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Necrotizing ulcerative periodontitis Extension of NUG into the periodontal structures, leading to loss of attachment and bone loss Two types

Non-AIDS type NUP

AIDS-associated NUP

Non-AIDS Type NUP all the characteristic clinical features of necrotizing ulcerative gingivitis are seen, i.e. i. Ulceration and necrosis of gingival margin, which gets covered by a pseudomembranous slough. ii. The ulcerated margins are surrounded by an erythematous halo. iii. The lesions are extremely painful and bleed spontaneously. iv. Localized lymphadenopathy, fever and malaise long-standing cases, can extend to the deeper periodontal structures resulting in deep, crater-like osseous lesions especially in interdental areas NUP

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AIDS-Associated NUP similar findings that are seen in non-AIDS associated necrotizing ulcerative periodontitis may leads to NS and NOMA.

REFRACTORY PERIODONTITIS “those cases which do not respond to any treatment provided, whatever the thoroughness or frequency”

Etiology

Risk Factors Responsible for Refractory Cases

a. Abnormal host response.

b. Resistant strains of pathogenic periodontal microflora.

c. Failure to eliminate plaque-retentive factors

d. smoking

e. systemic diseases

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Microbial Specificity: three major microbial complexes in refractory periodontitis cases. 1. B. forsythus, F. nucleatum and C. rectus. 2. S. intermedius, P. gingivalis and P. micros. 3. S. intermedius and F. nucleatum.

Treatment

Antimicrobial therapy killing subgingival pathogens that remain after conventional mechanical periodontal therapy

intrasulcular irrigation with 10% povidone-iodine solution and chlorhexidine

local drug delivery system (gels, fibers or chips)

HMT

SDD 20mg BD

NSAIDs

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Periodontitis As A Manifestation Of Systemic Disease Some diseases in which either defective numbers of neutrophils or defective neutrophil function. Some of the conditions associated with defective neutrophils are a. Papillon-Lefévre syndrome.

b. Chédiak-Higashi syndrome.

c. Down’s syndrome.

d. Hypophosphatasia.

e. Neutropenia.

f. Leukocyte adhesion deficiency

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Papillon-Lefévre Syndrome

hyperkeratotic skin lesions

severe destruction of the periodontium

changes may appear before the age of 4 years

Skin lesions are—hyperkeratosis of localized areas on palms, soles, knees and elbows

Periodontal involvement is

early inflammatory changes that lead to bone loss and exfoliation of teeth.

Primary teeth are lost by 5 or 6 years of age.

The permanent dentition erupts normally but within few years the permanent teeth are also lost

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Chédiak-Higashi Syndrome

Genetically transmitted disease

Melanocytes, Platelets & Phagocytes affected

defects in both neutrophils and monocytes

Causes partial Albinism, Mild Bleeding & Recurrent infections

Neutrophils contains abnormal large giant Lysosome that can fuse with phagosome but their ability to release their content is impaired

Killing of ingested microrganism is delayed

Aggressive Periodontitis

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Down’s Syndrome (Mongolism, Trisomy 21)

Congenital disease caused by chromosomal abnormality

Mental deficiency and growth retardation

Prevalance of periodontal disease in Down syndrome is 100% in patients younger than 30yrs

Deep Periodontal pocket & substantial plaque accumulation

Poor PMN chemotaxis and phagocytosis

Disease progresses rapidly

Acute necrotizing lesions are frequent

Increased P-intermedia in children with Down syndrome ►Factors for increased prevalence and increased severity of periodontal destruction

Reduced resistance to infections because of poor circulation (especially peripheral).

Defect in T-cell maturation and polymorphonuclear leukocyte chemotaxis.

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Hypophosphatasia

rare familial skeletal disease characterized by

rickets,

poor cranial formation,

premature loss of primary dentition particularly incisors.

low level of serum alkaline phosphatase.

Teeth are lost with no clinical evidence of gingival inflammation

and show reduced cementum formation.

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Leukocyte Adhesion Deficiency

Extreme acute inflammation

rapid bone loss,

profound defects in peripheral blood neutrophils and monocytes are seen.

Hence they are absent in gingival tissues.

Patients with LAD also have frequent

RTI and

Otitis media

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Treatment

Local debridement of lesions with scaling and root planing

Oral hygiene instructions

The use of ultrasonic instrumentation with copious irrigation

Locally applied antimicrobials,

systemic antibiotics

analgesics should be considered