enlargement of the gingival mucosa, an oversized extension of the marginal gingiva, or a discrete tumor like inter-proximal mass. Acute painful necrotizing ulcerative inflammatory involvement may occur in the crevice formed at the junction of the enlarged gingiva and the contiguous tooth surfaces. Patients with leukemia may also have a simple chronic inflammation without the involvement of leukemic cells and may present with the same clinical and microscopic features seen in patients without the systemic disease. Most cases reveal features of both simple chronic inflammation and leukemic infiltrate.
  47. 47. Histopathology •Areas of connective tissue infiltrated with a dense mass of immature and proliferating leukocytes •Engorged capillaries, edematous and degenerated connective tissue, and epithelium with various degrees of leukocytic infiltration and edema are found. • Isolated surface areas of acute necrotizing inflammation with a pseudomembranous meshwork of fibrin, necrotic epithelial cells, polymorphonuclear neutrophils (PMNs), and bacteria are often seen.
  48. 48. B) Granulomatous Diseases 1) WEGENER'S GRANULOMATOSIS: •Rare disease characterized by acute granulomatous necrotizing lesions of the respiratory tract, including nasal and oral defects. •Cause is unknown but it is considered as an immunologically mediated tissue injury. (Cotran RS 1989) • Renal lesions develop, and acute necrotizing vasculitis affects the blood vessels. •The initial manifestations of Wegener’s granulomatosis may involve the orofacial region and include: -oral mucosal ulceration -gingival enlargement -abnormal tooth mobility -exfoliation of teeth -delayed healing response. • The granulomatous papillary enlargement is reddish purple and bleeds easily on stimulation
  49. 49. Histopathology Chronic inflammation occurs with scattered giant cells and foci of acute inflammation and microabscesses covered by a thin acanthotic epithelium. 2) SARCOIDOSIS: granulomatous disease unknown etiology. It starts in individuals in their twenties or thirties, predominantly affects blacks  can involve almost any organ, including the gingiva, in which a red, smooth, painless enlargement may appear. Histopathology Sarcoid granulomas consist of discrete, noncaseating whorls of epithelioid cells and multinucleated, foreign body–type giant cells with peripheral mononuclear cells.
  50. 50. A) Benign Tumors of the Gingiva  Epulis is a generic term used clinically to designate all discrete tumors and tumorlike masses of the gingiva. It serves to locate the tumor but not to describe it. Neoplasms account for a comparatively small proportion of gingival enlargements and make up a small percentage of the total number of oral neoplasms. In a survey of 257 oral tumors, approximately 8 % occurred on the gingiva. (Mc Arthy 1941)  In another study of 868 growths of the gingiva and palate, of which 57% were neoplastic and the remainder inflammatory, the following incidence of tumors was noted: carcinoma, 11.0%; fibroma, 9.3%; giant cell tumor, 8.4%; papilloma, 7.3%; leukoplakia, 4.9%; mixed tumor (salivary gland type), 2.5%; angioma, 1.5%; osteofibroma, 1.3%; sarcoma, 0.5%; melanoma, 0.5%; myxoma, 0.45%; fibropapilloma, 0.4%; adenoma, 0.4%; and lipoma, 0.3%. (Bernick S 1948) NEOPLASTIC ENLARGEMENT (GINGIVAL TUMORS)
  51. 51. 1) 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 may be soft and vascular. •Fibromas are usually pedunculated. •Hard fibromas of the gingiva are rare; most of the lesions diagnosed clinically as “fibromas” are inflammatory enlargements. •Also called giant cell fibroma contains multinucleated fibroblasts. •In another variant of fibroma, mineralised tissue (bone, cementum like material, dystrophic calcification) may be found and is called peripheral ossifying fibroma. Histopathology Bundles of Well-formed collagen fibers with scattering of fibrocytes and a variable vascularity.
  52. 52. 2) Papilloma •Benign proliferations of surface epithelium associated with the human papilloma virus (HPV). •Viral subtypes HPV-6 and HPV-11 have been found in most cases of oral papillomas. •Appear as Solitary, wartlike or "cauliflower"-like protuberances and may be small and discrete or broad, hard elevations with minutely irregular surfaces. Histopathology Finger like projections of stratified squamous epithelium often hyperkeratotic, with a central core of fibrovascular tissue.
  53. 53. 3) Peripheral Giant Cell Granuloma •Giant cell lesions of the gingiva arise interdentally or from the gingival margin, occur most frequently on the labial surface, and may be sessile or pedunculated. •They vary in appearance from smooth, regularly outlined masses to irregularly shaped, multilobulated protuberances with surface indentations . •Ulceration of the margin is occasionally seen. •The lesions are painless, vary in size, and may cover several teeth. •They may be firm or spongy, and the color varies from pink to deep red or purplish blue. •Local irritation or trauma appears to be important for these lesions to occur. It has growth potential and may cause separation of teeth due to pressure exerted by the growth
  54. 54. Histopathology Numerous foci of multinuclear giant cells and hemosiderin particles in CT stroma. Areas of chronic inflammation are scattered throughout the lesion, with acute involvement occurring at the surface. Overlying epithelium is usually hyperplastic, with ulceration at the base. Bone formation occasionally occurs within the lesion
  55. 55. 4)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 cannot be diagnosed as any other disease. The cause of leukoplakia remains obscure, although it is associated with the use of tobacco (smoke or smokeless). Other probable factors are Candida albicans, HPV-16 and HPV-18, and trauma. Leukoplakia of the gingiva varies in appearance from a grayish white, flattened, scaly lesion to a thick, irregularly shaped, keratinous plaque. Histopathology • Leukoplakia exhibits hyperkeratosis and acanthosis. •Premalignant and malignant cases have a variable degree of atypical epithelial changes that may be mild, moderate, or severe, depending on the extent of involvement of the epithelial layers. •Inflammatory involvement of the underlying connective tissue is a common associated finding.
  56. 56. 5) Gingival Cyst •appear as localized enlargements that may involve the marginal & attached gingiva. •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. •Gingival cysts develop from odontogenic epithelium or from surface or sulcular epithelium traumatically implanted in the area. Histopathology A gingival cyst cavity is lined by a thin, flattened epithelium with or without localized areas of thickening. Less frequently, the following types of epithelium can be found: unkeratinized stratified squamous epithelium, keratin- ized stratified squamous epithelium, and parakeratinized epithelium with palisading basal cells
  57. 57. Other benign tumors or masses have also been described as rare or infrequent findings in the gingiva. These include: Nevus Myoblastoma Ameloblastoma Hemangioma Neurilemoma Neurofibroma Mucoceles
  58. 58. B) Malignant Tumors of the Gingiva Carcinoma Oral cancer accounts for less than 3% of all malignant tumors in the body. The gingiva is not a frequent site of oral malignancy (6% of oral cancers). (Krolls SO,1976) Squamous cell carcinoma is the most common malignant tumor of the gingiva.  It may be exophytic, presenting as an irregular outgrowth, or ulcerative, which appear as flat, erosive lesions.  It is often symptom free, often going unnoticed until complicated by inflammatory changes that may mask the neoplasm but cause pain; sometimes it becomes evident after tooth extraction. They are locally invasive, involving the underlying bone and periodontal ligament of adjoining teeth and the adjacent mucosa. mulberry-like tissue between 2nd PM and 1st M
  59. 59. Malignant Melanoma • Rare oral tumor that tends to occur in the hard palate and maxillary gingiva of older persons. • Usually darkly pigmented and is often preceded by localized pigmentation. • May be flat or nodular and is characterized by rapid growth and early metastasis. • Arises from melanoblasts in the gingiva, cheek, or palate. • Infiltration into the underlying bone and metastasis to cervical and axillary lymph nodes are common. Sarcoma • Fibrosarcoma, lymphosarcoma, and reticulum cell sarcoma of the gingiva are rare • Kaposi’s sarcoma often occurs in the oral cavity of patients with acquired immunodeficiency syndrome (AIDS), particularly in the palate and the gingiva Metastasis • Tumor metastasis to the gingiva occurs infrequently. • Such metastasis has been reported with various tumors, including adenocarcinoma of the colon, lung carcinoma, melanoma, renal cell carcinoma, hypernephroma, chondrosarcoma, and testicular tumor.
  60. 60.  False enlargements are not true enlargements of the gingival tissues but may appear as such as a result of increases in size of the underlying osseous or dental tissues.  The gingiva usually presents with no abnormal clinical features except the massive increase in size of the area.  Underlying osseous lesions  Enlargement of bone subjacent to the gingival area occurs most often in tori and exostoses but it can also occur in Paget’s disease, fibrous dysplasia, cherubism, central giant cell granuloma, ameloblastoma, osteoma, and osteosarcoma.  The gingival tissue can appear normal or may have unrelated inflammatory changes FALSE ENLARGEMENT Florid type fibrous dysplasia that induced osseous enlargement in mandibular molar areas appearing as gingival enlargement.
  61. 61. 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 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 termed developmental enlargement and often persists until the junctional epithelium has migrated from the enamel to the cementoenamel junction. Developmental gingival enlargements are physiologic and usually present no problems. However, when such enlargement is complicated by marginal inflammation, the composite picture gives the impression of extensive gingival enlargement Treatment to alleviate the marginal inflammation, rather than resection of the enlargement, is sufficient in these patients.
  62. 62. MANAGEMENT OF GINGIVAL ENLARGEMENTS Treatment of chronic inflammatory enlargement Treated by SCALING AND ROOT PLANING, (provided the size of the enlargement does not interfere with complete removal of deposits from the involved tooth surfaces). When chronic inflammatory gingival enlargements include a significant fibrotic component that does not undergo shrinkage after scaling and root planing or are of such size that they obscure deposits on the tooth surfaces and interfere with access to them, SURGICAL REMOVAL is the treatment of choice. FLAP OPERATION. Used when the enlarged gingiva remains soft and friable even after scaling and root planing GINGIVECTOMY Indicated if the gingivectomy incision removes all of the attached, keratinized gingiva, which will create a mucogingival problem Tumorlike inflammatory enlargements are treated by gingivectomy
  63. 63. Gingivectomy procedure
  64. 64. Treatment Of Drug induced gingival enlargement First, consideration should be given to the possibility of DISCONTINUING THE DRUG OR CHANGING THE MEDICATION. These possibilities should be examined with the patient’s physician. Simple discontinuation of the offending drug is usually not practical, but its SUBSTITUTION WITH ANOTHER MEDICATION might be an option. Second, the clinician should EMPHASIZE PLAQUE CONTROL as the first step in the treatment of drug-induced gingival enlargement Third, in some patients, gingival enlargement persists after careful consideration of the previous approaches. These patients may require SURGERY, either PERIODONTAL FLAP OR GINGIVECTOMY.
  65. 65. DRUG SUBSTITUTES  Alternative medications to the anticonvulsant PHENYTOIN include CARBAMAZEPINE AND VALPROIC ACID, both of which have been reported to have a lesser effect in inducing gingival enlargement.  For patients taking NIFEDIPINE, which has a reported prevalence of gingival enlargement of up to 44%, other CALCIUM CHANNEL BLOCKERS, SUCH AS DILTIAZEM OR VERAPAMIL, may be viable alternatives. Their reported prevalence of inducing gingival enlargement is 20% and 4%, respectively.  Also, consideration may be given to the use of another class of ANTIHYPERTENSIVE medications rather than calcium channel blockers, none of which is known to induce gingival enlargement.  For cyclosporine, TACROLIMUS is another immunosuppressant. The incidence of gingival enlargement in patients under tacrolimus therapy is approximately 65% lower than in those taking cyclosporine.  Clinical trials have also shown that the substitution of cyclosporine by tacrolimus results in a significant decrease in the severity of gingival enlargement when compared to patients who are kept on cyclosporine therapy
  66. 66. Treatment of drug induced enlargement
  67. 67. Treatment of Leukemic gingival enlargement  The patient’s bleeding and clotting times and platelet count should be checked, and the hematologist should be consulted before periodontal treatment is instituted.  After acute symptoms subside, attention is directed to correction of the gingival enlargement.  The rationale for therapy is to remove the local irritating factors to control the inflammatory component of the enlargement.  The lesion is treated by scaling and root planing performed in stages with topical and local anesthesia and instructing the patient in oral hygiene for plaque control.  This portion of the therapy may include, at least initially, the daily use of chlorhexidine mouthwashes. Oral hygiene procedures are extremely important in these patients and should be performed by the nurse if necessary.  Progressively deeper scaling is carried out at subsequent visits. Treatments are confined to a small area of the mouth to facilitate the control of bleeding.  ANTIBIOTICS are administered systemically the evening before and for 48 hours after each treatment to reduce the risk of infection.
  68. 68. Treatment of gingival enlargement in pregnancy Treatment requires elimination of all local irritants responsible for precipitating the gingival changes in pregnancy. Elimination of local irritants early in pregnancy is a preventive measure against gingival disease. This is preferable to treatment of gingival enlargement after it occurs. Marginal and interdental gingival inflammation and enlargement are treated by scaling and root planing. Treatment of tumorlike gingival enlargements consists of surgical excision and scaling and planing of the tooth surface. The enlargement will recur unless all of the irritants are removed.
  69. 69. Timing of Treatment and Indications Gingival lesions in 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.  Gingival enlargements will shrink after pregnancy but may not completely disappear. After pregnancy, the entire mouth should be reevaluated, a full set of radiographs taken, and the necessary treatment undertaken. Lesions should be removed surgically during pregnancy only if they interfere with mastication or produce an esthetic disfigurement that the patient wants removed. In pregnancy, the emphasis should be on preventing gingival disease before it occurs and treating existing gingival disease before it worsens.  All patients should be seen as early as possible in pregnancy.
  70. 70. Treatment of gingival enlargement in puberty Gingival enlargement in puberty is treated by performing scaling and curettage, removing all sources of irritation, and controlling plaque. Surgical removal may be required in severe cases. Those without gingival disease should be checked for potential sources of local irritation and should be instructed in plaque control procedures. Those with gingival disease should be treated promptly, before the effects of pregnancy on the gingiva become apparent.

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