PERIODONTOLOGY

1. GOOD MORNING

2. GINGIVAL
ENLARGEME
NT

3. CONTENT
S
DEFINITION
CLASSIFICATIONS
CLINICAL-FEATURES,ETIOLOGY,
HISTOPATHOLOGY AND
TREATMENT
SYNDROMES ASSOCIATED
CONCLUSION
REFERENCES

4. DEFINITION
Increase in size of gingiva or
gingival overgrowth.
Carranza11th edition.

5. 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.
III.Enlargement 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 causing 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. ON THE BASIS OF LOCATION AND DISTRIBUTION
LOCALIZED
GENERALISED
MARGINAL

7. PAPILLARY
DIFFUSE
DISCRETE

8. THE DEGREE OF GINGIVAL ENLARGEMENT CAN BE
SCORED AS FOLLOWS
Grade 0- No signs of gingival
enlargement.
Grade I-Enlargement confined to
interdental papilla.
Grade II-Enlargement involves
papilla and marginal gingiva.
Grade III-Enlargement covers three
quarters or more of the crown.

9. CHRONIC INFLAMMATORY ENLARGEMENT
CLINICAL FEATURES
 Site - interdental papilla and marginal gingiva.
 Shape -Life preserver shaped bulge  can increase in size
until it covers part of crowns.
 May be localized or generalized.
 Progresses slowly and painlessly.
 Painful ulceration sometimes.

10. CHRONIC INFLAMMATORY

11. HISTOPATHOLOGY
• Exudative and proliferative features.
• Lesions that are clinically deep red or bluish
redsoft and friable,bleed easily due to vascular
engorgement.
• Lesions that are relatively firm,resilient and pink
hue have a greater fibrotic component with an
abundance of fibroblasts and collagen fibres.

12. TREATMENT
Scaling and Curettage.
Surgical removal
Gingivectomy and Flap operation.
Enlargment with significant
fibrotic component
If the size of enlargemrnt
interferes to root surface
deposits

13. ETIOLOGY
• Prolonged exposure to dental plaque
• poor oral hygiene
• irritation by anatomic abnormalities
• improper restorative & orthodontic appliances.
• Mouth breathing habit .

14. ACUTE INFLAMMATORY ENLARGEMENT
GINGIVAL ABSCESS
ETIOLOGY
Bacteria carried deep into the tissues when a foreign
substance like toothbrush bristles, piece of apple core etc.is
forcefully embedded into gingiva
CLINICAL FEATURES:
• site - marginal gingiva or interdental papilla
• localized, painful, rapidly expanding.
• Within 24 to 48 hrs lesion becomes fluctuant & pointed
with a surface orifice from which a purulent exudate may
be expressed.

15. GINGIVAL ABSCESS

16. HISTOPATHOLOGY
 Surfaceepithelium
• Varying degree of intra and extracellular oedema.
• Leukocytic invasion & ulceration
 Connective tissue
• purulent focus surrounded by PMNs.
• edematous tissue
• vascular engorgement.
PERIODONTAL ABSCESS
• involves the supporting periodontal tissues.

17. TREATMENT
 Cause of the abscess should be removed.
 Drainage can be established .
 If lesion persists it can be curetted under L.A. or incised.
 If persistent and severe systemic antibiotic may be
prescribed.
 Any residual pockets  subgingival curettage or localized
gingivectomy.

18. DRUG INDUCED GINGIVAL ENLARGEMENT
 Anticonvulsants
 Immunosuppressants
 Calcium channel blockers
• affects the speech, mastication, tooth eruption, and
aesthetics problems.
General clinical features:
• site - interdental papilla, facial and lingual gingival
margins

19. • Starts as a painless beadlike enlargement of the interdental
papilla
• mulberry shaped , firm , pale pink, resilient
• no tendency to bleed
• appears to project from beneath the gingival margin
separated by a linear groove .
• Plaque control becomes difficult resulting in
secondary inflammation.
produce
• red, bluish discoloration, obliterate lobulated surface
demarcations and increase bleeding tendency.
• Regress spontaneously within few months after
discontinuation of the drug.

20. HISTOPATHOLOGY
• Epithelium - acanthosis, elongated rete pegs .
• Connective Tissue - densely arranged collagen bundles,
fibroblasts, neovascularisation
• abundance of amorphous ground substance .
• CYCLOSPORINE- Highly vascularised & foci of chronic
inflammatory cells.
• PHENYTOIN - fibroblast to collagen ratio normal,
oxytalan fibers are numerous .

21. ANTICONVULSANTS
• First gingival enlargement reported .
• Introduced by Merritt and Putnam in 1938.
• Drugs used for the treatment of epilepsy.
• Phenytoin, ethotoin, mephenytoin, succinimides etc.
• 50% of the patients
• younger patients more prone .
• appears in saliva
• systemic administration accelerates the healing of
gingival wounds in non- epileptic humans.

22. • MECHANISM(PHENYTOIN )
Fibroblasts from a phenytoin induced gingival
overgrowth show increased synthesis of sulfated
glycosaminoglycans in vitro
Phenytoin may induce a decrease in collagen-degradation as
a result of the production of an inactive fibroblastic
collagenase.

23. PHENYTOIN INDUCED

24. IMMUNOSUPPRESSANTS
• CYCLOSPORINES used to prevent organ transplant
rejection & to treat autoimmune origin diseases.
• if dosage > 500mg/day reported to induce gingival
enlargement.
• 30% patient.
• More vascularised .
• associated with nephrotoxicity, hypersensitivity,
hypertension, hyperthricosis.

25. CYCLOSPORINE INDUCED

26. CALCIUM CHANNEL BLOCKERS
(nifedipine,diltiazem, felodipine, nitrendipine and verapamil)
• used for CVS disorders, hypertension , angina pectoris,
coronary artery spasm & cardiac arrhythmia.
• Nifedipine induces enlargement in 20% cases
• Nifedipine + cyclosporines (for kidney transplant)
• larger overgrowth
• dose dependent growth

27. NIFEDIPINE INDUCED

29. IDIOPATHIC GINGIVAL ENLARGEMENT
• termed as gingivostomatitis, elephantiasis,
idiopathicfibromatosis, hereditary gingival hyperplasia &
congenital familial fibromatosis.
ETIOLOGY :
• unknown
• hereditary basis (autosomal dominant or recessive)
• begins with primary & secondary dentition eruption.

30. CLINICAL FEATURES:
• Site - attached gingiva, gingival margin, and interdental
papilla
• pink,firm and leathery with pebbled surface.
• Teeth are completely covered.
• Severe cases jaw appears distorted due to bulbous
enlargement
• secondary inflammation

31. HISTOPATHOLOGY:
• Epithelium -thickened & acanthotic with elongated rete
pegs.
• Connective Tissue- relatively avascular, densely arranged
collagen bundles & numerous fibroblasts

32. ENLARGEMENT ASSOCIATED WITH SYSTEMIC DISEASES
• Many systemic diseases  oral manifestations  two
different mechanisms
1. Magnification of existing inflammation initiated by
dental plaque.. “Conditioned enlargement”
2. Manifestation of the systemic disease independent of the
inflammatory status of the gingiva.This group is described
as “ Systemic diseases causing gingival enlargement”.

33. CONDITIONED ENLARGEMENT
• systematic condition of the patient exaggerates the usual
gingival response to dental plaque.
• bacterial plaque is necessary for its initiation.
a). Hormonal conditions (pregnancy & puberty)
b). Nutritional (vitamin C deficiency)
c). Non- specific conditioned enlargement

34. ENLARGEMENT IN PREGNANCY
marginal and generalized or single or multiple tumor
like masses.
ETIOLOGY - increase in progesterone and estrogen till 3rd
trimester.
increased vascular permeability and gingival edema.
1.MARGINAL ENLARGEMENT
results from aggravation of previous inflammation.

35. 2.TUMOR LIKE GINGIVAL ENLARGEMENT
(pregnancy tumor)
• inflammatory response to bacterial plaque
CLINICAL FEATURES
• lesions are discrete, mushroom like, flattened spherical
masses
• sessile, pedunculated base
• exhibits deep red pin point markings.
• Painful ulcerations may occur.

36. HISTOPATHOLOGY (angiogranuloma)
• central mass of connective tissue.
• neovascularisation lined by cuboidal endothelial
cells.
• varying degree of edema & chronic inflammatory
infiltrate
• epithelium thickened, prominent retepegs.

37. TREATMENT
 minimize the potential exaggerated inflammatory
response related to hormonal alteration.
Plaque control,scaling and root planing should be
non emergent procedures performed.
Long stressful appointment and periodontal
surgical procedures should be postponed until
postpartum.
No medications and radiographs
Marginal and interdentalScaling and curettage.
Tumor like enlargementSurgical excisionif
possible postpone.

38. ENLARGEMENT IN PUBERTY
CLINICAL FEATURES :
• -marginal & interdental (often facial gingiva)
• - associated with chronic gingival disease.
• -reduces after puberty.
• -Capnocytophaga sp.. & P. intermedia

39. HISTOPATHOLOGY
• chronic inflammation with edema.
TREATMENT
• Scaling,curretage and oral hygiene instructions.
• Surgical removal may be performed in severe cases.

40. ENLARGEMENT IN VITAMIN C DEFICIENCY
CLINICAL FEATURES :
• Marginal gingivitis
• hemorrhage on slight provocation and surface necrosis
with pseudomembrane formation.

41. HISTOPATHOLOGY(VIT-C)
• chronic inflammatory cellular infiltrate with superficial
acute response
• scattered areas of hemorrhage
• diffuse edema, collagen degeneration & scarcity of
collagen.

42. PLASMA CELL GINGIVITIS
(atypical gingivitis,plasma cell gingivostomatitis )
• site- marginal and attached gingiva .
CLINICAL FEATURES :
• red, friable, bleeds easily
• site-oral aspect of attached gingiva

43. HISTOPATHOLOGY(Plasma Cell Gingivitis)
• Epithelium- spongiosis and infiltrated with chronic
inflammatory cells.
• lower spinous layer and basal layer damaged
• plasma cells infiltrate

44. NON SPECIFIC
CONDITIONED ENLARGEMENT (pyogenic granuloma)
• Tumor like gingival enlargement.
• conditioned response to minor trauma.
CLINICAL FEATURES:
• discrete spherical tumor like mass
• red friable with ulceration,purulent exudation.
• Involute to become fibroepithelial papilloma.

45. HISTOPATHOLOGY
• chronic inflammation with granulation tissue
• vascular spaces & epithelial atrophy
TREATMENT
removal of lesion and local irritating factors .

46. SYSTEMIC DISEASES CAUSING GINGIVAL
ENLARGEMENT
LEUKEMIA
CLINICAL FEATURES :
• diffuse or marginal
• localized or generalized tumor
like mass in interproximal spaces
• red, friable, firm and hemorrhagic
• painful necrotising
• ulcerative inflammation

47. HISTOPATHOLOGY
• Epithelium - varying degree of leukocytic infiltration &
edema
• Psuedomembranous meshwork of fibrins, necrotic
epithelial cells, PMNS & bacteria.
• Connective Tissue - infiltrated with a dense mass of
immature & proliferating leukocytes
• engorged capillaries.

48. TREATMENT
In leukemic patients (in general)
 Refer the patient to physician.
 Prior to chemotherapy, a complete periodontal treatment
plan should be prepared.
Treatment plan
 Monitor hematological lab values daily
 Administer antibiotics prior to any periodontal therapy
 Extract non-maintainable or potentially infectious
teeth,atleast 10 days prior to initiation of chemotherapy.
 Thorough periodontal debridement is done and oral
hygiene instructions are given

49. During acute phases of leukemia,patients should receive only
emergency periodontal care.
• If there is a persistent gingival bleeding
• Cleanse the area with 3 percent hydrogen peroxide.
• Carefully explore the area and remove any etiologic local
factors
• Recleanse with 3 percent H2O2 place the cotton pellet
soaked in thrombin against bleeding point.
• Cover with a gauze
• If oozing persists after removal of gauze,replace cotton and
then place a periodontal dressing over the area for 24
hours.

50. GRANULOMATOUS DISEASES
WEGENER’S GRANULOMATOSIS
ETIOLOGY :
• cause unknown (immunologically mediated tissue injury)
• characterized by acute granulomatous necrotising lesion of
respiratory tract involving the orofacial region .
CLINICAL FEATURES :
• reddish purple bleeds easily.
HISTOPATHOLOGY:
• chronic inflammatory giant cells & foci of acute
inflammation, microabscesses covered by a thin acanthotic
epithelium.

51. SARCOIDIOSIS
ETIOLOGY
• unknown.
• red, smooth, painless enlargement .
HISTOPATHOLOGY
• discrete, noncaseating whorls of epitheloid cells &
multinucleated
• foreign-body-type giant cells

52. NEOPLASTIC ENLARGEMENT (GINGIVAL TUMORS)
Benign tumors of gingiva Malignant tumors
 Epulis Squamous cell carcinoma
 Fibroma Malignant melanoma
 Papilloma Sarcoma
 Peripheral giant cell granuloma Fibrosarcoma
 Cental giant cell granuloma Lymphosarcoma
 Leukoplakia Reticulum cell carcinoma
 Gingival Cyst Kaposis sarcoma
 Other benign masses like nevus Renal cell carcinoma

53. FALSE ENLARGEMENT
• Not true enlargement but appear as an increase in size of
underlying osseous or dental tissues.
•
A). Underlying osseous lesions
• Enlargement of bone - exostosis or tori
(paget’s disease, fibrous dysplasia, cherubism, central giant
cell granuloma, ameloblastoma osteoma, osteosarcoma)

54. B). Underlying dental tissues
• during stages of eruption particularly primary dentition.
• labial gingiva- bulbous marginal distortion
called developmental enlargement
• & persists until junctional epithelium has migrated from
enamel to CEJ
• Physiologic
• complicated by marginal inflammation.

56. CONCLUSION
• The treatment of gingival enlargement depends on the type
of clinical enlargement encountered.
• The enlargement can be inflammatory,fibrotic or a
combination of both.
• Plaque induced inflammation appears to be a general
stimulating effect regardless of the mechanism of gingival
enlargement.
• In recent years,flap surgery have been used more often to
treat gingival enlargement than gingivectomy.

57. REFERENCES
 Clinical periodontology and Implant dentistry(5th
Edition) Jan Lindhe Vol 1.
Carranza’s Clinical Periodontology Eleventh edition.
Outline of periodontics,J.D.Manson,B.M.Eley.
Essentials Of Periodontology,Sahitya Reddy S.
Glickman:Hyperplasia of the gingiva associated with
Dilantin therapy.
Hallmon WW,Rossman JA:The role of drugs in the
pathogenesis of gingival overgrowth.
Slavin J,Taylor J :Cyclosporine,nifedipine and gingival
hyperplasia .
Rushton MA:Hereditary or Idipathic hyperplasia of the
gums

58. THANK YOUTHANK YOU