Medicine and Oral health

1. GINGIVAL ENLARGEMENT

2. CONTENTS
• Introduction
• Classification
• Indices
• Inflammatory Enlargement
• Enlargements associated with systemic diseases
• Neoplastic enlargement
• Drug-induced enlargement
• Idiopathic gingival enlargement
• False enlargement
• Conclusion
• References

3. INTRODUCTION
Hypertrophic
gingivitis
Gingival enlargement
Gingival overgrowth
Gingival
hyperplasia

4. CLASSIFICATION
A] Based on etiologic factors and pathologic changes
I. Inflammatory Enlargement
-Acute
- Chronic
II. Drug-induced enlargement
III. Enlargements associated with systemic diseases
ii) Systemic diseases causing
1. Leukemia
2.Granulomatous diseases (Wegener's
granulomatosis, sarcoidosis)
i) Conditioned enlargement
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5. B] Based on location and distribution
I. Localized
II. Generalized
III. Marginal
IV. Papillary
V. Diffuse
VI. Discrete

6. INDICES
Bokenkamp & Bohnhorst 1994
Grade 0  No signs of gingival enlargement
Grade 1  Enlargement confined to IDP
Grade 2  Enlargement involves IDP & marginal gingiva
Grade 3  Enlargement covers three quarters / more of
crown

7. Degree of gingival hyperplasia according to modified index
by Angelopoulos & Goaz 1972
Grade Hyperplasia Size Tooth
coverage
0 No Normal No
1 Minimal <2 mm Cervical 3rd
or less
2 Moderate 2-4 mm Middle 3rd
3 Severe >4 mm More than
2/3rd

8. Gingival overgrowth index- Mc Gaw et al 1987
Grade 0  No overgrowth, feather edge gingival margin
Grade 1  Blunting of gingival margin
Grade 2  Moderate gingival overgrowth (one third crown
length)
Grade 3  Marked gingival overgrowth (more than one
thirds of crown)

9. Clinical index for drug induced gingival overgrowth
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3. buccolingual dimension of upto
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4. Probing ≤ 6mm
5. Papillae retractable
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4. The probing depth ≥ 6mm
5. Papillae retractable
1. Severe overgrowth, profound
thickening of gingiva
2. Large % of the clinical crown is
covered
3
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5.buccolingual dimension 3mm

10. 1. INFLAMMATORY ENLARGEMENT
CHRONIC
INFLAMMATORY
Gingival
abscess
ACUTE
Periodontal
abscess

11. a. Chronic inflammatory enlargement
Etiology
Plaque
accumulation &
retention
Poor oral
hygiene
Anatomic
abnormalities
Improper
restoration
Orthodontic
appliances
Malocclusion

12. Clinical Features
1.
Slight ballooning of IDP & marginal gingiva
Life preserver shaped bulge
Smooth , edematous , bleed easily
Localised / generalised
Progress- slowly and painlessly
Pseudopockets

13. Discrete sessile or
pedunculated tumor like mass
Interproximal / marginal or
attached gingiva
Slow growing and painless
Clinical Features
1. 2.

14. Histopathology
1.Soft and friable
2.Firm and resilient

15. B. ACUTE INFLAMMATORY
ENLARGEMENT
1. GINGIV
ALABSCESS
Etiology
 Foreign substances
Clinical features
 Marginal gingiva or IDP
 Red swelling
 smooth shiny surface
 Fluctuant and pointed with
a surface orifice
 expresses purulent exudate

16. 2. PERIODONTALABSCESS
Lateral abscess / parietal abscess
Depending on location
- Gingival
- Periodontal (Acute / Chronic)
- Pericoronal
Meng et al ’99
Depending on number
- Single
- Multiple

17. Etiology
PERIODONTITIS RELATED
Extension of infection from PD
pocket
Lateral extension of
inflammation
Pocket with a tortuous course
Incomplete removal of calculus

18. Etiology
NON PERIODONTITIS
RELATED
Impaction of foreign bodies
Endodontic perforation
Lateral cyst infection
Factors affecting morphology
of root

19. Signs and symptoms
Acute abscess
- Mild to severe discomfort
- Localized red, ovoid swelling
- Periodontal pocket
- Mobility
- Tooth elevation in the socket
- Tenderness to percussion or
biting
- Suppuration
- Elevated temperature
- Regional lymphadenopathy
Chronic abscess
- No pain or dull pain
- Localized inflammatory lesion
- Slight tooth elevation
- Intermittent exudation
-Fistulous tract often associated
with deep pocket
- Usually without systemic
involvement

20. ENLARGEMENTS ASSOCIATED WITH
SYSTEMIC DISEASES
Two mechanisms
1. Magnification of an existing inflammation initiated by
dental plaque
- conditioned enlargement
2. Manifestation of the systemic disease independently of the
inflammatory status of the gingiva
- systemic disease causing enlargement

21. 1. Conditioned enlargement
• Systemic condition exaggerates or distorts usual gingival
response to plaque
• Bacterial plaque
Types
1. Hormonal – pregnancy , puberty
2. Nutritional – vitamin C deficiency
3. Allergic
Non specific conditioned

22. 1. Marginal and generalised enlargement
2. Single or multiple tumor like masses
Hormonal changes
- Progesterone and estrogen
- Vascular permeability – edema , inflammatory response
Subgingival microbiota – P. intermedia
a. Enlargement in pregnancy

23. 1. Marginal enlargement
- Generalised , more prominent
interdentally
- Bright red or magenta colour
- Friable , smooth & shiny
surface
- Bleeding – spontaneously or
on slight provocation
“ Pregnancy rhinitis”

24. 2. Tumor like gingival enlargement
“Pregnancy tumor”
- Discrete mushroomlike , flattened
spherical mass
- Dusky red or magenta , smooth
glistening surface
- Doesnot invade underlying bone
- Semifirm – soft , friable
- sessile or pedunculated
- Painless unless its size and shape foster
accumulation of debris

25. Angiogranuloma
Thickened epilthelium
Newly formed, engorged
capillaries
Fibrous stroma
Inflammatory infiltrate
Histopathology

26. Treatment
• Removal of plaque and calculus
• Tumor like gingival enlargement - surgical excision and
SRP
• Recurrence
• Spontaneous reduction – termination of pregnancy

27. • Male and female adoloscents
• Areas of plaque accumulation
• Facial surface
• Marginal and interdental
Histopathology
- Similar to Chronic inflammation
Difference
b. Enlargement in puberty

28. c. Enlargement in vitamin C deficiency
• Classic description of scurvy
• Acute deficiency – hemorrhage , collagen degeneration , edema
• modify response to plaque
Clinical features
- Bluish red , soft , friable, boggy
- smooth & shiny surface
- Haemorrhage – spontaneous /
slight provocation
- Surface necrosis with
pseudomembrane formation

29. d. Plasma cell gingivitis
• Atypical gingivitis / plasma cell gingivostomatitis
• Plasma cell granuloma – localised form
• Allergic in origin
Clinical features

30. • Pyogenic granuloma
Clinical features
• Discrete spherical , tumorlike mass , pedunculated ,
smooth surface
• Bright red or purple , friable or firm
• Painless
• Hemorrhage
e. Nonspecific conditioned enlargement

31. 2.Systemic Disease That Cause Gingival
Enlargement
1. Leukemia
malignant neoplasia of WBC precursors
-diffuse replacement of bone marrow – proliferating
leukemic cells
- abnormal number and forms of immature WBCs
- widespread infiltrates
Acute myeloid leukemia

32. Clinical features
• Diffuse / marginal
• Localised / generalised
• Overextension of marginal
gingiva
• Discrete tumorlike
interproximal mass
• Bluish red , shiny surface
• Firm
• Hemorrhage

33. Leukemic infiltration
Leukemic cell infiltration of
gingival corium
Gingival thickness
Gingival pockets
Plaque accumulation
Secondary inflammatory lesion

34. Histopathology
- Connective tissue – dense mass of immature and
proliferating leukocytes , engorged capillaries , edema
- Epithelium – degree of leukocytic infiltration and edema

35. 2. Granulomatous disease
a.Wegeners granulomatosis
- Acute granulomatous necrotising lesions of respiratory
tract , nasal and oral defects
- Acute necrotising vasculitis
Clinical features
-oral mucosal ulcerations
-delayed healing
-Papillary enlargement –
reddish purple ,
- bleeds easily
-Strawberry gingiva

36. Etiology
- Unknown
- Immunologically mediated tissue injury
Histopathology

37. b. Sarcoidosis
- Unknown etiology
- Involve any organ
Clinical features

38. NEOPLASTIC ENLARGEMENT
1. Benign tumors of gingiva
Epulis
a. Fibroma
i) Giant cell fibroma
ii) Peripheral ossifying fibroma

39. b. Papilloma
- Proliferations of surface epithelium associated with HPV
- HPV 6 & 11

40. c. Peripheral Giant Cell Granuloma
Peripheral giant cell tumors
d.Central Giant Cell Granuloma
- Arise within the jaw – central cavitation

41. e. Leukoplakia
• WHO: White patch or plaque that does
not rub off & cannot be diagnosed as any other disease
• Associated  use of tobacco
Other probable factors: Candida, HPV-16, HPV-18 &
Trauma

42. Gingival Cyst:
Develop from odontogenic epithelium or traumatically
implanted sulcular epithelium

43. 2. Malignant tumors of gingiva
Squamous cell carcinoma:
12th - females
• 90% of all Oral cancer
• 6th –most common cancer in males
•
• Most common malignant tumor of gingiva

44. Malignant melanoma:
• Rare tumor  hard palate, maxillary gingiva -older persons
• Darkly pigmented, rapid growth, early metastasis

45. Thankyou

46. GINGIVAL ENLARGEMENT

47. Contents
• Introduction
• Classification
• Indices
• Inflammatory Enlargement
• Enlargements associated with systemic diseases
• Neoplastic enlargement
• Drug-induced enlargement
• Idiopathic gingival enlargement
• False enlargement
• Conclusion
• References

48. Drug induced gingival enlargement
• Side effect – non dental treatment
• First case – Kimball 1939
Drugs associated with gingival overgrowth
Anticonvulsants
Phenytoin
Sodium valproate
Phenobarbitone
Vigabatrin
Immunosuppressants
Cyclosporin
Calcium channel
blockers
Dihydropyridines
Nifedipine
Felopdipine
Amlodipine
Phenylalkylamine
Verapamil
Benzothiazepine
Diltiazem

49. Prevalence of DIGO
• 50 % - phenytoin
(Angelopoulous & Goaz 1972)
• 30% - Cyclosporine
• 10% - Nifedipine
(Seymour 1987 , Barclay 1992)
• In India, 57% of epileptic children - aged 8-13 years -
phenytoin therapy
Prasad et al 2002

50. Risk factors for DIGO
Risk factors
Age
Sex
Drug
variables
Concomitant
medication
Genetic
factors
Periodontal
variables

51. •Early studies on phenytoin – teenagers
, hospitalised or institutionalised
•Two community based studies –
1. mean age 40.6 years –
Thomason 1992
2.Younger age – Casetta 1997
•Cyclosporin - children
(Daley 1994)
•Calcium channel blockers – not
applicable
•Middle age and older
Circulating androgen +
gingival fibroblasts
Testosterone – 5α
dihydrotestosterone
PHT – enhances metabolism
Circulating androgen –
adoloscents and teenagers
Age

52. •Phenytoin – no difference
Hassell 1981
•CsA- Male
•CCBs – male 3 times more
Sex Concomitant
medication
•Nifedipine + cyclosporin –
increases prevalence but not the
severity
•Polypharmacy – PHT –
metabolised by P450
•other anticonvulants – induce
P450 isoenzyme

53. Drug
variables
1. Drug dosage – poor predictor
•Dose / pts body weight
•PHT & CCB – therapeutic drug level 7-10 days
•Cyclosporin – trough concentration
•Area under plasma/ serum concentration time curve (AUC)
2. Type of preparation
CsA– solution - 37 % - early onset – higher in saliva
capsules – 43%
(Wondimu 1996)
3. Salivary concentration
PHT &CsA– salivary concentration positive correlation with OG
4. GCF – nifedipine

54. Genetic
factors
Cytochrome P450 gene
polymorphism
HLA- DR1 – protection against
OG
HLA-DR2 – OG susceptible
Pernu 1994
Periodontal
variables
Plaque scores & gingival
inflammation – exacerbate
OG

55. General features of DIGO
Painless beadlike
enlargement of IDP
Marginal gingiva
Massive tissue fold
Plaque control
difficult
Secondary
inflammatory process
Combined
enlargement

56. • Generalised
• Not in edentulous areas
• Chronic , slow
• Recurs
• Discontinuation of drug – spontaneous reduction

57. Histopathology

58. Anticonvulsants
• Epilepsy –
• First antiepileptic drug – phenytoin – DOC
• Merritt & Putman 1938
• 1st DIGO case
• Active metabolite – 5 parahydroxyphenyl – 5
phenylhydantoin
• Other hydantoins – ethotoin , mephenytoin
• Other anticonsulvant – succinimides , valproic acid

59. Anticonvulsant properties
1. Reduces excessive discharge
2. Reduces spread of excitation
Stabilising neuronal membrane
Na – prevents influx
K – blocks outward flow
Ca – decreases calcium influx

60. • Clinical features
1. Esthetic disfigurement,
2. Malpositioning of teeth,
3. Interfere masticatory function,
4. Speech,
5. Oral hygiene

61. Theories of pathogenesis
1. Gingival fibroblasts
1. High activity
2. Low activity
Hasell 1983

62. 2. Lack of collagen breakdown
• FBS – inactive collagenase
• mRNA collagenase levels are diminished
• Gene expression of MMP-1, 2, and 3 was reduced by
phenytoin administration,
• the TIMP-1 mRNA was markedly augmented
2005, Kato et al
• macrophages pretreated with phenytoin - lower production
of MMPs
• intracellular pathway - related to a lower expression of
α2β1-integrin

63. 3. Non collagenous matrix
• Non collagenous matrix – 20% of dry weight
• Increased hexoamine , uronic acid
• Increased sulphated GAG
• Higher volume density of non collagenous protein
compared to collagenous
Dahllof et al 1984

64. 4. Role of growth factors
• TGF-β - stimulating collagen biosynthesis
• latency-associated protein (LAP) - TGF-β inactive
• CTGF levels are increased
• Epithelial mesenchymal transition
• PDGF – PHT facilitated expression of PDGF B
– 6 times

66. 5.Immunosuppression
sIgA - decreased
Repair process
Gingival overgrowth

67. 6. PHT andAdrenal gland
Suppression ofACTH production
Suppression of adrenocortical
function
Reduction of glucocorticoid
synthesis
compensatory increase in the
Somatotrophic hormone
Fibroblast proliferation

68. 7. PHT and folic acid depletion
Decreases
absorption of
folic acid
Blocks transport
- intestinal
epithelium
Enzyme folate
reductase
Folic acid – DNAsynthesis
Impaired maturation –
sulcular epithelium
CT susceptible to inflammation

69. Cyclosporin induced gingival overgrowth
• Cyclosporin (CsA) - 1972 James Borel
• Organ transplantation , autoimmune disease
• Monotherapy - CsA
• 2 drugs – CsA+ cortisone / dihydropyridine
• 3 drugs – CsA+ cortisone + azathiprine
• Cyclosporin-induced gingival overgrowth –
1983 Rateitschak- Plu¨ss et al

70. Cyclosporin and T cells
• a) Inhibits T cell helper function to accessory cells -
interleukin 1
• b) Prevents the formation of receptors to interleukin I on
the membrane of the T-cell.
• c) Renders T-cells unresponsive to - interleukin 2 .

72. Pathogenesis of Cs GO
Cyclosporin
Cytokines
Extracellular
matrix
metabolism
Cell
proliferation
Apoptosis
Synthesis
Degradation
-I/C pathway
-E/C pathway

73. • More in labial aspect
• Soft, red or bluish-red, extremely fragile and bleed easily,
more hyperemic than PIGO

74. Histopathology

75. Calcium channel blockers
• CCB’s introduced in 1980’s
• Used extensively in the management of CV
disorders(HTN, angina, coronary artery spasm, cardiac
arrythmia)
• NIFEDIPINE  angina, mild to moderate HTN
• Relaxes smooth muscles and dilates the coronary arteries
• NIGO 1984 by Lederman et al

76. Pathogenesis:
Nifedipine
• Affects calcium metabolism similar to phenytoin
• Role of TGF beta
• Heparan GAG
Verapamil
Subpopulation of fibroblast

77. • IDPmarginal attached
• Lobulated and nodular
• Anteriorly, facial surface
• Inflammation  Combination enlargement

79. Idiopathic gingival enlargement
• Gingivomatosis , Elephantiasis, Idiopathic fibromatosis,
Hereditary gingival hyperplasia , Congenital familial
fibromatosis , Hereditary gingival fibromatosis
• rare oral disease
• autosomal dominant
• hypertrichosis, mental retardation and epilepsy

80. • Nodular form
• Symmetric form- most common type
• During eruption of permanent teeth

81. • most common effects
• diastemas,
• Malpositioning of teeth
• prolonged retention of primary teeth
• cover the dental crowns
• the alveolar bone is not affected (Bittencourt et al. 2000).

83. TGF 1
Increased
proliferation
HGF cells
Low levels of
MMP 1, MMP 2
Myofibroblasts
High level of
extracellular
matrix proteins
(collagen)
TGF 1
Gingival
overgrowth

84. False enlargement
a. Underlying osseous lesions
• Commonly  Tori, Exostosis
• Also seen in  Paget’s disease, Fibrous dysplasia,
Cherubism, Central giant cell granuloma,Ameloblastoma,
Osteoma and Osteosarcoma

85. b. Underlying dental lesions
• Various stages of eruption of primary dentition  labial
gingiva
• Developmental enlargement

86. Conclusion
Gingival enlargement are multifactorial and complex in
nature , which may be in respone to various interaction
between host and environment. GO considerably reduce the
quality of life and may result in serios emotional and social
problems due to esthetics and functionality hence the
prevention and treatment based on the understanding the
cause and underlying pathologic changes ,

87. References
• Newman MG , Takei HH , Klokkevold PR , Carranza FA .
Carranza’s Clinical Periodontology, 10th edition
• Marshall R , Bartold M A clinical review of drug induced
gingival overgrowth Australian dental journal 1999 ;44:4 219-
232
• Seymour RA, Ellis JS, Thomason JM: Risk factors for drug-
induced gingival overgrowth.J Clin Periodontol 2000; 27: 217–
223.
• Seymour RA , Thomasan JM Pathogenesis of Drug Induced
Gingival Overgrowth- J Clin Periodontol 1996;23:165-175
• Strawberry –like gingival tumor as first sign of Wegener’s
Granulomatosis. J Periodontol 2008; 79: 1297-1303
• Seymour RA and Heasman PA: Drugs and the periodoniium. J
Clin Periodontol 1988: 15: 1-16

88. • Jˆoice Dias Corrˆea et al Phenytoin-Induced Gingival Overgrowth: A
Review of the Molecular, Immune, and Inflammatory Features ISRN
Dentistry 2011,1-8
• Williamw . Hallmo&n J Effrey A. Rossmann The role of drugs in the
pathogenesis of gingival overgrowth A collective review of current
concepts Periodontology 2000, Vol. 21, 1999, 176-196
• Paulom. Camargo, Philip R.Melnick, Flavia Q. M. Pirih, Rodrigo Lagos
& Henry H. Takei Treatment of drug-induced gingival enlargement:
aesthetic and functional considerations Periodontology 2000, Vol. 27,
2001, 131–138
• Dustin Tedesco and Lukas Haragsim Cyclosporine: A Review Journal of
Transplantation Volume 2012
• Bitu CC, Sobral LM, Kellermann MG, Martelli-Junior H, Zecchin KG,
Graner E, Coletta RD. Heterogeneous presence of myofibroblasts in
hereditary gingival fibromatosis. J Clin Periodontol 2006; 33: 393–400

89. Thankyou