1. GINGIVAL ENLARGEMENT

2. CLASSIFICATION BASED ON ETIOLOGY
INFLAMMATORY ENLARGEMENT
Acute
Chronic
FIBROTIC ENLARGEMENT
drug induced enlargement
Idiopathic enlargement

3. enlargement associated with systemic disease
Conditioned enlargement
Puberty
Vita C deficiency
Pregnancy
Plasma cell gingivitis
Nonspecific conditioned enlargement(granuloma pyogenicum)
Systemic diseases causing gingival enlargement
Leukemia
Granulomatous disease(sarcoidosis,wegener’s granulomatosis)

4. Neoplastic enlargement
Benign tumors
Malignant tumors
False enlargement
Underlying osseous lesion
Underlying dental tissues

5. Criteria for assessing ge
Grade I-
Grade II-
Grade III-
Grade IV-

6. CLASSIFICATION BASED ON LOCATION & DISTRIBUTION
LOCALISED: 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 & attached gingiva & papilla
Discrete :an isolated sessile or pedunculated tumor like enlargement

7. PREDISPOSING FACTORS AGE-younger age groups are more affected
SEX-males are more affected
SITE-anterior facial areas especially the canine region is more prone
INFLAMMATION-predisposes to enlargement

8. Age AGE-younger age groups are more affected
Higher dosage may be administered
As age advances the metabolic process in gingival tissue like glycosaminoglycans synthesis reduces

9. Sex SEX-males are more susceptible
Progesterone a female sex harmone decreases glycosaminoglycan synthesis by human gingival fibroblasts.

10. SITE
Anterior regions are more affected especially the canine region is more prone
Buccal side is more affected than lingual.
Dentulous areas are more prone than edentulous area
Related to plaque control & drying of mucosa .
Temperature difference.

11. INFLAMMATION INFLAMMATION-predisposes to enlargement.
Enlargement may predisposes to plaque accumulation

12. Drug induced gingival enlargement
Calcium channel blockers
Immuno suppressants
Anti-epileptic

13. Calcium channel blockers
Nifedipine
Amlodipine
Verapamil
Dilitiazem
Oxodipine

14. Drug discovered-1960
Therapeutic usage-1980
Class I-affect the heart(verapemil)
Class II-affect mainly blood vessels &vasodilation(dihydropyridines)
Class III-minimal or slight inotropic effects(dilitiazem)

15. M.O.A-alter the Ca++ metabolism ,the influx of Ca++ across the cell membrane is decreased due to reduced membrane permeability.
Contraction of muscle cells occurs when increased intracellular Ca++ binds to trophonin & in the presence of ATP causes the myosin bridge to contract the actin filaments.

16. Although dosage & duration of medication were cited as possible explanations no clear evidence available.

17. Histologic features Hyperkeratosis Acanthosis
Elongation of rete pegs(test tube shape)
Fibroblast with prominent RER

18. Pathogenesis
Apoptosis is characterized by nuclear & cytoplasmic condensation,membrane budding,formation of apoptotic bodies, on-random fragmentation of DNA.
Calcium plays an important signaling pathway in triggering apoptosis

19. Prolongation of cell life through inhibition of keratinocyte apoptosis.
Ca++ is needed for keratinocyte DNA fragmentation.
Low Ca++ expresses Bcl-2 gene which suppresses apoptosis
High Ca++ expresses Bax gene which induces apoptosis

20. Indirect action of nifedipine may occur by stimulating either production of IL-2 by T-cells or metabolites of testosterone by gingival fibroblasts which in turn stimulates proliferation or increased collagen synthesis.
Responsiveness of the cells appear to be inversely proportional to the IL-1 β levels.
Medullasin(a neutrophil elastase-like proteases) plays a role in development of inflammation & mechanism is not known.

21. A role of TGFβ,bFGF & heparan sulphate glycosaminoglycan.
The site specificity in the accumulation of collagenous proteins in the ECM may be due to the relatively slow synthesis of these proteins in other tissues or because of altered deposition/resorption in susceptible tissues.

22. Immuno suppressants
Cyclosporine
Tacrolimus

23. cyclosporin Liphophilic cyclic endecapeptide
Used in the prevention of organ transplant rejection
Peak plasma conc. reached after 3 hrs.
Serum half life 17-40hrs.
mostly bound to erythrocytes & lipoproteins. only 5% free in plasma.
Therapeutic conc-135μg

24. The total amount of drug per weight in tissue can be upto 20-fold greater than in plasma & varies between organs & individuals.

25. Pharmacological action
Cs suppresses T-helper cell function leaving T-suppresser cells un affected.
Cs selectively suppresses the cellular immune response by interfering with IL-2 production.

26. MOA
Drug cyclophilin complex binds & inhibits calcineurin a calcium & calmodulin dependent serine threonine phosphatase.
This inactivation prevents dephosphorylation of nuclear factor of activated T-cells(NF-AT) the nuclear import of NF-AT complex & the formation of a transcriptionally active NF-AT complex. the net consequence is inhibition of IL-2.

27. Pathogenesis
During plaque induced inflammation the humoral response replaces the cell mediated response.
Several cytokines that play important role in humoral response are known to influence connective tissue homeostasis.
IL-1β & IL-6 are cytokines known to play regulatory function in periodontal tissue turnover with IL-1β inducing & IL-6 reducing tissue break down.

28. IL-6 is a multifactorial cytokine found to induce final maturation of B-cells into immunoglobulin producing plasma cells.
The increase in plasma cell number may promote Cs induced alteration of the cytokine profile within gingival tissue, resulting in disruption of normal connective tissue turn over

29. The immunosuppresed pts had markedly lower no of NK cells which could enhance the ability of Cs to induce proliferative activity not directly, but by disrupting the complex conn tissue-homeostasis mechanism.
Cs stimulates TGF-β1,PDGF which promote fibroblast growth & matrix production.
Cs reduces the level of MMP-1 & MMP-2 & increases the level of TIMP.

30. Cs reduces gingival prostacyclin(PGI2)synthesis.
PGI2 has an antiproliferative effect via increasing cAMP thus gingival overgrowth may result.

31. Perlecan a type of proteoglycans is increased.
It has high affinity for growth factors has been attributed to this proteoglycans ,which ia able to retain these factors inside the basement membrane.
Perlecan acts as a major reservoir of FGF-2.

32. Cs could mimic endogenous signals for wound repair or remodelling,but at the usual therapeutic dosage levels& in the absence of any specific inflammatory process, its effect is sub threshold.
However when specific inflammatory processes take place within localized & specific areas the effects of Cs could act synergistically with endogenous signals stimulating excessive repair or growth.

33. Side effects of Cs Hypertension
Dihydropyridines are Ca ++ channel blockers used to treat hypertension

34. Rx Conversion to other drugs in the same group-tacrolimus
Reduction or withdraval of the drug under medical suoervision if indicated
gingivectomy

35. Anti-epileptic
Phenytoin
Sodium valproate
Phenobarbital
Vigabatrin

36. Phenytoin
Macrophages differ in respect to location, morphology & function & they have been recognized to be major mediator of connective tissue turnover,maintenence & repair.

37. Macrophage 27E10-asociated with production of pro inflammatory cytokines-IL-1,IL-6 & TNF-α
A reparative/proliferative Macrophage phenotype RM3/1 associated with production of PDGF- β,TGF- β1,bFGF.
Expression of 25F9 antigen is connected with maturation of macrophage & relative decrease in 25F9 indicates that maturation of tissue macrophages have been altered.

38. decreases the level of EGF receptors in gingival fibroblast resulting in increased cellular responsiveness to EGF,which can stimulate cellular DNA synthesis.
Phenytoin can stimulate testosterone metabolism & increases the level of 5α-dihydrotestosterone a stimulator of fibroblast growth.

39. Phenytoin interferes with folic acid metabolism & hence causes folic acid deficiency
Folic acid is necessary for DNA synthesis, thus tissues with a high turn over could be adversely affected
PHT can cause immuno suppresion in long term use like decreased salivary IgA which could favor inflammation.

40. PHT & its metabolite P-HPPA induces the release of factors from monocytes which activate quiescence gingival fibroblast to synthesize DNA.
Decreases ACTH which leads to increased somatotrophic harm one which increases fibroblast proliferation.

41. PHT leads to production of collagenase which is inactive.
Increased PGE2 leading to increased hyaluronic acid .

42. Rx Conversion to other drugs in the same group
Reduction or withdraval of the drug under medical suoervision if indicated
gingivectomy

43. Others
Erythromycin

44. Acute inflammatory enlargement
Gingival abscess
Localised,painful expanding lesion that is usually of sudden onset.
Generally limited to marginal gingiva or interdental papilla.
Red, swelling with a smooth shiny surface.

45. Within 24-48hrs the lesion usually becomes fluctuant & pointed with a surface orifice from which a purulent exudates may be expressed.
The adjacent teeth are often sensitive to percussion.

46. Etiology
Bacteria carried deep into tissues when a foreign substance such as toothbristle,small traumatic injury.

47. Histopathology Polymorphonuclear leucocytes. Edematous tissue
Vascular engorgement

48. Rx
Incision and drainage.

49. Chronic inflammatory enlargement
Slight ballooning of the interdental papilla &/or the marginal gingiva.
Early stages it produces a life preserver –like bulge around the teeth.
Progresses slowly & painless.
Enlargement is generally papillary or marginal.

50. Occasionally it may occur as a discrete sessile or pedunculated mass resembling a tumor.
Painful ulceration sometimes may occur

51. Etiology Prolonged exposure to dental plaque.
Factors that favor plaque accumulation
Poor oral hygiene
Abnormal relationship of adjacent teeth
Overhanging margin
Food impaction
Orthodontic appliance
RPD
Nasal obstruction
Improperly contoured restoration & pontics

52. Histopathology
Exudative & proliferative features of chronic inflammation is seen.
Edematous tissue
Inflammatory cells
Vascular engorgement
Fibrotic tissue
Abuntance of fibroblasts & collagen fibers

53. Treatment Removal of plaque Control of inflammation
Scaling & root planning
Fibrotic enlargement –gingivectomy.

54. Enlargement associated with mouth breathing
Gingiva appears red & edematous
Diffuse surface shininess of the exposed area
Common site-maxillary anterior region.
Attributed to irritation from surface dehydration

55. Idiopathic gingival enlargement
Gingivostomatosis
Elephantiasis
Diffuse fibroma
Familial elephantiasis
Idiopathic fibromatosis
Hereditary gingival hyperplasia
Congenital familial fibromatosis

56. Clinical features
It affects the attached gingiva as well as the marginal gingiva & interdental gingiva.
Pink, firm & almost leathery in consistency & has a characteristic minutely pebbled surface.
In severe cases the teeth are almost covered & projects into the vestibule.
Jaws appears distorted because of bulbous enlargement.

57. Combined enlargement
Gingival hyperplasia is complicated by secondary inflammatory changes because it produces conditions favorable for accumulation of plaque by accentuating the depth of gingival sulcus.
It consist of 2 portions.
A primary or basic hyperplasia of the connective tissue & epithelium.
A secondary complicating inflammatory component

58. Enlargement associated with systemic disease
Conditioned enlargement
The condition itself does not cause the condition, the altered tissue metabolism accentuates the response to local irritants.
Magnification of an existing inflammation initiated by dental plaque.
Puberty
Pregnancy(harmonal)
Vita C deficiency (nutritional disturbances)

59. Enlargement in pregnancy
Pregnancy does not cause the condition, the altered tissue metabolism in pregnancy accentuates the response to local irritants.
Gingival enlargement in pregnancy is called ANGIOGRANULOMA.
Enlargement may be marginal, mostly generalized & more prominent in interdental papilla.
Sometimes it occur as a discrete, mushroom like flattened spherical mass attached by a sessile pedunculated base.

60. Puberty

61. Vita C

62. Non specific conditioned enlargement
Granuloma pyogenicum – is a tumour like enlargement that is considered an exaggerated response to minor trauma.

63. Systemic diseases causing gingival enlargement
Leukemia
Granulomatous disease
Sarcoidosis
wegener’s granulomatosis

64. Neoplastic enlargement
Benign tumors
Epulis – is a generic term used clinically to designate all discrete tumors & tumor like masses of the gingiva.
Most epulis are inflammatory rather than neolastic.

65. Benign tumors Fibroma Papilloma Peripheral giant cell granuloma
Central giant cell carcinoma
Gingival cyst
Leukoplakia

66. Malignant tumors Squamous cell carcinoma Malignant melanoma Metastasis
Adenocarcinoma of colon
Lung carcinoma
Primary hepatocellular carcinoma
Renal cell carcinoma
Hypernephroma
Chondrosarcoma
Testicular tumor

69. Apoptosis

70. Rx
gingivectomy