9.1 perio conditions

gingival color: reddish pink → more vascular

contour: rounded gingival margin

consistency: Softer and less fibrotic due to less dense connective tissue and fewer organized collagen fibers

surface texture: Smooth surface, stippling usually absent or minimal in early childhood

children

gingival color: coral pink

contour: knife edge gingival margin

consistency: firm and resilient

surface texture: stippling present

adults

features:

• gingival inflammation

• reversible

• critically, features no loss of attachment or bone

plaque-induced gingivitis

prevalence:

• low in early childhood

• peaks during puberty

• 60% of teens exhibit gingival bop

plaque-induced gingivitis

etiology:

• plaque dependent

• steroid hormones (puberty, pregnancy, menstruation, oral contraceptives)

• local factors: crowding, eruption, calculus

plaque-induced gingivitis

features:

• enlargement of interdental papilla and/or marginal gingiva

• appearance ranges from pale and fibrotic to red and friable

• can be generalized or localized

plaque-induced gingival inflammation

etiology:

• caused by prolonged exposure to plaque

• common local contributory factors - mouth breathing and orthodontic appliances

plaque-induced gingival inflammation

dental management:

• requires thorough oral hygiene routines

• in severe cases, gingivectomy or gingivoplasty may be required

plaque-induced gingival inflammation

mouth breathing may include presence of what three things?

orthodontic appliances may include presence of what three things?

what three drug types may induce DIGE?

• anticonvulsants

• immunosuppressants

• calcium channel blockers

phenytoin, sodium valproate, phenobarbitone

anticonvulsants

cyclosporine, sirolimus, tacrolimus

immunosuppressants

nifedipine, nitrendipine, diltiazem, amlodipine

calcium channel blockers

clinical features of DIGE?

• Painless fibro-epithelial growth of interdental papillae/marginal gingiva

• May cover crowns

• Related to plaque control (does not occur in edentulous areas)

• Regresses after drug cessation

treatment for DIGE

• Replace drug if possible

• Professional prophylaxis

• Azithromycin (beneficial post-debridement for cyclosporine patients)

• Chlorhexidine rinse

• Gingivectomy/gingivoplasty

presentation of localized juvenile spongiotic hyperplasia

• Red hyperplastic lesion with a highly vascular appearance and velvet-like texture

• Involves marginal and/or attached gingiva

• Not associated with plaque or calculus

• Typically, asymptomatic but poses esthetic concerns. May resolve spontaneously

management of localized juvenile spongiotic hyperplasia

• Surgical excision must be approached with caution due to the risk of gingival recession (recurrence rate is around 25%)

• Insufficient evidence exists to prove the effectiveness of alternative treatments (cryotherapy, laser ablation, surface cauterization, topical steroids)

three presentations of localized juvenile spongiotic hyperplasia

what is a pyogenic granuloma?

benign, reactive hyperplasia of CT. responds to trauma, chronic irritation, or elevated estrogen/progesterone. bleeds easily upon stimulation.

appearance and location of pyogenic granuloma

• painless, smooth, lobulated blue-red colored mass

• features a pedunculated base that commonly involves the gingiva

treatment of pyogenic granuloma

complete surgical excision coupled with the removal of underlying irritant

three features of pyogenic granuloma

• Localized, painful sudden onset

• Bacterial infection post-trauma (e.g., embedded popcorn, fingernail)

• Managed via debridement, irrigation, drainage

(no PARL, no adj caries, etc)

gingival abscess

• Inflammation of flap covering partially erupted molar (mostly 3rd molars)

• Food trap leads to bacterial growth. Very painful due to occlusal trauma

• Managed via debridement, antibiotics, chlorhexidine, extraction

pericoronitis

• Edematous, spongy gingiva with non-specific appearance

• Spontaneous bleeding, impaired wound healing

• Managed by treating deficiency and plaque control

vitamin C - deficiency gingivitis

• Rapid, painful onset. Soft tissue necrosis/ulceration with malodor

• Linked to spirochetes, Prevotella Intermedia, stress, smoking. Peak in late teens/20s

• Managed via ultrasonic debridement, NSAIDs, penicillin/metronidazole

ANUG (Acute Necrotizing Ulcerative Gingivitis)

what are the three distinct forms of perio disease?

periodontitis, necrotizing perio, perio as manifestation of systemic condition

describe phases and dynamic clinical loop of perio

what three things are done is diagnostic phase for establishing baseline?

clinical probing, radiographic standards, risk assessment (PRA)

for peds when do you start comprehensive probing? when you would probe early?

after eruption of first permanent molars and incisors

before if if clinical/radiographic findings indicate disease → bop in primary teeth indicates high susceptibility

generalized gingivitis is ≥(?)% affected

30

which radiographic type is standard for diagnostic phase

bitewing

which radiograph rules out root resorption for anterior mobility?

periapical

for primary dentition normal height from CEJ to crest is?

1 ± 0.5 mm

bone loss for peds is

>2mm

a pseudopocket >3mm may be present around partially and newly erupted teeth

true

why would radiographs be essential for definitive perio diagnosis?

severe bone loss can exist beneath deceptively healthy-looking gingival tissue

severity and extent of disease

staging

Assesses the future risk of periodontitis progression and anticipated treatment outcomes

grading

perio stage and grade

staging

grading

perio risk assessment <13 y/o

perio risk assessment ≥13 y/o

HIGH RISK INDICATED BY:

• Periodontal probing depths > 5 mm

• Bleeding on probing > 25% of sites

≥13 y/o

HIGH RISK INDICATED BY:

• Periodontal probing depths > 3 mm

• Bleeding on probing (any amount)

<13 y/o

what are some age modifiers for high risk perio

GOAL: Debridement, scaling, and root planing to remove subgingival plaque, calculus and contaminated cementum

Hand instruments – smoother root surfaces

Ultrasonic scalers – less soft-tissue trauma, faster but avoid for patients unable to expectorate or at risk of aspiration

(systematic reviews show similar results)

phase I: mechanical plaque and local factor control

what are some restorative factors to consider?

• Restore open, cavitated lesions causing food impaction

• Smooth or replace defective restorations with overhangs

• Ensure preformed crowns are well-adapted, contoured, and crimped

what are some orthodontic and enamel factors?

• Suspend orthodontic treatment if the patient cannot maintain proper oral hygiene

• Use desensitizing toothpastes, fluoride varnishes, and sealants for enamel defects (amelogenesis imperfecta) to reduce sensitivity and improve brushing compliance

14 y/o pt w aggressive perio characterized by rapid attachment loss and pocket depths of 5mm. do you prescribe antibiotics? if using adjunctively what is the gold standard?

ab but also srp! no stand alone ab

antimicrobial adjuncts

when do you refer?

what are some surgical interventions (phase II)?

can you place implants on a 15 y/o? why or why not?

no, not until all bone growth complete 18 for gurls 21 for boys, otherwise infraocclusion and twisting of implant w growth

diagnostic standard for implant placement

chronological age is insufficient, skeletal maturation must be assessed via cephalometric analysis or hand-wrist radiographs

what would be the best management for periodontally compromised teeth if implants/regen are not viable?

extraction

which phase

maintenance

long term success relies entirely on quality of supportive perio therapy to prevent disease relapse