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MODERATED BY: Dr Harpreet Grewal Dr Mridula Goswamy Dr Gyanendra Dr Meera Dr Ashok

A Presentation by: Shruti Goel

Greater sulcus depth (1.42.1mm)

Inflammatory

Disease of gingiva and deeper tissues of periodontium Characterized by pocket formation and destruction of supporting alveolar bone. Distance of alveolar crest to CEJ

2-3 mm= questionable bone loss >3 mm= definite bone loss

In

preschool children- no recession, gingival erythema and edema (Delaney)

Pubertal

Adult

Periodontitis

Juvenile

Rapidly Progressing

Used

as a generic term to describe a heterogeneous group of periodontal diseases occuring in young individuals who are otherwise healthy.

Localized Juvenile Early-Onset Prepubertal Generalized

Localized Juvenile Early-Onset Prepubertal Generalized

severe attachment and bone loss around the first molars and incisors (but not involving more than two additional non first molar/incisor teeth), which occurs between the ages of 12 to 26 years.

severe attachment and bone loss involving more than two teeth in addition to first molar/incisor teeth.

Fairly Generalized

Chronic Slowly Progressive

Acute Progressive

Juvenile Periodontitis

Bacteria (certain kind)

Actinobacillus actinomycetemcomitans

Host response

Impaired PMNs (phagocytosis, chemotaxis and decreased receptors)

Possibly genes

may be AD inheritance

PMN Dysfunction

Susceptibility to infection

A. Actinomycetemcomitans

Serum Amplification leukotoxins

Antibody

Neutralisation

Local PMN and Macrophage destruction

Accelerated Disease

Loss of attachment and alveolar bone around permanent incisors and first molars Detected at ages 10-15 Diagnosis made when 3 sites have CAL of 5mm or greater Familial Aggregation Lack of clinical inflammation despite the presence of deep pockets Premature and excessive mobility of affected teeth

Regional lymphadenopathy

Distolabial migration of maxillary incisors with diastema formation Apparent increase in the size of clinical crown

Rapid progression- Rate of bone loss is 3-4 times more than typical periodontitis. Denuded root surfaces become sensitive to thermal and tactile stimuli. Deep, dull radiating pain
Periodontal abscesses Small amount of plaque, calculus rarely

Vertical alveolar bone loss around the first molars and incisors.

Arc shaped bone loss extending from the distal surface of the second premolar to the mesial surface of the first molar.

Arc like bone loss

Gram

negative, facultative anaerobic, coccobacillus Makes leukotoxin kills macrophages Why is A.a the culprit?
None or low levels of A.a found at non diseased sites Extermination of A.a = Clinical Success Presence of A.a after treatment resulted in progressive attachment loss

Lost

Teeth:

Over a 6 year period


Untreated 43% lose teeth

35%

cases of untreated LAP lead to Generalized Aggressive Periodontitis

Five-year maintenance follow-up of early-onset periodontitis patients. J Clin Periodontol. 2003 Jun;30(6):562-72 Study:

25 patients with JP Received Supportive Periodontal Therapy (SPT) for 5 year period SRP and Localized Antibiotic Placement

Average 12-13 sessions of SPT over the 5 year period


Improvements in pocket depths, clinical attachment loss and gingival index However, 134 sites showed CAL greater than or equal to 2mm

Bacteria most prevalent in these failures:


P. gingivalis T. denticola

Note: Confounded by smoking and stress

Actinobacillus actinomycetemcomitans as indicator for aggressive periodontitis by two analyzing strategies. J Clin Periodontol. 2007 July;34(7):566-573 60 patients with JP or Chronic Periodontitis samples taken of subgingival plaque using paper points Plaque analyzed for A.a, T. forsythensis, P. gingivalis and T. denticola Higher levels of A.a in LAP versus Chronic Periodontitis Lower levels of other pathogens in A.a versus Chronic Periodontitis

Study:

Comparative evaluation of surgical and conservative treatment modalities of juvenile periodontitis patients. Afr J Med Med Sci. 2001 Dec;30(4):313-8. Study: 12 patients, 6 mon longitudinal study Split mouth tx: 1 side conservative 1 side surgical and antibiotic therapy Look at mobility and CAL Use SRP and systemic antibiotic use It was therefore concluded that surgical debridement with systemic administration of tetracycline is more effective than the conservative technique in the treatment of juvenile periodontitis, although both gave improvement

Hypophosphatasia

Papillon-Lefevre syndrome

Histiocytosis-X

Neutropenia

Cyclic Neutropenia

Early Diagnosis

Depends upon
Infectionfree environment for healing Use of antibiotics

DNA test kit Clinical Examination Radiographic Interpretation


DMDx test kit (Microdentex) Aids in establishing the risk of JP confirms the response to antibiotic therapy

History

week course of Doxycycline hyclate (1 g per day) Sometimes combined with metronidazole Rationale- concentrations of tetrracyclines achieved in GCF is 2-10 times greater than that in plasma

Meticulous

scaling and root planing Concomitant irrigation to probing depth of saturated inorganic salts and 1% chloramine T. Home care treatment : Daily application of a paste of sodium bicarbonate and 3% hydrogen peroxide and inorganic salt irrigations.

Localized Juvenile Early-Onset Prepubertal Generalized

Prepubertal Periodontitis

Localized

Generlized

Localized attachment loss and alveolar bone loss only in the primary dentition in an otherwise healthy individual Etiology
Abnormalities in host defences Extensive proximal caries facilitating plaque retention Familial

Clinical Features:
Onset- around 4 yrs of age Abnormal probing depths with minor gingival inflammation, rapid bone loss, and minimal to varying amounts of plaque Advanced stages show signs of gingival inflammation with gingival crests and localized ulceration of gingival margin.

Occurs

in families More common in females This suggests X-linked pattern of inheritence Defect may also be acquired and might have resulted from a inhibition of chemotaxis derived from periodontal bacteria

Onset-

during or soon after eruption of primary teeth History of recurrent infections: otitis media, skin infections, URTIs Severe gingival inflammation, generalized CAL, tooth mobility, rapid alveolar bone loss with premature exfoliation of teeth(by 3 yrs of age). Initially gingiva is minorly inflamed with minimal plaque. Chronic cases- clefting and pronounced recession with accute inflammation

Early Diagnosis Consultation with physician to rule out systemic disease Dental curettage

Root planing
Prophylaxis

OHI
Restoration of decayed teeth Removal of primary teeth that have lost bony support Use of antimicrobial rinses(chlorhex), and therapy with broad spectrum antibiotics (amoxycillin, tetracycline)

(Precocious Periodontitis)

First

described by two French physicians, Papillon and Lefvre, in 1924 Prevalence of 1-4 cases per million persons Consanguinity between parents in 1/3 of cases Males and females are equally affected with no racial predominance Rare genetic disorder Autosomal recessive

The palmoplantar keratoderma typically has onset between the ages 1 to 4 years The sharply demarcated erythematous keratotic plaques may occur focally, but usually involve the entire surface of palms and soles resulting in foulsmelling odor Well-demarcated psoriasiform plaque occur on elbows and knees, this may worsen in winter and be associated with painful fissures

Early onset of severe periodontitis starts at the age 3 or 4 years. Development and eruption of deciduous teeth proceeds normally eruption is associated with gingival inflammation and rapid destruction of the periodontium. unresponsive to traditional treatment modalities primary dentition is exfoliated prematurely by age 4 to 5 years. After exfoliation, the inflammation subsides and gingiva appears healthy. In permanent dentition the process of gingivitis and periodontitis is repeated Without treatment, most of the permanent teeth may also be lost by age 17.

Of tentorium falx cerebri and choroid plexus

Radiographic features are characterized by generalized loss of alveolar bone, rapid bone loss. Incomplete root formation Unerupted teeth assume abnormal positions Low Hb Marked predisposition for infections

Pyogenic liver abscess is increasingly recognized as a complication of PLS because of impairment of the immune system. The risk of pyogenic liver abscess should be kept in mind in evaluating these patients when they present with fever of unknown origin. A course of antibiotics should be tried to control the active periodontitis in an effort to preserve the teeth and prevent bacteremia and subsequently pyogenic liver abscess. The most common etiologic agent is S aureus, and most often a solitary abscess is found

PLS
Cathepsin C gene mutation Palmoplantar keratosis 2126CT substitution Y

NS-PPP
1040AG substitution N

Progressive periodontal disease


Teeth effected Patterns of familial transmission

Y
Generalized AR

Y
Generalized or Localized AD and AR

PLS
CTSC gene defect A. a. Reduced chemotaxis PMN defect Teeth effected Y Y Y Y Generalized

LJP
N Y Y Y Localized

multidisciplinary approach is important for the care of patients with PLS, skin manifestations are usually treated with emollients Salicylic acid and urea may be added to enhance their effects Oral retinoids including acitretin, etretinate, and isotretinoin are used in treatment of both the keratoderma and periodontitis associated with PLS

Treatment may be more beneficial if it is started during the eruption and maintained during the development of the permanent teeth Therapy: aggressive local measures to control plaque including rigorous oral hygiene, chlorhexidine mouth rinses, frequent professional prophylaxis, and periodic appropriate antibiotic therapy needed for long-term maintenance The periodontitis in PLS is usually difficult to control. These patients often end up wearing dentures or and implant-supported prosthesis

Initially

recognized by Rathbun in 1948, hypophosphatasia is a rare inborn error of metabolism caused by low activity of the tissue-nonspecific isoenzyme of alkaline phosphatase

Familial

disorder of inborn error of metabolism Autosomal recessive/ dominant inheritance

Infantile Type Birth- 6 months

Childhood type 6-14 months

Adult type Manifests during chilhood

Abnormal

mineralization of bone and teeth Premature exfoliation of primary teeth Only the deciduous teeth are affected

Physical Findings
Consistent clinical history

Low serum alkalinase activity

Wide

variety of treatments have been attempted without a proven success Like oral phosphate supplements, i.v. infusion of plasma etc.

Reactive disorder in which the proliferation of langerhans cells results from disturbances in immunoregulation Langerhans cell is of marrow origin and is found in the epidermis. Oral manifestations:

Ulcerative necrotizing lesions of the gingiva root exposure Increased mobility of teeth Halitosis Osteolytic areas of alveolar bone in the radiographic examination giving the appearance of floating teeth

Disappearance

of neutrophils occurs periodically, approx. every 3 weeks After 5-8 days,the neutrophils begin to reappear Autosomal recessive trait Periodic symptoms- skin and ear infections Mucus membrane ulcerations, severe stomatitis and profound neutropenia develop over a recurrent period of 14-24 days Neutropenic conditions are usually accompanied by or slightly preceeded by monocytosis

Attached,

papillary and marginal gingiva are enlarged, edematous and erythematous and bleed easily on a gentle provocation. Antibiotics are ineffective and bone resorption progresses rapidly to the teeth. During neutropenic stage periodontal disease and destruction occurs and during non neutropenic stage oral health returns.

Caused

by microbial plaque Attachment loss in initial stage is 1-2 mm True periodontal pockets of 45mm Incipient crestal alveolar bone loss >0.5 mm Mesial and distal sites on first molars and incisors most commonly affected Slow progression

Incidence

increases after puberty with age Increased attachment loss and bone loss in poorly controlled diabetes Increased susceptibility to infections Reduced wound healing Due to

Decreased neutrophil function Collagen crosslinking Formation of AGEs

Necrotizing

ulcerative periodontal disease Necrosis and loss of papillary and marginal gingiva and bone Spontaneous gingival bleeding Deep, aching pain May progress to cancrum oris or noma in undernourished or debilitated individuals

Increased attachment loss and bone loss at an earlier age Characteristic periodontal changes include

Fibrotic gingiva Reduced gingival bleeding Anterior recession Maxillary palatal surfaces often more severely affected Nicotine staining

Poorer response to periodontal treatment, maybe refractory periodontitis Neutrophil function affected More susceptible to necrotizing ulcerative gingivitis (NUG)

High

level of spirochetes and P. intermedia invasion of the tissues Factors that predispose children to NPD include

Viral infections including HIV Malnutrition Emotional stress Lack of sleep A variety of systematic diseases

Presence

of interproximal necrosis and ulceration and rapid onset of gingival pain Pts. may be febrile

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