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GINGIVAL ENLARGEMENT
CONTENTS
• Introduction
• Classification
• Indices
• Inflammatory Enlargement
• Enlargements associated with systemic dise...
INTRODUCTION
Hypertrophic
gingivitis
Gingival
hyperplasia
Gingival enlargement
Gingival overgrowth
CLASSIFICATION
A] Based on etiologic factors and pathologic changes
I. Inflammatory Enlargement
- Acute
- Chronic
II. Drug...
B] Based on location and distribution
I. Localized
II. Generalized
III. Marginal
IV. Papillary
V. Diffuse
VI. Discrete
INDICES
Bokenkamp & Bohnhorst 1994
Grade 0  No signs of gingival enlargement
Grade 1  Enlargement confined to IDP
Grade ...
Degree of gingival hyperplasia according to modified index
by Angelopoulos & Goaz 1972
Grade Hyperplasia Size Tooth
covera...
Gingival overgrowth index- Mc Gaw et al 1987
Grade 0  No overgrowth, feather edge gingival margin
Grade 1  Blunting of g...
Clinical index for drug induced gingival overgrowth
Ingles et al 1999
G
r
a
d
e
0
G
r
a
d
e
1
G
r
a
d
e
2
G
r
a
d
e
3
G
r
...
1. INFLAMMATORY ENLARGEMENT
CHRONIC
ACUTE
INFLAMMATORY
Gingival
abscess
Periodontal
abscess
a. Chronic inflammatory enlargement
Etiology
Plaque
accumulation &
retention
Poor oral
hygiene
Anatomic
abnormalities
Impr...
Clinical Features
1.
Slight ballooning of IDP & marginal gingiva
Life preserver shaped bulge
Smooth , edematous , bleed ea...
Discrete sessile or
pedunculated tumor like mass
Interproximal / marginal or
attached gingiva
Slow growing and painless
Cl...
Histopathology
1.Soft and friable
2.Firm and resilient
B. ACUTE INFLAMMATORY
ENLARGEMENT
1. GINGIVALABSCESS
Etiology
 Foreign substances
Clinical features
 Marginal gingiva or...
2. PERIODONTAL ABSCESS
Lateral abscess / parietal abscess
Depending on location
- Gingival
- Periodontal (Acute / Chronic)...
Etiology
PERIODONTITIS RELATED
Extension of infection from PD
pocket
Lateral extension of
inflammation
Pocket with a tortu...
Etiology
NON PERIODONTITIS
RELATED
Impaction of foreign bodies
Endodontic perforation
Lateral cyst infection
Factors affec...
Signs and symptoms
Acute abscess
- Mild to severe discomfort
- Localized red, ovoid swelling
- Periodontal pocket
- Mobili...
ENLARGEMENTS ASSOCIATED WITH
SYSTEMIC DISEASES
Two mechanisms
1. Magnification of an existing inflammation initiated by
de...
1. Conditioned enlargement
• Systemic condition exaggerates or distorts usual gingival
response to plaque
• Bacterial plaq...
1. Marginal and generalised enlargement
2. Single or multiple tumor like masses
Hormonal changes
- Progesterone and estrog...
1. Marginal enlargement
- Generalised , more prominent
interdentally
- Bright red or magenta colour
- Friable , smooth & s...
2. Tumor like gingival enlargement
“Pregnancy tumor”
- Discrete mushroomlike , flattened
spherical mass
- Dusky red or mag...
Angiogranuloma
Thickened epilthelium
Newly formed, engorged
capillaries
Fibrous stroma
Inflammatory infiltrate
Histopathol...
Treatment
• Removal of plaque and calculus
• Tumor like gingival enlargement - surgical excision and
SRP
• Recurrence
• Sp...
• Male and female adoloscents
• Areas of plaque accumulation
• Facial surface
• Marginal and interdental
Histopathology
- ...
c. Enlargement in vitamin C deficiency
Clinical features
- Bluish red , soft , friable, boggy
- smooth & shiny surface
- H...
d. Plasma cell gingivitis
• Atypical gingivitis / plasma cell gingivostomatitis
• Plasma cell granuloma – localised form
•...
• Pyogenic granuloma
Clinical features
• Discrete spherical , tumorlike mass , pedunculated ,
smooth surface
• Bright red ...
2.Systemic Disease That Cause Gingival
Enlargement
1. Leukemia
malignant neoplasia of WBC precursors
- diffuse replacement...
Clinical features
• Diffuse / marginal
• Localised / generalised
• Overextension of marginal
gingiva
• Discrete tumorlike
...
Leukemic infiltration
Leukemic cell infiltration of
gingival corium
Gingival thickness
Gingival pockets
Plaque accumulatio...
Histopathology
- Connective tissue – dense mass of immature and
proliferating leukocytes , engorged capillaries , edema
- ...
2. Granulomatous disease
a.Wegeners granulomatosis
- Acute granulomatous necrotising lesions of respiratory
tract , nasal ...
Etiology
- Unknown
- Immunologically mediated tissue injury
Histopathology
b. Sarcoidosis
- Unknown etiology
- Involve any organ
Clinical features
NEOPLASTIC ENLARGEMENT
1. Benign tumors of gingiva
Epulis
a. Fibroma
i) Giant cell fibroma
ii) Peripheral ossifying fibroma
b. Papilloma
- Proliferations of surface epithelium associated with HPV
- HPV 6 & 11
c. Peripheral Giant Cell Granuloma
Peripheral giant cell tumors
d.Central Giant Cell Granuloma
- Arise within the jaw – ce...
e. Leukoplakia
• WHO: White patch or plaque that does
not rub off & cannot be diagnosed as any other disease
• Associated ...
Gingival Cyst:
Develop from odontogenic epithelium or traumatically
implanted sulcular epithelium
2. Malignant tumors of gingiva
Squamous cell carcinoma:
• 90% of all Oral cancer
• 6th –most common cancer in males
• 12th...
Malignant melanoma:
• Rare tumor  hard palate, maxillary gingiva -older persons
• Darkly pigmented, rapid growth, early m...
Thankyou
GINGIVAL ENLARGEMENT
Contents
• Introduction
• Classification
• Indices
• Inflammatory Enlargement
• Enlargements associated with systemic dise...
Drug induced gingival enlargement
• Side effect – non dental treatment
• First case – Kimball 1939
Drugs associated with g...
Prevalence of DIGO
• 50 % - phenytoin
( Angelopoulous & Goaz 1972)
• 30% - Cyclosporine
• 10% - Nifedipine
(Seymour 1987 ,...
Risk factors for DIGO
Risk factors
Age
Sex
Drug
variables
Concomitant
medication
Genetic
factors
Periodontal
variables
•Early studies on phenytoin – teenagers
, hospitalised or institutionalised
•Two community based studies –
1. mean age 40....
•Phenytoin – no difference
Hassell 1981
•CsA- Male
•CCBs – male 3 times more
Sex Concomitant
medication
•Nifedipine + cycl...
Drug
variables
1. Drug dosage – poor predictor
•Dose / pts body weight
•PHT & CCB – therapeutic drug level 7-10 days
•Cycl...
Genetic
factors
Cytochrome P450 gene
polymorphism
HLA- DR1 – protection against
OG
HLA-DR2 – OG susceptible
Pernu 1994
Per...
General features of DIGO
Painless beadlike
enlargement of IDP
Marginal gingiva
Massive tissue fold
Plaque control
difficul...
• Generalised
• Not in edentulous areas
• Chronic , slow
• Recurs
• Discontinuation of drug – spontaneous reduction
Histopathology
Anticonvulsants
• Epilepsy –
• First antiepileptic drug – phenytoin – DOC
• Merritt & Putman 1938
• 1st DIGO case
• Active...
Anticonvulsant properties
1. Reduces excessive discharge
2. Reduces spread of excitation
Stabilising neuronal membrane
Na ...
• Clinical features
1. Esthetic disfigurement,
2. Malpositioning of teeth,
3. Interfere masticatory function,
4. Speech,
5...
Theories of pathogenesis
1. Gingival fibroblasts
1. High activity
2. Low activity
Hasell 1983
2. Lack of collagen breakdown
• FBS – inactive collagenase
• mRNA collagenase levels are diminished
• Gene expression of M...
3. Non collagenous matrix
• Non collagenous matrix – 20% of dry weight
• Increased hexoamine , uronic acid
• Increased sul...
4. Role of growth factors
• TGF-β - stimulating collagen biosynthesis
• latency-associated protein (LAP) - TGF-β inactive
...
5.Immunosuppression
sIgA - decreased
Repair process
Gingival overgrowth
6. PHT and Adrenal gland
Suppression of ACTH production
Suppression of adrenocortical
function
Reduction of glucocorticoid...
7. PHT and folic acid depletion
Decreases
absorption of
folic acid
Blocks transport
- intestinal
epithelium
Enzyme folate
...
Cyclosporin induced gingival overgrowth
• Cyclosporin (CsA) - 1972 James Borel
• Organ transplantation , autoimmune diseas...
Cyclosporin and T cells
• a) Inhibits T cell helper function to accessory cells -
interleukin 1
• b) Prevents the formatio...
Pathogenesis of Cs GO
Cyclosporin
Cytokines
Extracellular
matrix
metabolism
Cell
proliferation
Apoptosis
Synthesis
Degrada...
• More in labial aspect
• Soft, red or bluish-red, extremely fragile and bleed easily,
more hyperemic than PIGO
Histopathology
Calcium channel blockers
• CCB’s introduced in 1980’s
• Used extensively in the management of CV
disorders(HTN, angina, co...
Pathogenesis:
Nifedipine
• Affects calcium metabolism similar to phenytoin
• Role of TGF beta
• Heparan GAG
Verapamil
Subp...
• IDPmarginal attached
• Lobulated and nodular
• Anteriorly, facial surface
• Inflammation  Combination enlargement
Idiopathic gingival enlargement
• Gingivomatosis , Elephantiasis, Idiopathic fibromatosis,
Hereditary gingival hyperplasia...
• Nodular form
• Symmetric form- most common type
• During eruption of permanent teeth
• most common effects
• diastemas,
• Malpositioning of teeth
• prolonged retention of primary teeth
• cover the dental cro...
TGF 1
Increased
proliferation
HGF cells
Low levels of
MMP 1, MMP 2
Myofibroblasts
High level of
extracellular
matrix prote...
False enlargement
a. Underlying osseous lesions
• Commonly  Tori, Exostosis
• Also seen in  Paget’s disease, Fibrous dys...
b. Underlying dental lesions
• Various stages of eruption of primary dentition  labial
gingiva
• Developmental enlargement
Conclusion
Gingival enlargement are multifactorial and complex in
nature , which may be in respone to various interaction
...
References
• Newman MG , Takei HH , Klokkevold PR , Carranza FA .
Carranza’s Clinical Periodontology, 10th edition
• Marsh...
• Jˆoice Dias Corrˆea et al Phenytoin-Induced Gingival Overgrowth: A
Review of the Molecular, Immune, and Inflammatory Fea...
Thankyou
 Gingival enlargement
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Gingival enlargement

  1. 1. GINGIVAL ENLARGEMENT
  2. 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. 3. INTRODUCTION Hypertrophic gingivitis Gingival hyperplasia Gingival enlargement Gingival overgrowth
  4. 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 IV. Neoplastic enlargement (gingival tumors) Benign tumors Malignant tumors V. False enlargement ii) Systemic diseases causing gingival enlargement 1. Leukemia 2.Granulomatous diseases (Wegener's granulomatosis, sarcoidosis) i) Conditioned enlargement 1. Pregnancy 2. Puberty 3. Vitamin C deficiency 4. Plasma cell gingivitis 5. Nonspecific conditioned enlargement
  5. 5. B] Based on location and distribution I. Localized II. Generalized III. Marginal IV. Papillary V. Diffuse VI. Discrete
  6. 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. 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. 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. 9. Clinical index for drug induced gingival overgrowth Ingles et al 1999 G r a d e 0 G r a d e 1 G r a d e 2 G r a d e 3 G r a d e 4 1.No overgrowth 2. slight stippling, no/slight granular appearance 3. knife edge margin 4. no increase in the density or size 1. Early overgrowth slight increase in density 2.marked stippling and granular appearance 3.tip of the papillae is round 4.probing depth ≤ 3mm 1.Moderate overgrowth increase in size of the papillae and rolled gingival margins 2. The contour concave or straight 3. buccolingual dimension of upto 2mm 4. Probing ≤ 6mm 5. Papillae retractable 1. Marked overgrowth encroachment on the clinical crown 2. The contour convex 3. Buccolingual dimension ≥ 3 mm 4. The probing depth ≥ 6mm 5. Papillae retractable 1. Severe overgrowth, profound thickening of gingiva 2. Large % of the clinical crown is covered 3. Papillae - retractable 4. Probing depth ≥ 6mm 5.buccolingual dimension 3mm
  10. 10. 1. INFLAMMATORY ENLARGEMENT CHRONIC ACUTE INFLAMMATORY Gingival abscess Periodontal abscess
  11. 11. a. Chronic inflammatory enlargement Etiology Plaque accumulation & retention Poor oral hygiene Anatomic abnormalities Improper restoration Orthodontic appliances Malocclusion
  12. 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. 13. Discrete sessile or pedunculated tumor like mass Interproximal / marginal or attached gingiva Slow growing and painless Clinical Features 1. 2.
  14. 14. Histopathology 1.Soft and friable 2.Firm and resilient
  15. 15. B. ACUTE INFLAMMATORY ENLARGEMENT 1. GINGIVALABSCESS 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. 16. 2. PERIODONTAL ABSCESS Lateral abscess / parietal abscess Depending on location - Gingival - Periodontal (Acute / Chronic) - Pericoronal Meng et al ’99 Depending on number - Single - Multiple
  17. 17. Etiology PERIODONTITIS RELATED Extension of infection from PD pocket Lateral extension of inflammation Pocket with a tortuous course Incomplete removal of calculus
  18. 18. Etiology NON PERIODONTITIS RELATED Impaction of foreign bodies Endodontic perforation Lateral cyst infection Factors affecting morphology of root
  19. 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. 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. 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. 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. 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. 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. 25. Angiogranuloma Thickened epilthelium Newly formed, engorged capillaries Fibrous stroma Inflammatory infiltrate Histopathology
  26. 26. Treatment • Removal of plaque and calculus • Tumor like gingival enlargement - surgical excision and SRP • Recurrence • Spontaneous reduction – termination of pregnancy
  27. 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. 28. c. Enlargement in vitamin C deficiency Clinical features - Bluish red , soft , friable, boggy - smooth & shiny surface - Haemorrhage – spontaneous / slight provocation - Surface necrosis with pseudomembrane formation • Classic description of scurvy • Acute deficiency – hemorrhage , collagen degeneration , edema • modify response to plaque
  29. 29. d. Plasma cell gingivitis • Atypical gingivitis / plasma cell gingivostomatitis • Plasma cell granuloma – localised form • Allergic in origin Clinical features
  30. 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. 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. 32. Clinical features • Diffuse / marginal • Localised / generalised • Overextension of marginal gingiva • Discrete tumorlike interproximal mass • Bluish red , shiny surface • Firm • Hemorrhage
  33. 33. Leukemic infiltration Leukemic cell infiltration of gingival corium Gingival thickness Gingival pockets Plaque accumulation Secondary inflammatory lesion
  34. 34. Histopathology - Connective tissue – dense mass of immature and proliferating leukocytes , engorged capillaries , edema - Epithelium – degree of leukocytic infiltration and edema
  35. 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. 36. Etiology - Unknown - Immunologically mediated tissue injury Histopathology
  37. 37. b. Sarcoidosis - Unknown etiology - Involve any organ Clinical features
  38. 38. NEOPLASTIC ENLARGEMENT 1. Benign tumors of gingiva Epulis a. Fibroma i) Giant cell fibroma ii) Peripheral ossifying fibroma
  39. 39. b. Papilloma - Proliferations of surface epithelium associated with HPV - HPV 6 & 11
  40. 40. c. Peripheral Giant Cell Granuloma Peripheral giant cell tumors d.Central Giant Cell Granuloma - Arise within the jaw – central cavitation
  41. 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. 42. Gingival Cyst: Develop from odontogenic epithelium or traumatically implanted sulcular epithelium
  43. 43. 2. Malignant tumors of gingiva Squamous cell carcinoma: • 90% of all Oral cancer • 6th –most common cancer in males • 12th - females • Most common malignant tumor of gingiva
  44. 44. Malignant melanoma: • Rare tumor  hard palate, maxillary gingiva -older persons • Darkly pigmented, rapid growth, early metastasis
  45. 45. Thankyou
  46. 46. GINGIVAL ENLARGEMENT
  47. 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. 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. 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. 50. Risk factors for DIGO Risk factors Age Sex Drug variables Concomitant medication Genetic factors Periodontal variables
  51. 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. 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. 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. 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. 55. General features of DIGO Painless beadlike enlargement of IDP Marginal gingiva Massive tissue fold Plaque control difficult Secondary inflammatory process Combined enlargement
  56. 56. • Generalised • Not in edentulous areas • Chronic , slow • Recurs • Discontinuation of drug – spontaneous reduction
  57. 57. Histopathology
  58. 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. 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. 60. • Clinical features 1. Esthetic disfigurement, 2. Malpositioning of teeth, 3. Interfere masticatory function, 4. Speech, 5. Oral hygiene
  61. 61. Theories of pathogenesis 1. Gingival fibroblasts 1. High activity 2. Low activity Hasell 1983
  62. 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. 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. 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
  65. 65. 5.Immunosuppression sIgA - decreased Repair process Gingival overgrowth
  66. 66. 6. PHT and Adrenal gland Suppression of ACTH production Suppression of adrenocortical function Reduction of glucocorticoid synthesis compensatory increase in the Somatotrophic hormone Fibroblast proliferation
  67. 67. 7. PHT and folic acid depletion Decreases absorption of folic acid Blocks transport - intestinal epithelium Enzyme folate reductase Folic acid – DNA synthesis Impaired maturation – sulcular epithelium CT susceptible to inflammation
  68. 68. 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
  69. 69. 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 .
  70. 70. Pathogenesis of Cs GO Cyclosporin Cytokines Extracellular matrix metabolism Cell proliferation Apoptosis Synthesis Degradation -I/C pathway -E/C pathway
  71. 71. • More in labial aspect • Soft, red or bluish-red, extremely fragile and bleed easily, more hyperemic than PIGO
  72. 72. Histopathology
  73. 73. 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
  74. 74. Pathogenesis: Nifedipine • Affects calcium metabolism similar to phenytoin • Role of TGF beta • Heparan GAG Verapamil Subpopulation of fibroblast
  75. 75. • IDPmarginal attached • Lobulated and nodular • Anteriorly, facial surface • Inflammation  Combination enlargement
  76. 76. 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
  77. 77. • Nodular form • Symmetric form- most common type • During eruption of permanent teeth
  78. 78. • 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).
  79. 79. 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
  80. 80. 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
  81. 81. b. Underlying dental lesions • Various stages of eruption of primary dentition  labial gingiva • Developmental enlargement
  82. 82. 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 ,
  83. 83. 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
  84. 84. • 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
  85. 85. Thankyou

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