L14 Acute Conditions

Acute Gingival and Periodontal Conditions¹²³

The University of Western Australia

Dr Emma Perry | BDSc, AssocDeg DH, GradCert HPEd Lecturer (Clinical Dentistry) | UWA Dental School

Content courtesy of Dr Anna Hughes and Dr Tina Choo

Acknowledgement of country

On Noongar land. Our university is located alongside the Derbal Yerrigan (Swan River) on Whadjuk Noongar Boodja (land). The University of Western Australia acknowledges that we are situated on Noongar land and that Noongar people remain the spiritual and cultural custodians of their land and continue to practise their values, languages, beliefs and knowledge.

Artist: Dr Richard Barry Walley OAM

Everyone is welcome

Learning Outcomes and Lecture Outline⁴⁵

Learning outcomes

• Diagnose and classify the most common acute gingival and periodontal conditions by recognising risk factors and clinical presentation
• Explain the aetiology of acute gingival and periodontal conditions
• Describe the rationale and methods for management of the most common acute gingival and periodontal conditions

Clinical Characteristics

Unlike chronic periodontal disease, acute conditions are characterized by rapid onset, pain, and tissue destruction.

Lecture outline

Necrotising periodontal diseases

• Necrotising gingivitis (NG)
• Necrotising periodontitis (NP)
• Viral lesions
  • Acute Herpetic Gingivostomatitis
• Abscesses of the periodontium
  • Gingival abscess
  • Pericoronitis
  • Periodontal abscess
• Other less common conditions
  • Desquamative gingivitis and Neoplasia
• Endo-perio lesions covered in dedicated lecture from DENT4212 endodontics module

Characteristics of Acute Conditions⁶⁷

• Rapid onset
• Patients seek urgent care because they are in significant pain and may have difficulty eating or drinking.
• Pain or discomfort
• Tissue destruction +/- infection
• Often involves the death of tissue (necrosis).
• Patients usually seek urgent care (pain)
• Underlying Causes: These conditions usually occur because a patient is compromised; they do not typically arise from simple short-term neglect (e.g., missing one day of brushing).
• Recurrence: If the underlying cause is not addressed, the condition is likely to recur.

It is important to identify and eliminate predisposing factors to prevent recurrence.

Periodontal Treatment Planning⁸⁹

PERIODONTAL TREATMENT PLAN

EMERGENCIES PHASE OF PERIODONTAL TREATMENT Item Proposed Item Completed

RISK MANAGEMENT PHASE OF PERIODONTAL TREATMENT (step1) Item Proposed Item Completed

FUNDAMENTAL PHASE OF PERIODONTAL TREATMENT (step1&2) Item Proposed Item Completed

RE-EVALUATION PHASE OF PERIODONTAL TREATMENT (step3) Item Proposed Item Completed

CORRECTIVE PHASE OF PERIODONTAL TREATMENT (step3) Item Proposed Item Completed

MAINTENANCE PHASE (step4) Item Proposed Item Completed

PROPOSED MAINTENANCE INTERVAL

• 3 Months
• 6 Months
• 12 Months
• Other

Student Signature Tutor Signature

Periodontal Treatment Step

Step 0 PREREQUISITE TO THERAPY - Educate, classification, diagnosis, risk assess, care plan

Emergency Phase

Acute conditions fall into the “emergency” or “palliative” phase of the treatment plan (Step 0). Steps 1 and 2 of periodontal therapy can often be performed simultaneously with Step 0. Most conditions require biofilm removal and risk factor control.

Step 1 RISK - Risk factor control, OHI, adjuncts for GI, PMPR, supra-gingival scaling

Step 2 INTERVENE - Sub-gingival biofilm & calculus removal ± adjuncts

Step 3 CHECK - Non-responder sites: Re-RSD/surgery

Step 4 EXIT - plan longer-term care (above)

C Supportive care/rehabilitation

E

Necrotising Periodontal Diseases¹⁰¹¹

• NG and NP appear to be the same disease but at different stages.

Disease Progression

Necrotising diseases involve tissue death and are considered a progression of the same disease process. Unlike “garden variety” chronic gingivitis, necrotising gingivitis will usually progress to periodontitis if left untreated.

• Differentiated by:
  • Severity
  • Extent of tissue destruction

Glick et al 1994, Robinson et al 1998

NG, necrotizing gingivitis; NP, necrotizing periodontitis; NS, necrotizing stomatitis

^a^ Mean plasma and serum concentrations of retinol, total ascorbic acid, zinc, and albumin markedly reduced, or very marked depletion of plasma retinol, zinc, and ascorbate; and saliva levels of albumin and cortisol, as well as plasma cortisol concentrations, significantly increased

^b^ Living in substandard accommodations, exposure to debilitating childhood diseases, living near livestock, poor oral hygiene, limited access to potable water and poor sanitary disposal of human and animal fecal waste

^c^ Measles, herpes viruses (cytomegalovirus, Epstein-Barr virus-1, herpes simplex virus) chicken pox, malaria, febrile illness

Aetiology and Risk Factors

Aetiology¹²

• Opportunistic / dysbiotic microbiome in a susceptible host
• Fusiform bacteria, Prevotella intermedia, & spirochaetes
• Bacterial invasion of soft tissues occurs
• Intense release of cytokines and tissue destruction

Falkler et al 1987, Stevens et al 1984

Risk Factors¹³

• Poor oral hygiene
• Smoking
• Insufficient sleep & Psychological STRESS – inability to cope with stress
  • Exhaustion and being “run down” (e.g., end of semester)
• HIV +ve patients & Immunosuppressed patients
• Severe malnutrition
• Developed countries - Young people (15-34yrs)
• Developing countries - children

Epidemiology¹⁴

• Unclear, but low in developed countries
• Higher in developing countries - 5-25%
• Higher in children - 54-68% are children <10 yrs
• HIV +ve patients 2% (30% if not on HAART)
• Higher in military population
• High during WWI & WWII
  • Historically known as “Trench Mouth” due to high prevalence in military populations during WWI and WWII (linked to stress, smoking, and poor hygiene)

Necrotising Gingivitis Clinical Features¹⁵¹⁶

• Sudden Onset - Rapid development and painful, more common to affect anterior teeth
• Starts with ulceration of interdental papilla, leading to papillary necrosis
• “Punched out” papillae appearance
  • Papillae may appear brown or “mushy”
• Fibrinous pseudomembrane
• +/- Fever, lymphadenopathy, malaise
• No bone loss
• Bleeding
• Malodour

Fig. 19-9 Healing of necrotizing gingivitis lesions in the upper anterior sextant. (a) Active lesions with necrosis the interdental papillae. (b) Complete resolution after 60 days.

(Source: Courtesy of Dr. Nidia Castro dos Santos and Dr. Mauro Santamaria.)

Essential clinical features¹⁷

• Lesions are painful
• Lesions are gingival ulcers, punched-out crater-like affecting the interdental papilla and may involve marginal gingiva
• Gingival ulcers bleed spontaneously or readily
• The acute condition may occur from an existing chronic gingival condition or de novo

Non-essential clinical features

• “Pseudomembrane” of sloughed necrotic debris & bacteria covering the ulcerated area
• Bad breath
  • Pungent, “metallic” smell
• Fever, malaise
• Lymphadenopathy – (submandibular & cervical)

Necrotising Periodontitis Clinical Features¹⁸¹⁹²⁰

• Lesions extend into alveolar bone
• Exposed bone, gingival recession, tooth mobility
• Malodour, lymphadenopathy, fever and malaise
• Severe pain and spontaneous bleeding
• Exfoliation of teeth within months of onset of NP
  • Rapid destruction of the alveolar bone
  • Visible bone fragments (sequestra)
  • Teeth may become loose and “drop out” within months if untreated

Fig. 19-8 Necrotizing periodontitis: presence of necrosis/ulcer of the interdental papillae.

(Source: Courtesy of Dr. Mauro Santamaria.)

Management of Necrotising Periodontal Diseases^21222324

• Needs urgent treatment

• Disease can progress rapidly (necrotic bone & soft tissue)

• If left untreated: NG → NP

• Gentle debridement with ultrasonic (with LA) to remove slough, plaque & necrotic tissues, saline irrigation

• Rx metronidazole 400mg 12-hourly for 3-5 days, pain management, OHI (gentle)

• Mouthwash for 2-3 weeks, 2 x daily for 1 min

  • CHX 0.2%
  • OR
  • H2O2 1.5%

• Stop smoking!

• Review 2-3 days later - further Rx may be needed

Robinson et al 1998

Access by University of Western Australia (CAUL) Therapeutic Guidelines > Oral and Dental > Necrotising periodontal disease

Necrotising periodontal disease

metronidazole 400 mg orally, 12-hourly for 3 to 5 days.

Metronidazole Contraindications

• Allergy
• First trimester of pregnancy
• Alcohol consumption (causes severe vomiting)
• Potential interaction with Warfarin

If pain and inflammation restrict oral hygiene practices, recommend short-term use of a mouthwash to reduce plaque formation; use:

1. hydrogen peroxide 3% solution 5 mL, mixed with 5 mL of warm water, rinsed in the mouth for 1 minute then spat out, 12-hourly until pain has reduced OR
2. hydrogen peroxide 1.5% solution 10 mL, rinsed in the mouth for 1 minute then spat out, 12-hourly until pain has reduced OR
3. chlorhexidine 0.2% mouthwash 10 mL rinsed in the mouth for 1 minute then spat out, 8- to 12-hourly until pain has reduced [Note 1] OR
4. chlorhexidine 0.12% mouthwash 15 mL rinsed in the mouth for 1 minute then spat out, 8- to 12-hourly until pain has reduced [Note 1]

Response to treatment is diagnostic

At 1-2 week review:

• Subgingival debridement if necessary (earlier may hinder regenerative potential of tissues) and treat chronic disease if present

• Reinforce oral hygiene

• Review again - maintenance or needs surgery?

• Failure to resolve may be due to incomplete debridement/ stress/ malnutrition/ smoking/ immunological conditions

• Regimen shown to have 94% resolution within 1 week & 100% within 1 month

• If not resolved, you need to rule other non-infective conditions that resemble NG, e.g. desquamative gingivitis

Robinson et al 1998

Longer term management^2526272829

• Review at 1 month
• If resolved, place on 3/12 maintenance, (may need periodontal surgery if deformities present)
• If no resolution, refer to periodontist or oral medicine specialist, (blood test, microbiological sample & biopsy -> histopathology investigations)
• Up to 30% of patients will experience recurrence within 2 years
• Maintenance of meticulous OH and scaling/debridement

Image courtesy of Dr Anna Hughes

IPD-P03848 Eng-Patent (27)

Viral Lesions

Acute Herpetic Gingivostomatitis³⁰³¹³²

• Herpes Simplex virus

• 70-80% of population exposed

• Less in developed countries

• Young adults & children

• Affects whole mouth & gingiva

• 1-2mm blisters that rupture to form small, shallow, painful & irregular ulcers, 7-10 days

• Ulcers covered by a yellowish-gray center & surrounded by a red halo

• Ulcers may take up to 2 weeks to heal

• Heal with no scarring

• Rare to get gingival recession

• Sore to touch, food & drinks

• Worse with salty, acidic, hard foods

• Fever & malaise

• Ddx recurrent apthous ulcers?

  • These are not seen on keratinised tissues

Table 4. Differences in clinical features of necrotizing ulcerative gingivitis (NUG) and acute herpetic gingivostomatitis (AHG)

Site of ulcers NUG: Interdental papilla, Marginal gingival AHG: Gingiva, no predilection for interdental papilla; Entire oral mucosa

Character of ulcers NUG: Punched-out, crater-like; Covered by yellow/white/gray slough; Bleed readily or spontaneously; Painful on stimulation AHG: Multiple vesicles that coalesce and form shallow, fibrin-covered, regular-shaped ulcers; No marked tendency to bleed; Not specially tender

Fever NUG: Doubtful or slight only AHG: 38 °C (or more)

Symptoms NUG: Painful gums, ‘dead-feeling teeth’ AHG: Sore mouth

Duration of ulcers and discomfort NUG: Short-lived (1–3 days), with appropriate therapy AHG: More than 1 week, even with therapy

Management³³

• Pain relief: analgesics & topical anaesthetics rinses
• Advice to have adequate fluid intake & food
• Use of antiviral medication questioned: ACYCLOVIR, only if started immediately
• Systemic Acyclovir can be prescribed if started within the first 5 days.
• Inform - AHG is CONTAGIOUS!
• Dental treatment should be deferred to prevent self-inoculation, such as herpetic whitlow on fingers or ocular herpes in the eyes.
• Review in 2wks to confirm correct diagnosis
• Recurrence can occur - dental tx, stress, fever, trauma

Reactivation of Viruses³⁴

Herpes simplex virus Cold sores Varicella Zoster Shingles (from chicken pox)

Varicella Zoster Presentation

Reactivation of the chickenpox virus presents along dermatomes (nerve pathways) and is extremely painful. In the mouth, it may stop exactly at the midline of the palate.

Fig. 20.4 Herpetic vesicles recurred in the lip. (A) Early stage. (B) Late stage, showing brownish, crusted lesions. (From Sapp JP, Eversole LR, Wysocki GP. Contemporary oral and maxillofacial pathology. ed2, St Louis, 2002, Mosby.)

Fig. 20.5 Recurrent intraoral herpetetic vesicles are seen (A) in the palate and (B) in the gingiva. The latter location is rare. (From Sapp JP, Eversole LR, Wysocki GP. Contemporary oral and maxillofacial pathology, ed 2, St Louis, 2002, Mosby.)

Abscesses of the Periodontium³⁵

Definition

An abscess is a localized collection of pus (purulent exudate) involving a massive inflammatory response.

Classification of Abscesses³⁶³⁷

Classified based on aetiology

Periodontal abscess in periodontitis patients (in a pre-existing periodontal pocket)

• Acute exacerbation
  • Untreated periodontitis
  • Non-responsive to therapy periodontitis
  • Supportive periodontal therapy
• After treatment
  • Post-scaling
  • Post-surgery
  • Post-medication
    • Systemic antimicrobials
    • Other drugs: nifedipine

Periodontal abscess in non-periodontitis patients (not mandatory to have a pre-existing periodontal pocket)

• Impaction

  • Dental floss, orthodontic elastic, toothpick, rubber dam, or popcorn hulls

• Harmful habits

  • Wire or nail biting and clenching

• Orthodontic factors

  • Orthodontic forces or a cross-bite

• Gingival overgrowth

• Alteration of root surface

  • Severe anatomic alterations
    • Invaginated tooth, dens evaginatus or odontodysplasia
  • Minor anatomic alterations
    • Cemental tears, enamel pearls or developmental grooves
  • Iatrogenic conditions
    • Perforations
  • Severe root damage
    • Fissure or fracture, cracked tooth syndrome
  • External root resorption

• Pericoronal Abscess (Pericoronitis)

• Gingival Abscess

• Periodontal Abscess

  • Combined perio-endo abscess
  • Other acute abscesses

Pericoronitis^38394041

• Easy to diagnose as can see partially erupted tooth with inflamed gum flap
• Gingiva in 3rd molar area appear red & swollen, infection may be due to biofilm, trauma, food debris
• Location: Inflammation/infection of the operculum (gum flap) over a partially erupted tooth
• Danger: Can lead to difficulty swallowing or breathing, which requires immediate hospital referral
• Infection may spread posteriorly into the oropharyngeal area and medially to the base of the tongue and involve the regional lymph nodes, may have difficulty swallowing
• Patients may have a history of pericoronitis
• Gram-negative anaerobic pathogens

Management⁴²

• Acute phase and initial Treatment:
  • debride & irrigate under the pericoronal flap
• Rx. Antibiotics if systemic involvement (fever, lymphadenopathy), warm salt water mouthwash
• Manage underlying condition:
  • operculectomy
  • distal debridement
  • extract third molar(s)

Gingival Abscess⁴³⁴⁴

• Localised purulent infection - smooth, red, painful swelling
• Confined to marginal gingival tissue, often at previously non-diseased sites
• Usually an acute inflammatory response (1-2 days) to plaque, trauma or foreign substances forced into the gingiva (Piksters, dental floss, food)
• Etiology: Often caused by a local injury or foreign body, such as a popcorn husk, stuck in the gingiva
• If left untreated, lesion may ruptre spontaneously
• Diagnosis - find & retrieve the offending foreign material if applicable
• Treatment: debride & irrigate pocket

Periodontal Abscess^45464748

• 3rd most common emergency in general practice (UK data)

• 8-14% of all dental emergencies

• More common in patients with untreated gum disease (60%) vs patients undergoing active periodontal treatment (13.5%)

• Patients in maintenance – 38% (5-29yrs follow up)

• Usually around molars & lower incisors

• Rapid destruction of periodontal tissues, with a negative effect on the prognosis of the affected tooth. Bacterial invasion of soft tissues ulceration of the PE occurs.

• May lead to tooth loss

• During SPT, main reason for tooth extraction

• Teeth with repeated abscess formation – prognosis considered “hopeless”

• Severe systemic consequences can occur

Herrara et al 2018

Aetiology and Microbiology

why?

• Untreated periodontitis
• Poor access/residual calculus - anatomical difficulties in furcations, vertical defects, root concavities
• Non-inflammatory - root fractures/perforations
• Systemic antimicrobial intake, without subgingival debridement
• Poorly controlled diabetics - higher risk
• Triggered by “superficial healing” where the pocket margin tightens after a quick scale, trapping bacteria at the base

Microbial composition similar to periodontitis

Most prevalent bacterial species were Porphyromonas gingivalis (50-100%), Prevotella intermedia, Prevotella melaninogenica, Fusobacterium nucleatum, Tannerella forsythia, Treponema species, Campylobacter species, Capnocytophaga species, Aggregatibacter actinomycetemcomitans or gram-negative enteric rods

Herrara et al 2018

Clinical Presentation and Diagnosis⁴⁹⁵⁰

• Confined to marginal gingival tissue

• Ovoid swelling in gum

• Gingiva is oedematous & red, with a smooth, shiny surface

• Very common - Pus may be expressed from the gingival margin by gentle digital pressure, or by probing

• Uncommon - Fistula

• Symptoms vary from a slight discomfort, tender gums, to severe pain & swelling, or tooth “elevation”

• The tooth may feel “high” or “popped up” in the socket

• Increased tooth mobility, TTP or soreness with chewing

• Extra-oral uncommon – swollen face (3.6%)

• Lymphadenopathy, fever & malaise (7-40%)

Periodontal abscess diagnosis

• Deep probing depths >5mm (7-9mm on average)

• Positive response to pulp vitality test

  • The tooth is usually vital (responds to cold tests), which differentiates it from an endodontic abscess

• Radiographs – no apical radiolucency or endodontic lesion, but bone loss observed

• Can occur in patients undergoing perio tx, during maintenance, or untreated perio patients

• Usually in patients with a history of periodontitis & smokers

• May occur post scaling due to remaining subgingival calculus on root surface - deep periodontal pockets, furcations, & intrabony defects

• May occur when antibiotics Rx without debridement in patients with periodontal disease

Management and Complications⁵¹

management

• Drain abscess by debriding through the pocket or an incision & removing plaque, calculus, & other irritants
• Occlusal adjustment
  • Necessary if the tooth is elevated and causing pain on biting
• CHX mouthwash
• Rx. Analgesics
• Resolution 2-7 days
• Recurring abscess – surgery to access site to find other cause for abscess

management

Rarely needed! Only if spreading locally + mild systemic involvement

• Phenoxymethylpenicillin 500mg x4 daily for 5 days or Amoxycillin 500mg tds for 5 days (plus metronidazole 400mg bds 5 days) TG
• PENICILLIN ALLERGY: CLINDAMYCIN 300mg tds for 5 days
• If severe systemic + spreading - immediate referral to a hospital!!

without treatment…

• Tooth loss
• Spread of infection to other parts of the body – bacteraemia, lung infection, brain abscess
• Life-threatening systemic spread such as cellulitis

Differential Diagnosis and Other Conditions⁵²

Differentiation of Necrotizing Ulcerative Gingivitis, Chronic Desquamative Gingivitis, and Chronic Periodontal Disease

Necrotizing Ulcerative Gingivitis	Desquamative Gingivitis	Chronic Destructive Periodontal Disease
Bacterial smears show fusospirochetal complex	Bacterial smears reveal numerous epithelial cells and few bacterial forms	Bacterial smears vary
Marginal gingiva affected	Diffuse involvement of marginal and attached gingivae and other areas of oral mucosa	Marginal gingiva affected
Acute history	Chronic history	Chronic history
Painful	May or may not be painful	Painless if uncomplicated
Pseudomembrane	Patchy desquamation of gingival epithelium	Usually no desquamation, but purulent material may appear from pockets
Papillary and marginal necrotic lesions	Papillae do not undergo necrosis	Papillae do not undergo noticeable necrosis
Affects adults of both genders and occasionally affects children	Affects adults, most often women	Usually found in adults, occasionally found in children
Characteristic fetid odor	No odor	Some odor but not strikingly fetid

Less Common Acute Conditions^53545556

**Acute Candida infection in a cancer patient receiving chemotherapy

• Fungal infection, often seen in immunocompromised patients (e.g., those on chemotherapy).
• Neoplasia: Oral cancers can sometimes mimic the appearance of an abscess or pericoronitis.**

Desquamative gingivitis in a patient with auto-immune disease⁵⁷

• Characterized by the sloughing off of squamous cells.
• The gingiva appears severely ulcerated and “nasty,” often linked to systemic autoimmune conditions. Allergic reactions
• Can cause acute gingival swelling.

References and Further Reading⁵⁸⁵⁹

Chapter 14 Non-Plaque-Induced Gingival Diseases Palle Holmstrup¹ and Mats Jontell² ¹ Department of Periodontology, School of Dentistry, University of Copenhagen, Copenhagen, Denmark ² Oral Medicine and Pathology, Institute of Odontology, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden

Chapter 19 Abscesses, Necrotizing Lesions of the Periodontium, and Endo-Periodontal Lesions David Herrera¹ and Magda Feres² ¹ ETEP (Etiology and Therapy of Periodontal and Peri-Implant Diseases) Research Group, Complutense University of Madrid, Madrid, Spain ² Department of Periodontology, Dental Research Division, Guarulhos University, Guarulhos, São Paulo, Brazil and The Forsyth Institute, Cambridge, MA, USA

The University of Western Australia

Questions?

emma.perry@uwa.edu.au

Images in presentation not otherwise credited are licence-free from https://www.freepik.com/

Recommended Resources

• Therapeutic Guidelines: The primary resource for evidence-based prescribing (accessible on clinic computers).
• eMIMS: Used to check drug formulations and packaging sizes.
• Textbook: Refer to the specific chapter on acute periodontal conditions for further detail.

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Audio Appendix

Additional Audio Content

The following sections from the lecture audio did not correspond to any heading in the main document.

Case Study: 18-Month-Old Baby

An 18-month-old baby presented with constant screaming and refusal to eat. The mother had a healing cold sore. The baby was diagnosed with acute herpetic gingivostomatitis after contracting the virus from the mother.

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Case Study: Young Male Smoker

The lecturer observed a case of necrotising gingivitis in a young male patient who was “partying a lot” and smoking heavily. The diagnosis was tipped off by the classic “punched-out” appearance of the papilla and the patient’s heavy smoking habit.

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