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GINGIVAL ENLARGEMENT
Presented by :
Dr.Varsha vishwakarma
 Introduction
 Classification
 Inflammatory enlargement
 Drug induced gingival enlargement
 Enlargement associated with
systemic diseases.
 Idiopathic gingival enlargement
 Neoplastic enlargement
 False enlargement
 Introduction
 Attrision
 Abrasion
 Abfraction
 Erosion
GINGIVAL ENLARGEMENT WASTING DISEASESOFTEETH
 Increase in the size of the gingiva is known as gingival
enlargement or gingival overgrowth
 Earlier it was also erroneously connoted as Hypertrophic
gingivitis or gingival hyperplasia
There are two ways to classify gingival
enlargement :
1 .According to etiological factor and
pathological changes.
2 .According to location and distribution.
ACCORDING TO ETIOLOGICAL FACTOR AND
PATHOLOGICAL CHANGES
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. Non specific conditioned enlargement (pyogenic granuloma )
B. Systemic disease causing gingival enlargement
1.Leukemia
2. Granulomatous diseases (e.g.wegner’s granulomatosis,
sarcoidosis)
IV.Neoplastic enlargement (gingival tumor)
A. Benign tumors
B.Malignant tumor’s
V. False enlargement
ACCORDING TO LOCATION AND DISTRIBUTION
 Localized :limited to gingiva adjacent to a single tooth or
group of teeth.
 Generalized :involving the gingiva throughout the mouth
 Marginal: confined to marginal gingiva
 Papillary : confined to inter dental papilla
 Diffuse: involving the marginal and attached gingiva and
papilla
 Discrete : an isolated sessile or pedunculated, tumor like
enlargement.
 It results from chronic or acute inflammatory changes ,chronic
changes are much more common . Inflammatory
enlargements usually are a secondary complication to any of
the other types of enlargement therefore it is important to
understand the double etiology and treat them adequately
CHRONIC INFLAMMATORY ENLARGEMENT
CLINICAL FEATURE
 Originates as a slight ballooning of the
interdental papilla and marginal gingiva
 Enlargement may be localized or generalized
 Occasionally ,it may occur as a discrete
sessile or pedunculated mass resembling a
tumor
 The lesion are slow growing masses and
usually painless
 They may undergo spontaneous reduction in
size, followed by exacerbation and continued
enlargement
ETIOLOGY
 Prolonged exposure to dental plaque and
factors that favor plaque accumulation
and retention like poor oral hygiene,
irritation by anatomic abnormalities and
improper restorative and orthodontic
appliance .
 GINGIVAL CHANGES ASSOCIATED WITH
MOUTH BREATHING
Gingivitis and gingival enlargement are
often seen in mouth breathers.
CLINICAL FEATURE:
 Gingiva appears red and edematous, with a diffuse surface
shininess of exposed area
 It mainly involves maxillary anterior region
 It’s harmful effect is generally attributed to irritation from
surface dehydration
ACUTE INFLAMMATORY ENLARGEMENT
A. GINGIVAL ABSCESS
- Gingival abscess is the localized , painful,
rapidly expanding lesion usually of
sudden onset
- most common site is marginal or
interdental gingiva
ETIOLOGY
 Caused by bacteria carried deep into the
tissues when a foreign substance is
forcefully embedded into the gingiva
CLINICAL FEATURE
 Initially it appears as red swelling with a smooth shiny
surface
 Within 24 to 48 hours , lesion become fluctuant and pointed
with a surface orifice from which purulent exudate may be
expressed .
 Adjacent teeth are often sensitive to percussion
B. PERIODONTAL (LATERAL ) ABSCESS
 Produce enlargement of gingiva , but they also involve the
supporting periodontal tissues .
DRUG INDUCED GINGIVAL ENLARGEMENT
 It is a consequence of the administration of certain drugs
mainly -
Anticonvulsants
Immunosuppressants
Calcium channel blocker
ANTICONVULSANTS
 drug induced gingival enlargements were first produced by
Phenytoin (Dilantin ).
 Other anticonvulsants known to induce gingival enlargement
are ethotoin and mephenytoin methsuxinamide andValproic
acid .
 It occurs more often in younger patient .
 Occurrence and severity are not necessarily related to the
dosage after a threshold level has been exceeded .
 Tissue culture experiments indicate that Phenytoin stimulates
proliferation of fibroblast like cells and epithelium with
increased synthesis of sulfated glycosaminoglycans in vitro .
IMMUNOSUPPRESSANT
 Cyclosporin is a potent immunosuppressive agent used to
prevent organ transplant rejection and to treat several
disease of autoimmune origin .
 It has a role in gingival enlargement .
 Dose 500 mg/day .
 Enlargement are more vascularized than phenytoin
enlargement .
 Occurs more commonly in children .
CALCIUM CHANNEL BLOCKERS
 These are the drugs used for cardiac conditions like
Hypertension , Angina pectoris ,Coronary artery spasms, and
cardiac arrhythmia.
 Examples include :-
1.Dihydropyridine derivatives -Felodipine,nicardipine ,nifidipine
2.Benzothyazine derivatives- diltiazem
3.Phenylalkaline derivatives- verapamil
 NIFIDIPINE one of the most important drug causing gingival
enlargement can be substituted by dihydropyridine derivative
isradipine to reduce gingival enlargement in some instances.
CLINICAL FEATURES
 Starts as a painless , bead like enlargement of the interdental
papilla and extends to the facial and lingual gingival margins
 As condition progresses , marginal and papillary enlargement unite
and develop into massive tissue fold covering a considerable
portion of the crown ,thus interfering with occlusion
 When uncomplicated by inflammation , the lesion is mulberry
shaped, firm, pale pink, and resilient , with a minutely lobulated
surface and no tendency to bleed .
 Enlargement characteristically appears to project from beneath
the gingival margin
 Presence of enlargement makes the plaque control difficult
resulting in a secondary inflammatory process.
 RESULTANT ENLARGEMENT = INCREASE IN SIZE (DRUG
INDUCED ) +INFLAMMATION (BACTERIA INDUCED )
 SITE OF OCCURANCE : Usually generalized through out mouth
 Severely effects maxillary and mandibular anterior regions
 Enlargement disappears in areas from which teeth are extracted
 Hassel et al. have hypothesized that in non-inflammed gingiva ,
fibroblasts are less active or even quiescent and do not respond
to the circulating phenytoin ,whereas fibroblast within
inflammed tissue are in an active state as a result of the
inflammatory mediators and the endogenous growth factors
presents
 Enlargement is chronic and slowly increases in size .
 When surgically removed it recurs spontaneously within a few
months after discontinuation of the drug .
 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.
2. Manifestation of systemic disease independent of
inflammatory status of gingiva.
 It occurs when the systemic condition
of the patient exaggerates or distorts
the usual gingival response to dental
plaque.
 Bacterial plaque is necessary for the
initiation of this type of enlargement.
 It occurs in three conditions:
- hormonal (pregnancy, puberty)
- nutritional (vitamin c deficiency)
ENLARGEMENT IN PREGNANCY
 Pregnancy itself does not cause gingival
enlargement.
 Gingivitis in pregnancy leads to gingival
enlargement.
 The altered tissue metabolism in
pregnancy accentuates the gingival
response to plaque.
 Gingival enlargement in pregnancy can
be :
Marginal enlargement
Tumor like enlargement.
MECHANISM OF GINGIVAL ENLARGEMENT IN PREGNANCY
Increase in level of progesterone and estrogen
By end of 3rd trimester the level reaches 10-30 times the normal
level
Changes in vascular permeability
Gingival edema and increased inflammatory response to dental
plaque
ENLARGEMENT IN PUBERTY
 Gingival enlargement seen during
puberty may occur in both male and
female adolescents and occur in the areas
of plaque accumulation.
 It is marginal and interdental.
 It is characterized by prominent bulbous
interproximal papillae.
 Only the facial gingiva are enlarged and
the lingual surface are relatively
unaltered.
 Degree of enlargement and tendency to develop massive
recurrence distinguish pubertal gingival enlargement from
chronic inflammatory gingival enlargement.
 After puberty the enlargement undergoes spontaneous
reduction but does not disappear until plaque and calculus are
removed.
 There is high initial prevalence of gingival enlargement in
children during 11 to 17 years.
ENLARGEMENT IN VITAMIN C DEFICIENCY
 Enlargement of the gingiva is generally
included in classic description of scurvy.
 Acute vitamin C deficiency itself does
not cause gingival inflammation, but it
causes hemorrhage, collagen
degenaration and edema of the gingival
connective tissue.
 These changes modify the response of
gingiva to plaque so that extent of
inflammation is exaggerated.
 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 feature.
PLASMA CELL GINGIVITIS
 It is also referred to as atypical gingivitis or
plasma cell gingivomatitis.
 It is thought to be allergic in origin.
 It often consists of mild marginal gingival
enlargement that extends to the attached
gingiva.
 Gingiva appears red, friable, and
sometimes granular and bleeds easily.
 A localized lesion, referred to as plasma
cell granuloma, is located in the oral
aspect of the attached gingiva.
 An associated cheilitis and glossitis have
been reported.
NONSPECIFIC CONDITIONED ENLARGEMENT-
PYOGENIC GRANULOMA
 Pyogenic granuloma is a tumor like
gingival enlargement that is considered an
exaggerated conditioned response to
minor trauma.
 The lesion varies from a discrete spherical,
tumor like mass with a pedunculated
attachment to a flattened, red or purple
and either firm or febrile, depending on its
duration.
 In majority of cases it its present with
ulceration or purulent exudate.
1. LEUKEMIA :
 Leukemic enlargement may be diffuse or
marginal and localized or generalized.
 It may appear as a diffuse enlargement of
the gigival mucosa and extention of
marginal gingiva.
 Gingiva becomes bluish red and has a shiny
surface.
 There is tendency towards friability and
hemorrhage.
2. GRANULOMATOUS DISEASES :
A.Wegener’s granulomatosis is a rear disease characterized by
acute granulomatous nectrtizing lesions of the respiratory tract,
including nasal and oral defects.
 The initial manifestations ofWegener’s granulomatosis may
involve the orofacial region and include oral mucosal ulceration,
gingival enlargement, abnormal tooth mobility and delayed
healing response.
 Granulomatous papillary enlargement is reddish purple and
bleeds easily on stimulation.
B. SARCOIDOSIS:
 It is a granuloatous disease of unknown etiology.
 It involve almost any organ including gingiva.
 There is red, smooth, painless gingival enlargement.
 It is a rare condition of undetermined cause .
 Other designated term include -
Gingivomatosis
Elephantiasis gingiva
Idiopathic fibromatosis
Hereditary gingival Hyperplasia
Congenital Familial fibromatosis
IDIOPATHIC GINGIVAL ENLARGEMENT
Facial view Occlusal view
ETIOLOGY
 The cause is unknown .
 Some have hereditary basis .
 In some families the gingival enlargement may be
linked to impairment of physical development.
 Gingival enlargement have been described in tuberous
sclerosis which is an inherited condition characterized
by triad of epilepsy , mental deficiency and cutaneous
angiofibromas.
CLINICAL FEATURES
 The enlargement affects the attached gingiva ,as well as the
gingival margin and interdental papillae .
 The facial surfaces and lingual surfaces of the mandible and maxilla
are generally affected .
 The enlarged gingiva is pink ,firm and leathery in consistency and
has a characteristic pebbled surface .
 In severe cases the teeth are almost completely covered and the
enlargement completely projects into the oral vestibules .
 The jaw appears distorted because of the bulbous enlargement of
the gingiva .
 Secondary inflammatory changes are common at the gingival
margin .
 Neoplasms account for small proportion of gingival
enlargement.
 Epulis is a generic term used clinically to designate all
discrete tumor and tumor like masses of gingiva.
A. Benign tumors of gingiva
 Fibroma
 Papilloma
 Peripheral giant cell
granuloma
 Central giant cellgranuloma.
 Gingival cysts
B. Malignant tumors of
gingiva –
 Carcinoma
 Malignant melanoma
FIBROMA
 It arises from gingival connective tissue or from periodontal
ligament.
 Slow growing, spherical tumors that tend to be firm and
nodular but may be soft and vascular.
 Usually pedunculated.
 Giant cell fibroma contains multinucleated fibroblast.
 Peripheral ossifying fibroma contains mineralized
tissue(bone, cementum like material, distrophic calcifications)
PAPILLOMA
 Benign proliferation of surface epithelium
associated with human pappiloma virus
(HPV).
 Viral subtypes HPV-6 and HPV-11 have
been found in most cases.
 Appears as solitary, cauliflower-like
protuberances.
 They may be small and discrete or broad,
hard elevations with minutely irregular
surfaces
PERIPHERAL GIANT CELL GRANULOMA
 It arises from gingival margin , occur most
frequently on labial surface, may be sessile or
pedunculated.
 Vary in appearance from smooth regularly
outlined masses to irregularly shaped
multilobulated protuberance with surface
indentations.
 Marginal ulceration is seen occasionally
 Lesions are painless, vary in size ,may cover
several teeth.
 They may be firm or spongy, colour varies from
pink to deep red or purplish blue.
CENTRAL GIANT CELL GRANULOMA
 These lesion arises within the jaw and produce central
cavitation
 They occasionally create deformity of jaw that makes gingiva
appear enlarged.
GINGIVAL CYST
 It develop from odontogenic epithelium or from surface or
sulcular epithelium traumatically implanted in the area.
 They seldom reach to clinically significant size and when they
do, they appear as localized enlargement involving marginal
and attached gingiva.
 Occurs in mandibular canine and premolar areas, most often
in lingual surface.
 They are painless but with expansion, may cause resorption of
alveolar bone.
CARCINOMA
 It is the 6th most common cancer in
males and 12th in females.
 Squamous cell carcinoma is most
common malignant tumor of gingiva.
 It may be exophytic, presenting
irregular growth and ulcerative lesions.
 It go unnoticed till complicated with
inflammatory changes.
 Sometime it become evident after
extraction
 These are locally invasive involving bone and periodontal
ligament of adjoining teeth and adjacent mucosa.
 Metastasis remain confined to region above clavicle , most
extensive form may include lung, liver or bone.
MALIGNANT MELANOMA
 It arises from melanoblasts in gingiva, cheek or palate.
 It is rare tumor occur in hard palate and in gingiva of
older person.
 It may be flat or nodular characterized by rapid growth
and early metastasis.
 Infiltration into underlying bone and metastasis to
cervical and axillary lymph node are common.
 Fibrosarcoma, lymphosarcoma and reticulum cell
sarcoma of gingiva are rare
 Only isolated cases have been reported
 Kaposi sarcoma often occurs in oral cavity of patients
with AIDS
 Tumor metastasis to gingiva occurs infrequently
False enlargement are not true enlargement of gingival
tissue but may appear as a result of increase in size of the
underlying osseous or dental tissue
1) underlying osseous lesions
enlargement of bone subjacent to gingival area occurs
most often in tori and exostoses, it also occurs in Pagets
disease,fibrous dysplasia,cherubism, central giant cell
granuloma,ameloblastoma,osteoma and osteosarcoma
2)Underlying dental tissue
 During various stages of eruption, particularly of primary
dentition, labial gingiva may show bulbous marginal
distortion caused by superimposition of gingiva on
normal prominence of enamel in gingival half of crown.
 Enlargement persists until junctional epithelium has
migrated from enamel to CEJ
 This enlargement are physiologic and usually present no
problem
WASTING DISEASES OF TEETH
 It is the physiologic wearing away of teeth because of tooth
to tooth contact .
 Attrition is the simple wearing down of the cusps of the
posterior teeth and the incisal edges of the anterior teeth.
Types
Physiological attrition-attrition which occurs due to normal
process, due to mastication
Pathological attrition-due to abnormalities in occlusion and
due to abnormal habbits like bruxism
Shows serious attrition of 76 yr old man
who has been bruxing all life
Cusps of the molars have been worn down
exposing the yellow dentin underneath.
Treatment
 In patients having habbit of bruxism, night guards , bite
guards or splint are effective in reducing attrition
 Correction of malocclusion
Abrasion is the pathological loss of tooth structure by
abnormal mechanical forces.
Etiology
use of abrasive dentifrices, horizontal toothbrushing, holding
nails and improper use of floss
Types
 Toothbrush abrasion
 Habitual abrasion-seen in pipe smokers
 Occupational abrasion
Treatment
 Examination and modification of teeth cleansing
habbits will be indicated
 Elimination of causative agent
 Restoration for esthetics and to prevent further tooth
wear
 Abfraction is also called stress lesion.This term was
coined by Dr J.O. Grippo in early 1990’s
 It results from occlusal loading causing mechanical
microfractures and tooth loss in cervical area
 The theory of abfraction is controversial. Dentists
began noticing eroded or notched areas (erosions) on
teeth close to the gum line (which is called the cervix of
the tooth)
 Acid erosion, also known as dental erosion, is the irreversible
loss of tooth structure due to chemical dissolution by acids not
of bacterial origin.
 Dental erosion is the most common chronic disease of
children ages 5-7yrs
 Erosion is found initially in the enamel and, if unchecked, may
proceed to the underlying dentin.
TYPES
extrinsic-
occurs because of acidic beverages,citrus food
Intrinsic-
Dental erosion can occur by non-extrinsic factors too. Intrinsic
dental erosion is known as perimolysis, gastric acid from the
stomach comes into contact with the teeth. People with
diseases such as gastro esophageal reflux disease often suffer
from this
Management
 Prescription of flouride mouthwash is indicated
 Modification of brushing habbit and restoration of
defect by GIC
 These four mechanism of tooth wear-attrision ,abrasion ,
abfraction and erosion-can combine with each other resulting
in increased degree of tooth wear.
THANK YOU

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Gingival enlargement

  • 1. GINGIVAL ENLARGEMENT Presented by : Dr.Varsha vishwakarma
  • 2.  Introduction  Classification  Inflammatory enlargement  Drug induced gingival enlargement  Enlargement associated with systemic diseases.  Idiopathic gingival enlargement  Neoplastic enlargement  False enlargement  Introduction  Attrision  Abrasion  Abfraction  Erosion GINGIVAL ENLARGEMENT WASTING DISEASESOFTEETH
  • 3.  Increase in the size of the gingiva is known as gingival enlargement or gingival overgrowth  Earlier it was also erroneously connoted as Hypertrophic gingivitis or gingival hyperplasia
  • 4. There are two ways to classify gingival enlargement : 1 .According to etiological factor and pathological changes. 2 .According to location and distribution.
  • 5. ACCORDING TO ETIOLOGICAL FACTOR AND PATHOLOGICAL CHANGES 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
  • 6. 4.Plasma cell gingivitis 5. Non specific conditioned enlargement (pyogenic granuloma ) B. Systemic disease causing gingival enlargement 1.Leukemia 2. Granulomatous diseases (e.g.wegner’s granulomatosis, sarcoidosis) IV.Neoplastic enlargement (gingival tumor) A. Benign tumors B.Malignant tumor’s V. False enlargement
  • 7. ACCORDING TO LOCATION AND DISTRIBUTION  Localized :limited to gingiva adjacent to a single tooth or group of teeth.  Generalized :involving the gingiva throughout the mouth  Marginal: confined to marginal gingiva  Papillary : confined to inter dental papilla  Diffuse: involving the marginal and attached gingiva and papilla  Discrete : an isolated sessile or pedunculated, tumor like enlargement.
  • 8.  It results from chronic or acute inflammatory changes ,chronic changes are much more common . Inflammatory enlargements usually are a secondary complication to any of the other types of enlargement therefore it is important to understand the double etiology and treat them adequately
  • 9. CHRONIC INFLAMMATORY ENLARGEMENT CLINICAL FEATURE  Originates as a slight ballooning of the interdental papilla and marginal gingiva  Enlargement may be localized or generalized  Occasionally ,it may occur as a discrete sessile or pedunculated mass resembling a tumor  The lesion are slow growing masses and usually painless  They may undergo spontaneous reduction in size, followed by exacerbation and continued enlargement
  • 10. ETIOLOGY  Prolonged exposure to dental plaque and factors that favor plaque accumulation and retention like poor oral hygiene, irritation by anatomic abnormalities and improper restorative and orthodontic appliance .  GINGIVAL CHANGES ASSOCIATED WITH MOUTH BREATHING Gingivitis and gingival enlargement are often seen in mouth breathers.
  • 11. CLINICAL FEATURE:  Gingiva appears red and edematous, with a diffuse surface shininess of exposed area  It mainly involves maxillary anterior region  It’s harmful effect is generally attributed to irritation from surface dehydration
  • 12. ACUTE INFLAMMATORY ENLARGEMENT A. GINGIVAL ABSCESS - Gingival abscess is the localized , painful, rapidly expanding lesion usually of sudden onset - most common site is marginal or interdental gingiva ETIOLOGY  Caused by bacteria carried deep into the tissues when a foreign substance is forcefully embedded into the gingiva
  • 13. CLINICAL FEATURE  Initially it appears as red swelling with a smooth shiny surface  Within 24 to 48 hours , lesion become fluctuant and pointed with a surface orifice from which purulent exudate may be expressed .  Adjacent teeth are often sensitive to percussion
  • 14. B. PERIODONTAL (LATERAL ) ABSCESS  Produce enlargement of gingiva , but they also involve the supporting periodontal tissues .
  • 15. DRUG INDUCED GINGIVAL ENLARGEMENT  It is a consequence of the administration of certain drugs mainly - Anticonvulsants Immunosuppressants Calcium channel blocker
  • 16. ANTICONVULSANTS  drug induced gingival enlargements were first produced by Phenytoin (Dilantin ).  Other anticonvulsants known to induce gingival enlargement are ethotoin and mephenytoin methsuxinamide andValproic acid .  It occurs more often in younger patient .  Occurrence and severity are not necessarily related to the dosage after a threshold level has been exceeded .  Tissue culture experiments indicate that Phenytoin stimulates proliferation of fibroblast like cells and epithelium with increased synthesis of sulfated glycosaminoglycans in vitro .
  • 17.
  • 18. IMMUNOSUPPRESSANT  Cyclosporin is a potent immunosuppressive agent used to prevent organ transplant rejection and to treat several disease of autoimmune origin .  It has a role in gingival enlargement .  Dose 500 mg/day .  Enlargement are more vascularized than phenytoin enlargement .  Occurs more commonly in children .
  • 19.
  • 20. CALCIUM CHANNEL BLOCKERS  These are the drugs used for cardiac conditions like Hypertension , Angina pectoris ,Coronary artery spasms, and cardiac arrhythmia.  Examples include :- 1.Dihydropyridine derivatives -Felodipine,nicardipine ,nifidipine 2.Benzothyazine derivatives- diltiazem 3.Phenylalkaline derivatives- verapamil  NIFIDIPINE one of the most important drug causing gingival enlargement can be substituted by dihydropyridine derivative isradipine to reduce gingival enlargement in some instances.
  • 21. CLINICAL FEATURES  Starts as a painless , bead like enlargement of the interdental papilla and extends to the facial and lingual gingival margins  As condition progresses , marginal and papillary enlargement unite and develop into massive tissue fold covering a considerable portion of the crown ,thus interfering with occlusion  When uncomplicated by inflammation , the lesion is mulberry shaped, firm, pale pink, and resilient , with a minutely lobulated surface and no tendency to bleed .  Enlargement characteristically appears to project from beneath the gingival margin  Presence of enlargement makes the plaque control difficult resulting in a secondary inflammatory process.  RESULTANT ENLARGEMENT = INCREASE IN SIZE (DRUG INDUCED ) +INFLAMMATION (BACTERIA INDUCED )
  • 22.  SITE OF OCCURANCE : Usually generalized through out mouth  Severely effects maxillary and mandibular anterior regions  Enlargement disappears in areas from which teeth are extracted  Hassel et al. have hypothesized that in non-inflammed gingiva , fibroblasts are less active or even quiescent and do not respond to the circulating phenytoin ,whereas fibroblast within inflammed tissue are in an active state as a result of the inflammatory mediators and the endogenous growth factors presents  Enlargement is chronic and slowly increases in size .  When surgically removed it recurs spontaneously within a few months after discontinuation of the drug .
  • 23.  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. 2. Manifestation of systemic disease independent of inflammatory status of gingiva.
  • 24.  It occurs when the systemic condition of the patient exaggerates or distorts the usual gingival response to dental plaque.  Bacterial plaque is necessary for the initiation of this type of enlargement.  It occurs in three conditions: - hormonal (pregnancy, puberty) - nutritional (vitamin c deficiency)
  • 25. ENLARGEMENT IN PREGNANCY  Pregnancy itself does not cause gingival enlargement.  Gingivitis in pregnancy leads to gingival enlargement.  The altered tissue metabolism in pregnancy accentuates the gingival response to plaque.  Gingival enlargement in pregnancy can be : Marginal enlargement Tumor like enlargement.
  • 26. MECHANISM OF GINGIVAL ENLARGEMENT IN PREGNANCY Increase in level of progesterone and estrogen By end of 3rd trimester the level reaches 10-30 times the normal level Changes in vascular permeability Gingival edema and increased inflammatory response to dental plaque
  • 27. ENLARGEMENT IN PUBERTY  Gingival enlargement seen during puberty may occur in both male and female adolescents and occur in the areas of plaque accumulation.  It is marginal and interdental.  It is characterized by prominent bulbous interproximal papillae.  Only the facial gingiva are enlarged and the lingual surface are relatively unaltered.
  • 28.  Degree of enlargement and tendency to develop massive recurrence distinguish pubertal gingival enlargement from chronic inflammatory gingival enlargement.  After puberty the enlargement undergoes spontaneous reduction but does not disappear until plaque and calculus are removed.  There is high initial prevalence of gingival enlargement in children during 11 to 17 years.
  • 29. ENLARGEMENT IN VITAMIN C DEFICIENCY  Enlargement of the gingiva is generally included in classic description of scurvy.  Acute vitamin C deficiency itself does not cause gingival inflammation, but it causes hemorrhage, collagen degenaration and edema of the gingival connective tissue.  These changes modify the response of gingiva to plaque so that extent of inflammation is exaggerated.
  • 30.  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 feature.
  • 31. PLASMA CELL GINGIVITIS  It is also referred to as atypical gingivitis or plasma cell gingivomatitis.  It is thought to be allergic in origin.  It often consists of mild marginal gingival enlargement that extends to the attached gingiva.  Gingiva appears red, friable, and sometimes granular and bleeds easily.  A localized lesion, referred to as plasma cell granuloma, is located in the oral aspect of the attached gingiva.  An associated cheilitis and glossitis have been reported.
  • 32. NONSPECIFIC CONDITIONED ENLARGEMENT- PYOGENIC GRANULOMA  Pyogenic granuloma is a tumor like gingival enlargement that is considered an exaggerated conditioned response to minor trauma.  The lesion varies from a discrete spherical, tumor like mass with a pedunculated attachment to a flattened, red or purple and either firm or febrile, depending on its duration.  In majority of cases it its present with ulceration or purulent exudate.
  • 33. 1. LEUKEMIA :  Leukemic enlargement may be diffuse or marginal and localized or generalized.  It may appear as a diffuse enlargement of the gigival mucosa and extention of marginal gingiva.  Gingiva becomes bluish red and has a shiny surface.  There is tendency towards friability and hemorrhage.
  • 34. 2. GRANULOMATOUS DISEASES : A.Wegener’s granulomatosis is a rear disease characterized by acute granulomatous nectrtizing lesions of the respiratory tract, including nasal and oral defects.  The initial manifestations ofWegener’s granulomatosis may involve the orofacial region and include oral mucosal ulceration, gingival enlargement, abnormal tooth mobility and delayed healing response.  Granulomatous papillary enlargement is reddish purple and bleeds easily on stimulation.
  • 35. B. SARCOIDOSIS:  It is a granuloatous disease of unknown etiology.  It involve almost any organ including gingiva.  There is red, smooth, painless gingival enlargement.
  • 36.  It is a rare condition of undetermined cause .  Other designated term include - Gingivomatosis Elephantiasis gingiva Idiopathic fibromatosis Hereditary gingival Hyperplasia Congenital Familial fibromatosis
  • 38. ETIOLOGY  The cause is unknown .  Some have hereditary basis .  In some families the gingival enlargement may be linked to impairment of physical development.  Gingival enlargement have been described in tuberous sclerosis which is an inherited condition characterized by triad of epilepsy , mental deficiency and cutaneous angiofibromas.
  • 39. CLINICAL FEATURES  The enlargement affects the attached gingiva ,as well as the gingival margin and interdental papillae .  The facial surfaces and lingual surfaces of the mandible and maxilla are generally affected .  The enlarged gingiva is pink ,firm and leathery in consistency and has a characteristic pebbled surface .  In severe cases the teeth are almost completely covered and the enlargement completely projects into the oral vestibules .  The jaw appears distorted because of the bulbous enlargement of the gingiva .  Secondary inflammatory changes are common at the gingival margin .
  • 40.  Neoplasms account for small proportion of gingival enlargement.  Epulis is a generic term used clinically to designate all discrete tumor and tumor like masses of gingiva.
  • 41. A. Benign tumors of gingiva  Fibroma  Papilloma  Peripheral giant cell granuloma  Central giant cellgranuloma.  Gingival cysts B. Malignant tumors of gingiva –  Carcinoma  Malignant melanoma
  • 42. FIBROMA  It arises from gingival connective tissue or from periodontal ligament.  Slow growing, spherical tumors that tend to be firm and nodular but may be soft and vascular.  Usually pedunculated.  Giant cell fibroma contains multinucleated fibroblast.  Peripheral ossifying fibroma contains mineralized tissue(bone, cementum like material, distrophic calcifications)
  • 43. PAPILLOMA  Benign proliferation of surface epithelium associated with human pappiloma virus (HPV).  Viral subtypes HPV-6 and HPV-11 have been found in most cases.  Appears as solitary, cauliflower-like protuberances.  They may be small and discrete or broad, hard elevations with minutely irregular surfaces
  • 44. PERIPHERAL GIANT CELL GRANULOMA  It arises from gingival margin , occur most frequently on labial surface, may be sessile or pedunculated.  Vary in appearance from smooth regularly outlined masses to irregularly shaped multilobulated protuberance with surface indentations.  Marginal ulceration is seen occasionally  Lesions are painless, vary in size ,may cover several teeth.  They may be firm or spongy, colour varies from pink to deep red or purplish blue.
  • 45. CENTRAL GIANT CELL GRANULOMA  These lesion arises within the jaw and produce central cavitation  They occasionally create deformity of jaw that makes gingiva appear enlarged.
  • 46. GINGIVAL CYST  It develop from odontogenic epithelium or from surface or sulcular epithelium traumatically implanted in the area.  They seldom reach to clinically significant size and when they do, they appear as localized enlargement involving marginal and attached gingiva.  Occurs in mandibular canine and premolar areas, most often in lingual surface.  They are painless but with expansion, may cause resorption of alveolar bone.
  • 47. CARCINOMA  It is the 6th most common cancer in males and 12th in females.  Squamous cell carcinoma is most common malignant tumor of gingiva.  It may be exophytic, presenting irregular growth and ulcerative lesions.  It go unnoticed till complicated with inflammatory changes.  Sometime it become evident after extraction
  • 48.  These are locally invasive involving bone and periodontal ligament of adjoining teeth and adjacent mucosa.  Metastasis remain confined to region above clavicle , most extensive form may include lung, liver or bone.
  • 49. MALIGNANT MELANOMA  It arises from melanoblasts in gingiva, cheek or palate.  It is rare tumor occur in hard palate and in gingiva of older person.  It may be flat or nodular characterized by rapid growth and early metastasis.  Infiltration into underlying bone and metastasis to cervical and axillary lymph node are common.
  • 50.  Fibrosarcoma, lymphosarcoma and reticulum cell sarcoma of gingiva are rare  Only isolated cases have been reported  Kaposi sarcoma often occurs in oral cavity of patients with AIDS  Tumor metastasis to gingiva occurs infrequently
  • 51. False enlargement are not true enlargement of gingival tissue but may appear as a result of increase in size of the underlying osseous or dental tissue 1) underlying osseous lesions enlargement of bone subjacent to gingival area occurs most often in tori and exostoses, it also occurs in Pagets disease,fibrous dysplasia,cherubism, central giant cell granuloma,ameloblastoma,osteoma and osteosarcoma
  • 52.
  • 53. 2)Underlying dental tissue  During various stages of eruption, particularly of primary dentition, labial gingiva may show bulbous marginal distortion caused by superimposition of gingiva on normal prominence of enamel in gingival half of crown.  Enlargement persists until junctional epithelium has migrated from enamel to CEJ  This enlargement are physiologic and usually present no problem
  • 55.  It is the physiologic wearing away of teeth because of tooth to tooth contact .  Attrition is the simple wearing down of the cusps of the posterior teeth and the incisal edges of the anterior teeth. Types Physiological attrition-attrition which occurs due to normal process, due to mastication Pathological attrition-due to abnormalities in occlusion and due to abnormal habbits like bruxism
  • 56. Shows serious attrition of 76 yr old man who has been bruxing all life Cusps of the molars have been worn down exposing the yellow dentin underneath.
  • 57. Treatment  In patients having habbit of bruxism, night guards , bite guards or splint are effective in reducing attrition  Correction of malocclusion
  • 58. Abrasion is the pathological loss of tooth structure by abnormal mechanical forces. Etiology use of abrasive dentifrices, horizontal toothbrushing, holding nails and improper use of floss Types  Toothbrush abrasion  Habitual abrasion-seen in pipe smokers  Occupational abrasion
  • 59.
  • 60. Treatment  Examination and modification of teeth cleansing habbits will be indicated  Elimination of causative agent  Restoration for esthetics and to prevent further tooth wear
  • 61.  Abfraction is also called stress lesion.This term was coined by Dr J.O. Grippo in early 1990’s  It results from occlusal loading causing mechanical microfractures and tooth loss in cervical area  The theory of abfraction is controversial. Dentists began noticing eroded or notched areas (erosions) on teeth close to the gum line (which is called the cervix of the tooth)
  • 62.
  • 63.  Acid erosion, also known as dental erosion, is the irreversible loss of tooth structure due to chemical dissolution by acids not of bacterial origin.  Dental erosion is the most common chronic disease of children ages 5-7yrs  Erosion is found initially in the enamel and, if unchecked, may proceed to the underlying dentin.
  • 64.
  • 65. TYPES extrinsic- occurs because of acidic beverages,citrus food Intrinsic- Dental erosion can occur by non-extrinsic factors too. Intrinsic dental erosion is known as perimolysis, gastric acid from the stomach comes into contact with the teeth. People with diseases such as gastro esophageal reflux disease often suffer from this
  • 66. Management  Prescription of flouride mouthwash is indicated  Modification of brushing habbit and restoration of defect by GIC
  • 67.  These four mechanism of tooth wear-attrision ,abrasion , abfraction and erosion-can combine with each other resulting in increased degree of tooth wear.