Healthy periodontium, Classification, Periodontitis, Gingival diseases, gingivitis, abscess, clinical features, treatment

1. PARITOSH KABRA
SINHGAD DENTAL COLLEGE & HOSPITAL, PUNE
DISEASES OF
PERIODONTIUM

2. INTRODUCTION
• Periodontal disease, also known as gum disease, is a set of inflammatory conditions
affecting the tissue surrounding teeth.
• Though there are many distinct types of chronic diseases of the periodontal tissues exist,
chronic plaque associated gingivitis and periodontitis are most common.
• Gingivitis
- Inflammation confined only to the marginal gingiva.
• Periodontitis
- Inflammation extending to involve the connective tissue attachment and
alveolar bone loss.

3. HEALTHY PERIODONTIUM
The periodontium ( peri- around, dontium- tooth ) or the attachment
apparatus incudes:
• The gingiva
• The periodontal ligamement
• The root cementum
• The alveolar bone

4. Page R C et al. 1997 – Prevalence of periodontal disease in adult population
90% Gingivitis
60% Chronic periodontitis
5 – 15% Aggressive periodontitis

5. CLASSIFICATION OF THE
PERIODONTAL DISEASE
1. GINGIVAL DISEASES: 2. CHRONIC PERIODONTITIS:
- Plaque Induced gingival disease - Localized
- Nonplaque induced gingival lesions - Generalized
3. NECROTIZING PERIODONTAL DISEASES: 4. AGGRESSIVE PERIODONTITIS:
- Necrotizing ulcerative gingivitis (NUG) - Localized
- Necrotizing ulcerative periodontitis (NUP) - Generalised
5. PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC DISEASES
6. PERIODONTITIS ASSOCIATED WITH 7. ABSCESSES OF PERIODONTIUM:
ENDODONTIC LESION: - Gingival abscess
- Endodontic-periodontal lesion - Periodontal abscess
- Periodontal-endodontic lesion - Pericoronal abscess
8. DEVELOPMENTAL OR ACQUIRED DEFORMITIES AND CONDITIONS:
- Mucoginingival deformities and conditions around tooth
- Mucoginingival deformities and conditions on edentulous ridges
9. OCCLUSAL TRAUMA

6. GINGIVA
• A healthy gingiva is a part of the masticatory mucosa covering the alveolar process and
surrounds the cervical portion of the tooth by snugly fitting into each interproximal
space between the teeth.
 Gingiva is anatomically differentiated into two parts:
• The free (marginal) gingiva
• The attached gingiva
 Features of healthy gingiva:
• Colour - Coral pink
• Stippled ‘orange peel’ surface
• Stippling is a form of adaptive
specialization.
• Reduction or a loss of stippling
is a common sign of gingival disease.
• In children- the gingiva is not
stippled and appears redder.
• Microscopically, gingival epithelium is stratified squamous and parakeratinized except
In the gingival sulcus & interdental area where it is nonkeratinized.

7. GINGIVAL DISEASES

8. PLAQUE INDUCED
GINGIVAL DISEASES

9. PLAQUE INDUCED GINGIVAL DISEASE
- Most common form of gingival disease.
- Result of the interaction of plaque bacteria and defence cells of the host.
 ETIOLOGY
- LOCAL FACTORS:
 Microorganisms
 Calculus
 Faulty or irritating restorations
 Mouth breathing
 Tooth maposition
- SYSTEMIC FACTORS:
 Nutritional deficiencies
 Drug action
 Allergy
 Heredity
 Endocrine changes associated with puberty, pregnancy, menstrual cycle & diabetes mellitus

10. 1. MICROORGANISMS
- Many varieties of microorganisms grow as biofilm or plaque, for the most part, on the
nonself-cleansing areas of the teeth such as –
Cervical convexity of the crown and in the cervical areas
- The normal oral flora is so vast & is made up of so many varities of microorganisms that it
has never been possible to prove conclusively that any one type of microorganism is of
greater importance than others.
- Plaque and plaque-induced endotoxins may act as irritants or antigens in both nonspecific
acute inflammatory responses and immune mechanisms of defence.
2. CALCULUS
- Whether in a supragingival or a subgingival position, calculus causes irritation of the
contracting gingival tissue.
- The irritation is probably caused by the byproducts of the microorganisms, although the
mechanical friction from the hard, rough surface of the calculus may also play a role.

11. 3. FOOD IMPACTION:
- The impaction of food and the accumulation of debris on the tooth because of oral neglect
result in gingivitis, through irritation of the gingiva by toxins of microorganisms growing in this
medium.
4. FAULTY OR IRRITATING RESTORATIONS:
- Faulty restorations may act as irritants to gingival tissues and thereby induce gingivitis.
- Overhanging margins of proximal restorations may directly irritate the gingiva and in
addition allow the collection of food debris.
- Prosthetic or orthodontic appliances impinging on the gingival tissue produce gingivitis as
a result of the pressure and of the tapping of food and microorganisms.
5. MOUTH BREATHING
- Drying of the oral mucous membrane due to mouth breathing, excessive environment heat or
excessive smoking causes gingival irritation.

12. 6. CHEMICAL OR DRUG APPLICATION
- Many drugs are potentially capable of inducing gingivitis, owing to a direct or systemic irritating
action
- For example, phenol, silver nitrate, volatile oils or aspirin, if applied to the gingiva, will provoke
an inflammatory reaction.
- An unusual type of gingivostomatitis termed ‘plasma cell gingivitis’ first appeared in the USA in
1968. They found out that the disease represented an allergic reaction to some components of
chewing gum. When the patients eliminated the use of chewing gum, the tissues returned to
normal.
7. PREGNANCY
- Many investigators have reported that the gingiva undergoes certain changes during pregnancy
which have termed ‘pregnancy gingivitis’.
- The clinical appearance of the gingiva in pregnant woman varies from an unchanged to smooth,
shiny, deeply reddened marginal gingiva with frequent focal enlargement & intense hyperemia
of the interdental papilla.
- Pregnancy induces a hypersensitive response to a mild injury which otherwise would have been
inoccous.
- It may occur near the end of first trimester and may regress or completely disappear at the term
-ination of pregnancy.

13. 8. DIABETES MELLITUS
- It has not been proved that diabetes is a specific cause of severe periodontal disease.
- However, in uncontrolled diabetes, many metabolic processes are affected including those
which make up resistance to infection or trauma causing the periodontal tissues to breakdown
more readily in such cases.

14. CLINICAL FEATURES
- Inflammation is limited only to the gingiva without underlying attachment loss.
- It may be localized or generalised.
- Bleeding from gingival sulcus following even mild irritation such as tooth brushing or
probing.
- Slight swelling of the gingiva and loss of stippling.
- Inflammatory swelling of the interdental papillae often produces a somewhat bulbous
appearance of these structures.

15. RADIOGRAPHIC FEATURES
Chronic gingivitis, in which the inflammation is limited strictly to the gingiva, does not
manifest changes in the underlying bone.
When bony changes become evident, the condition is termed ‘periodontitis’.

16. HISTOLOGIC FEATURES
- Infiltration of the connective tissue by varying numbers of lymphocytes, monocytes
and plasma cells.
- The capillaries of the connective tissue are usually engorged and sometimes increase in
number.
- The underlying periodontal ligament, except perhaps those fibers of the free gingival
group, is not involved.
- The junction of the epithelial attachment to the tooth represents a weak point in the
epithelial barrier to the oral environment, and at this point a collection of polymorpho-
nuclear leukocytes and lymphocytes are always found.
- The glycogen content of the granular and spinous layer of the epithelium increase as
the intensity of the underlying inflammation increases.
- The alkaline phosphatase activity increases somewhat in the inflamed gingiva.

17. TREATMENT & PROGNOSIS
- Most cases of chronic gingivitis are due to local irritation.
- If the irritants are removed at this stage, the inflammation with its attendant swelling
will disappear within a matter of hours or a few days, leaving no permanent damage.
- Mechanical removal of plaque can be aided by chemical plaque control measures such
as using mouthwashes containing chlorhexidine, listerine or triclosan.

18. NECROTIZING
GINGIVOSTOMATITIS

19.  Necrotizing ulcerative gingivitis, necrotizing ulcerative periodontitis and necrotizing
stomatitis are together termed as ‘ Necrotizing gingivostomatitis ’.
 They share many etiological and clinical characteristics.
 Predisposing factors may include emotional stress, immunosuppresion, HIV infection,
smoking, malnutrition and pre-existing gingivitis.
 Necrotizing periodontitis share many etiological and clinical characteristics of necrotiz-
ing ulcerative gingivitis in patients with no known systemic disease or immune dysfun-c
tion, except that patients with necrotizing periodontitis demonstrate attachment loss
Necrotizing ulcerative gingivitis Necrotizing stomatitisNecrotizing ulcerative Periodontitis

20. NECROTIZING ULCERATIVE
GINGIVITIS
VINCENT’S INFECTION /
TRENCH MOUTH /
ACUTE ULCEROMEMBRANOUS GINGIVITIS /
ACUTE NECROTIZING GINGIVITIS /
FUSOSPIROCHETAL GINGIVITIS

21. • Necrotizing ulcerative gingivitis is a specific type of gingivitis with characteristic signs &
symptoms.
• The disease manifests both acute and recurrent (sub-acute) phases; a chronic stage also has
been described.
• The inflammatory condition involves primarily the free gingival margin, the crest of the gingiva
and the interdental papillae.
• On rare occasions, the lesions spread to the soft palate and tonsillar areas, and in such instances
the term Vincent’s angina has been applied.
• Pain, interdental ulceration, and gingival bleeding are considered to be the diagnostic triad.
Necrotizing ulcerative gingivitis

22. EPIDEMIOLOGY
 Frequently occurs in an epidemic pattern, sweeping through groups of persons in close c
ontact, especially those living under similar conditions.
 Sporadic outbreaks occurred during World War I and II.
 The pattern of the spread of the disease, in many instances, indicated that it was a conta
gious infection, but this theory is not accepted now.
 Its occurrence in groups of persons can be explained on the basis of similar predisposing
conditions among the members of the group, which may cause gingivitis to develop in e
ach, even though there is no actual contact.

23. HISTORY
Features of the patient’s history-
 Sudden onset of symptoms
 Following an episode of debilitating disease or acute respiratory tract infection.
 Change in living habits
 Protracted work without rest
 Poor nutrition
 Tobacco use
 Psychological stress

24. ETIOLOGY
- Most investigators believe that NUG is caused by
a fusiform bacillus and Borrelia vincentii- a spirochete.
- Chung et al, found out significant increase in IgG
and IgM antibody titers to spirochetes and increased
antibody titers to Bacteroids melaninogenicus.
- MacDonald et al, concluded that
Bacteroids melaninogenicus , a motile gram negative
ananaerobic bacillus, was the true causative
agent of necrotizing ulcerative gingivitis.
A, Spirochete
B, Bacillus fusiformis
C, filamentous organism (Actinomyces)
D, Streptococcus
E, Vibrio

25. CLINICAL FEATURES
- Characterized by development of painful, hyperemic gingiva and sharply punched-out crater
like erosions of the interdental papillae of sudden onset.
- The ulcerated remnants if the papillae and free gingiva bleed when touched and generally
become covered by a grayish green, necrotic pseudomembrane.
- Fetid odour and increased salivation with the presence of metallic taste.
- Patient complains of a constant radiating gnawing pain (intensified by spicy or hot foods and
on chewing).
- Regional lymphadenopathy.

26. Generalized involvement of the
papillae and marginal gingiva,
with whitish necrotic lesions
Typical lesions with spontaneous
hemorrhage.

27. HISTOLOGIC FEATURES
• Histopathological changes are non-specific.
• Changes involves both the stratified squamous epithelium and the underlying connective
tissue.
• Surface epithelium is destroyed and replaced by a meshwork of fibrin, necrotic epithelial
cells, PMNs and many microorganisms. This is the zone which appears as pseudomembr-
ne.
• - At the border of necrotic pseudomembrane the epithelium is edematous and cells show
hydropic degeneration.
• - Infiltration PMNs in the intercellular spaces.
• Connective tissue is hyperemic with numerous engorged capillaries and dense infiltration
of PMNs.

28. TREATMENT & PROGNOSIS
- Varies depending upon individual dentists.
- Some prefer to treat this condition conservatively, instituting only superficial cleansing
of oral cavity with:
• Chlorhexidine
• Diluted hydrogen peroxide
• Warm saltwater
- Topical anaesthetic may be required to reduce the pain.
- Patients with moderate/severe NUG and local lymphadenopathy or other systemic sign
s or symptoms are placed on an antibiotic regimen of amoxicillin 500mg orally every 6
hours for 10 days.

29. GINGIVAL ABSCESS

30. • A gingival abscess is a localized, painful, rapidly expanding lesion that usually has a sudden onset.
• Generally limited to the marginal gingiva or interdental papilla.
• In its early stages, it appears as a red swelling with a smooth, shiny surface.
• Within 24 to 48 hours, the lesion usually becomes fluctuant and pointed with a surface orifice
from which a purulent exudate may be expressed.
• The adjacent teeth are often sensitive to percussion.
• Etiology
• Bacteria carried deep into the tissues when a foreign substance (e.g., toothbrush bristle, piece of
apple core, or lobster shell fragment) is forcefully embedded into the gingiva.

31. TREATMENT
Treatment of gingival abscess is aimed at-
• Reversal of acute phase
• When applicable immediate removal of the cause.
• Topical or local anaesthesia by infiltration is administered.
• When possible scaling and root planning are completed to establish
drainage and removal of microbial debris.
• Any foreign material (dental floss or impression material) removed.
• The area is irrigated with warm water and covered with moist
gauze under light pressure.
• After 24 hours area is reassessed, and if resolution is sufficient,
scaling not previously completed is undertaken.
Gentle digital pressure
applied to express
purulent discharge

32. PERICORONITIS

33. • Refers to inflammation of the gingiva in relation to the crown of an incompletely erupted tooth.
• Occurs most often in mandibular 3rd molar area
• Pericoronitis may be –Acute, sub acute or chronic.

34. CLINICAL FEATURES
 Partially erupted or impacted mandibular 3rd molar is the most common site of Pericoronitis.
 The space between crown of the tooth and the overlying gingival flap is an ideal area for the
accumulation of food debris and bacterial growth.
 Acute inflammatory involvement is a constant possibility and may be exacerbated by
 Trauma
 Occlusion
 Foreign body trapped underneath the tissue flap (e.g., Popcorn husk, nut fragment)
 The inflammatory fluid and cellular exudate increase bulk of flap that interferes with complete
closure of jaws and traumatized by contact with opposing jaw.
 Clinically appears as –
 Red
 Swollen
 Suppurating lesion
 Tender with radiating pain to ear, throat and floor of the mouth.
 - Patient uncomfortable because of foul taste and inability to close jaws.

35. TREATMENT
- Entrapped food debris must be removed.
- When the upper tooth is involved, it should
be grounded or extacted.
- If impacted, the tooth must be removed.
- If the involving tooth is in favourable position,
surgical removal of pericoronal flap is advocated
after acute symptoms subside.
Complication: Pericoronal abscess

36. GINGIVAL ENLARGEMENT

37. INTRODUCTION
• Gingival hyperplasia (“abnormal increase in the number of normal cells in a normal arr
angement in an organ or tissue, which increase in volume”) and gingival hypertrophy
(“enlargement or overgrowth of an organ or part due to an increase in size of its cons-
tituent cells”) have been used
• Gingival overgrowth is the general term that better describes this condition.
• Gingival enlargement or gingival overgrowth are strictly clinical descriptive terms and
avoid the erroneous pathologic connotations of terms in the past, such as "hypertroph
-ic gingivitis" or "gingival hyperplasia.

38. CLASSIFICATION
1. Inflammatory enlargement
• Chronic
• Acute
2. Drug-induced enlargement
3. Enlargements associated with systemic diseases or conditions
A. Conditioned enlargement
• Pregnancy
• Puberty
• Vitamin C deficiency
• Plasma cell gingivitis
B. Nonspecific conditioned enlargement
C. Systemic diseases causing gingival enlargement
• Leukemia
• Granulomatous diseases (e.g., Wegener's granulomatosis, sarcoidosis)
4. Neoplastic enlargement (gingival tumors)
1. Benign tumors 2. Malignant tumors
5. False enlargement

39. Conditioned enlargement
• Conditioned enlargement occurs when the systemic condition of the patient
exaggerates or distorts the usual gingival response to dental plaque.
• The specific manner in which the clinical picture of conditioned gingival enlargement
differs from that of chronic gingivitis depends on the nature of the modifying systemic
influence.
• Bacterial plaque is necessary for the interaction of this type of enlargement.
• The three types of conditioned gingival enlargement are
– Hormonal (pregnancy, puberty),
– Nutritional (associated with vitamin C deficiency)
– Allergic.

40. Enlargement in pregnancy

41. • In 1818 Pitcarin described the gingival hyperplasia in pregnancy
• The enlargement is usually generalized and occurs more prominently interproximally
than on the facial & lingual surfaces.
• The enlarged gingiva is bright red or magenta, soft and friable and has a smooth shiny su-
rface bleeding occurs spontaneously or on slight provocation.
• Tumor like gingival enlargement or pregnancy tumour.
• It usually appears after the third month of pregnancy but may occur earlier. The reported
incidence is 1.8 to 5%.
• Discrete mushroom like flattened spherical mass that protrudes from the gingival margin
or more commonly from the interproximal space
• Attached by a sessile or pedunculated base tends to expand laterally and pressure from
the tongue and cheek perpetuates its flattened appearance.

42. • Treatment requires elimination of all local irritants
• Elimination of local irritants early in pregnancy is preventive measure
• Marginal and interdental gingival inflammation and enlargement are treated with scaling and
root planning.
• Treatment of tumor-like gingival enlargements consists of surgical excision and scaling and
planning of the tooth surface.

43. Enlargement in
Vitamin C deficiency

44. • This enlargement is essentially a conditioned response to bacterial plaque.
• Acute vitamin C deficiency does not of itself cause gingival inflammation but it does cause
hemorrhage, collagen degeneration and edema of the gingival connective tissue.
• normal defensive delimiting reaction is inhibited and the extent of the inflammation is exagge-
rated.
• The combined effect of acute vitamin C deficiency and inflammation produces the massive
gingival enlargement in scurvy.
• Gingivitis with enlarged hemorrhagic bluish red gingiva is described as one of the classic signs
of vitamin C deficiency.

45. • Gingival enlargement is marginal, the gingiva is bluish red, soft & friable and has a smooth
shiny surface.
• Hemorrhage occur either spontaneously or on slight provocation and surface necroses
with pseudomembrane formation are common features.
• Although scorbutic changes in the gingival tissue may be observed throughout life. They
are commonly seen in the child under 2 yrs of age

46. TREATMENT
• Systemic treatment consists of supplementing the diet with vitamin C locally,
• Professional and chemical plaque control.

47. PLASMA CELL GINGIVITIS
( ALLERGIC GINGIVAL ENLARGEMENT)

48. •Plasma cell gingivitis is also referred to as atypical gingivitis and plasma cell gingivostomatitis
•often consists of mild marginal gingival enlargement that extends to the attached gingiva.
•more prevalent in young females and often extended over a period of many months.
•There is intense hyperemia, edema and inflammation of the free and attached gingiva which in
severe cases extends to involve the buccal and vestibular alveolar mucosa.
•If gingival inflammation is restricted to the free and attached gingiva it is demarcated from the
normal appearing vestibular mucosa with sharp line of demarcation.

49. •The gingiva appears red, friable and sometimes granular and bleeds easily. Usually it does
not induce a loss of attachment.
•This lesion is located in the oral aspect of the attached gingiva and therefore differs from
plaque induced gingivitis and association with cheilitis and glossitis have been reported.
• Plasma cell gingivitis is thought to be allergic in origin, possibly related to the components
of chewing gum, dentifrices or various diet components cessation of exposure to the allerge
n brings resolution of the lesion.
•In rare instances marked inflammatory gingival enlargements with a predominance
of plasma cells can appear associated with rapidly progressive periodontitis.

50. SYSTEMIC DISEASES
CAUSING
GINGIVAL ENLARGEMENT

51. LEUKEMIA
• Gingival hyperplasia is often an early finding in acute monocytic, lymphocytic or myelocy-
tic leukemia.
• Leukemia does not cause the gingivitis but the lowered resistance to infection due to
lack of normal functioning leukocytes tends to aggravate already present gingivitis and
the increased bleeding tendency.
• It also has been claimed that the large immature cells in acute monocytic leukemia may
act as emboli in the fine gingival capillary loops and create stasis.

52. CLINICAL FEATURES
• Leukemic enlargement may be diffuse or marginal, localized or generalized.
• The highest incidence in patients with acute monocytic leukemia (66.7%) followed by acute
myelocytic monocytic leukemia (18.7%) and acute myelocytic leukemia (3.7%).
• Leukemic gingival enlargement is not found in edentulous patients or in patients with chroni
c leukemia.

53. • Consists of a basic infiltration of the gingival corium by leukemic cells that creates gingival
pockets where bacterial plaque accumulates initiating a secondary inflammatory lesions
that contributes also to the enlargement of the gingiva.
• It appears as a diffuse enlargement or a discrete tumor like interproximal mass.
• In leukemic enlargement the gingiva is generally bluish red and has a shiny surface.
• consistency is moderately firm but there is tendency toward friability and hemorrhage occu-
rring either spontaneously or on slight irritation.
• Acute painful necrotizing ulcerative inflammatory involvement sometimes occurs in the
crevice formed at the junction of the enlarged gingiva and the contigous tooth surface.
• Patients with leukemia may also have simple chronic inflammation

54. TREATMENT
• The medical care of leukemic patients is often complicated by gingival enlargement with
superimposed painful anug,
• The patient's bleeding and clotting times and platelet count should be checked
• After acute symptoms subside, attention is directed to correction of the gingival enlarg-
ement.
• The rationale is to remove the local irritating factors to control the inflammatory compo-
nent of the enlargement.

55. PERIODONTITIS

56. CHRONIC PERIODONTITIS

57. Chronic Periodontitis can be defined as “an infectious disease resulting in
inflammation within the supporting tissues of the teeth, progressive attachment loss,
and bone loss.”
- Previously known as adult periodontitis or slowly progressive periodontitis.
- Occur as a result of extension of inflammation from the gingiva into deeper periodo
ntal tissue
- Most commonly seen in adults.

58. CLASSIFICATION
Based on Disease Distribution:
Localized:
– Periodontitis is considered localized when <30% of the sites assessed in mouth de
monstrate attachment loss and bone loss.
Generalized:
– Periodontitis is considered generalized when >30% of the sites assessed demonstr
ate attachment loss and bone loss.
– The pattern of bone loss in chronic periodontitis can be vertical or horizontal.
Based on severity:
Severity Pocket
Depths
CAL Bone Loss Furcation
Early 4-5 mm 1-2 mm Slight
horizontal
Moderate 5-7 mm 3-4 mm Sl – mod
horizontal
 involved
Advanced > 7 mm  5 mm Mod-severe
Horizontal &
Vertical
 involved

59. CLINICAL FEATURES
• Supra and subgingival plaque accumulation
(frequently associated with calculus)
• Gingival inflammation
• Pocket formation.
• Loss of periodontal attachment
• Occasional suppuration
• Poor oral hygiene – slightly to moderately swollen
• Color- pale red to magenta
• Consistency – soft or firm

60. • Surface topography – loss of stippling
• Blunted or rolled gingival margin
• Flattened or cratered papillae.
• Furcation
• Tooth mobility
• gum bleed
• space appear between teeth due to tooth movement
• May be painless (sleeping disease )goes unnoticed
• Some time pain due to caries , root hypersensitivity

61. Severe Periodontitis

62. MANAGEMENT
The treatment consists of –
1. Non-surgical procedures
– Scaling
– Root planing
– Curettage
2. Surgical procedure
– Pocket reduction surgery
• Resective
• Regenerative
– Correction of morphological / anatomic defects

63. AGGRESSIVE
PERIODONTITIS

64. • A rapid rate of disease progression.
• The disease affects only the permanent dentition. The primary teeth are not affected
and are not prematurely exfoliated because of destructive periodontal disease.
• The amount of local etiologic factors is not commensurate with the severity of period-
ontal destruction.
• Predominance in female subjects (female to male ratio - 3:1).
• The disease has a familial pattern.
• Microflora associated:
• Actinobacillus actinomycetemcomitans
• Porphyromonas gingivalis
• Bacteroids forsythus

65. CLINICAL FEATURES
LOCALIZED FORM
• Usually occurs around puberty
• Localized to the first molar and incisors
• There is attachment loss in at least two permanent
teeth, one of which is the first molar.
• A striking feature is the absence of clinical
inflammation with minimal local factors despite
the presence of deep periodontal pocket.
• The rate of alveolar bone loss is considerably
higher than in chronic periodontitis.

66. GENERALIZED FORM
• Usually affects patients under 30 years of age.
• It involves at least three teeth other than the first molar and incisor.
• Many cases represent the localized form which becomes generalised with time.
• The marked distinction between this and the localized form is the presence of large acc
umulation of plaque, calculus and gingival inflammation.

67. PAPILLON-LEFEVRE SYNDROME
• It is an autosomal recessive disorder that is characterized by cutaneous and oral manifes-
tations.
• The oral lesions are characterized by aggressive periodontitis leading to severe destruct-
ion of the alveolar bona involving both the deciduous and permanent dentition.
• Due to rapid bone loss, mobility and pathological migration occurs, which results in loss
of the entire dentition at a much younger age.

68. RADIOGRAPHIC FEATURES
- In the localized form, vertical bone loss is seen around the first molar and the incisor at
around the age of puberty in otherwise healthy patient.
- An arc-shaped bone loss extends from the distal surface of the second premolar to the
mesial surface of the second molar.
- In generalised form, bone loss may range from the involvement of one or two teeth to
a maximum number of teeth.

69. MANAGEMENT
• Antibiotics should be administered in combination with mechanical removal of plaque
and inflamed periodontal tissues.
• Periodontal surgery should be performed with prophylactic antibiotic cover and posto
perative usage of chlorhexidine mouthrinse.

70. THANK YOU!