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#Periodontology

Acute Periodontal Conditions

American academy of periodontology classification

3 common features

• rapid onset
• rapid tissue destruction
• acute pain or discomfort

Necrotising Ging, Perio and Stomatitis

Necrotising periodontal disease

• 
• diagnosed under many names for over 100 years
  • vincents disease, trench mouth, ANUG etc.
  • nectrotising periodontal diseases (AAP 1999)
• latest classification (Herrera et al 2017)
  • necrotising gingivitis -> marginal gingiva
  • necrotising periodontitis -> loss of attachment
  • necrotising stomatitis -> beyond mucogingival junction
  • cancrum oris / noma -> facial tissues
  • 
• 3 common typical features
  • necrosis of papilla
  • bleeding
  • sudden onset of pain
• pathogenesis
  • opportunistic infection of commensal bacteria within plaque coinciding with a temporary suppression in host immunity

Necrotising gingivitis

• clinical features
  • pain, especially on probing
  • gingival ulcers
  • punched out craters of papillae
  • may involve marginal gingiva
  • anterior mandible most common
  • spontaneous or readily bleed
• secondary features
  • halitosis
  • whitish/yellow pseudomembrane
  • lymphadenopathy
  • fever, malaise
  • sialorrhea (excessive salivation) in children
  • 
• typically due to specific bacteria
  • spirochaetes e.g. treponema spp, fusobacterium spp, prevotella intermedia (orange complex)
• 

Necrotising periodontitis clinical features

• loss of attachment
  • rarely deep pocketing as gingival necrosis accompanies bone loss
• deep interproximal craters divide papilla into facial and lingual
  • denudation of interdental alveolar bone
• sequestration of necrotic alveolar bone
• 

Necrotising Periodontal Disease

• local factors
  • poor OH
  • plaque retentive factors
  • pre existing gingivitis
  • history of NPD
• systemic factors
  • immunocompromised host (e.g. HIV)
  • stress
  • poor nutrition
  • smoking
  • alcohol
  • young age
• 
• acute phase treatment
  • pain relief and prevent disease progression
  • gentle debridement under LA
  • 3% H2O2 recommended by Robinson 2002
  • CHX rinse, care with mechanical OH, remove plaque but no further trauma to soft tissues
  • metronidazole 400mg bid 5 days + analgesia
  • prevent dehydration
• subsequent maintenance phase
  • treat pre existing periodontal disease
  • corrective therapy of gingival craters
  • HIV status if undiagnosed
  • address underlying cause of immunosuppression: i.e. stress, sleep nutrition, smoking, systemic health. for Necrotising perio: HIV, organ transplant, chemo etc.
  • early review
• 
• 

Necrotising stomatitis

• necrosis extending past perio into alveolar mucosa
• can present without prior NG/NP
• severely immunocompromised
• bone sequestra, large areas of osteitis (inflammation of the bone)
• becomes a noma if perforates cheek

differential diagnoses

• vesicullobullous disease (lichen planus, pemphigus, pemphigoid)
• herpetic gingivostomatitis
• toothbrush abrasion

Herpetic Gingivostomatitis

Disease

• etiology
• epidemiology
• clinical signs
• pathophysiology
• management

Herpetic gingivostomatitis (HGS)

• aetiology
  • initial exposure and systemic infection with herpes simplex virus (HSV)
• epidemiology
  • most frequent in infants, febrile illness with intraoral sequelae
  • most primary HSV are asymptomatic, HGS is most common manifestation and seen in 15-30% of cases
• clinical signs
  • one or two ulcerations +- widespread intraoral vesicles and ulceration
  • sudden onset
  • high fever, cervical lymphadenopathy
  • sore throat and mouth, fiery red gingiva
  • intra-epithelial vesicles can form within 24h of infection, typically tongue buccal mucosa palate and gingiva
    • vesicles rupture early to give numerous small round/irregular superficial greyish yellow ulcers with red halo
  • lesions take 10-14 days to heal (sometimes up to 21)
  • highly contagious (occurs 1 week after contact)
  • 
  • 
  • 
• pathophysiology
• management
  • supportive/ palliative care (soft diet, fluids, rest, analgesia, topical anaesthesia)
  • chlorhexidine rinse
  • antiviral agent
    • if immunocompromised child, IV acyclovir 10mg/kg 8 hourly until there are no new lesions
    • if immunocompetent but severe pain/dehydration within 72h onset of disease, acyclovir 10mg/kg (max 400mg) oral 5 per day until no new lesions
  • children who do not have control of oral secretions, should be excluded from childcare/school until sores have dried
• differential
  • Hand food mouth
  • herpangina
  • RAS
  • SJS
  • behcet

Reactivation of HSV

• primary illness leadss to infection of trigeminal ganglion
• can reactive as herpes labials (cold sore)
• herpetic ulceration
  • intraoral reactivation may occur following trauma e.g. surgery or local anaesthesia (palatal infil)
  • reactivated intraoral lesions, multiple clusters of small punctate ulcers
• 
• reportedly associated with COVID19 infection causing immunosuppression and respiratory distress

Periodontal Abscesses

• acute lesions characterised by localised accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination
• results in significant tissue destruction
• primary signs/symptoms
  • ovoid elevation in gingiva along lateral root
  • BOP, deep periodontal pocket, suppuration on probing (pocket or fistula)
  • Pain, swelling, redness
  • tooth feels higher than usual when biting (PDL is inflamed)
  • increase mobility
  • lymphadenopathy (10% of cases)
  • usually vital tooth but can be nonvital
  • radiology might not reveal anything
  • can cause rapid severe bone loss
• previously classified by location
  • gingival (foreign body in gingiva or sulcus)
  • periodontal (infection adjacent to pocket)
  • pericoronal (partially erupted tooth)
  • 
• 2017 classification (Herrera et al., 2017)
  • 
• **Etiology
  • in perio patients
    • represents period of disease exacerbation
    • presence of torturous pockets, furcation involvement, vertical defect
    • marginal closure of pocket - lack of coronal damage (leaving apical calculus but cleaning more coronally so gingiva heals and seals over the calculus)
    • changes in subgingival microbial composition
    • decrease in host defence
  • non perio patients
    • previously healthy site
    • foreign body (floss, fingernail, food particle, popcorn kernel)
    • harmful habit
    • ortho factors
    • alterations to root surface
  • can occur directly after debridement, due to dislodgement of calculus fragment into gingival wall
• epidemiology
  • 3rd most frequent reported dental emergency
  • most occur in perio patients
  • 60% untreated
  • 14% active treatment
  • 37% maintenance phase
  • 
    
    
    

Pathogenesis

• exact is unclear
• majority of abscesses occur in pre existing perio pockets
• inflamed pockets normally drain continuously
• occlusion of pocket prevents dranage
  • supragingival S/C
  • incomplete removal of calculus
  • altered root morphology (invaginations, furcations, ERR, cemental tears, endo perforations)
• bacteria remain at base of pocket
  • AB resistant strains (Topoll et al 1990)
  • Inflammatory infiltrate destroys pocket wall + CT

Histopathology

• DeWitt et al 1985
• 
• bacterial invasion of soft tissues surrounding the periodontal pocket
• attraction of inflammatory cells and products eg cytokines
• leads to destruction of connective tissues, encapsulation of bacterial infection and production of pus
• outside -> inside
  • normal oral epithelium and lamina propria
  • acute inflammatory infiltrate
  • intense focus of inflammation
  • presence of neutrophils and lymphocytes in an area of destroyed and necrotic connective tissue
  • destroyed and ulcerated pocket epithelium
• 

Microbiology

• no different to untreated chronic periodontitis
• non motile, gram -ve, strict anaerobic rods
  • Porphyromanas gingivalis 50-100%
  • Prevotella intermedia,
  • Prevotella melaninogenica
  • Fusobacterium nucleatum
  • Tannerella forsythia
  • Treponema species
  • Campylobacter species
  • Capnocytophaga species
  • Aggregatibacter actinomycetemcomitans
  • or gram‐negative enteric rods
• 

Acute Management

• drain abscess
• SRD
• +- occlusal adjustment
• Systemic antibiotics if signs of fever malaise
  • can be controversial
  • Antibiotics on their own to resolve acute symptoms first (Herrera et al 2000)
    • poorly localised infection or cant establish drainage
  • Antibiotics + supragingival scaling to avoid soft tissue trauma (Hafstrom et al 1994)
  • metronidazole best profile (400mg BID 3-5 days, 6-10 tabs) NEVER MIX WITH ALCOHOL OR YOUR STOMACH WILL BE VERY SORE
  • Azithromycin/amoxicillin work aswell
    • Amoxicillin 500mg orally, tid for 3-5 days
  • only for duration of acute phase
  • still need mechanical debridement
• Extraction if hopeless
• mouthwash to reduce plaque formation short term
  • hydrogen peroxide 3% 5ml mixed with 5ml water or 1.5% 10ml, rinse in mouth for 1 minute, then spit out, twice a day
  • chlorhexidine 0.2% mouthwash 10ml or 0.12% mouthwash 15ml rinse in mouth for 1 minute then spit out, 2-3 times a day
• follow up 24-48 hours

Differential

• other acute periodontal lesions
• periapical abscess
• root fracture
• pericoronitis
• lateral periodontal cysts
• perio as a manifestation of systemic disease
• postop infection
• self inflicted gingival injuries
• neoplasms

Endo-periodontal lesions

EPL

• clinical conditions involving both pulp and periodontal tissues and may occur in acute and chronic forms (Herrera et al 2017)

Anatomical pathways

• apical foramen
• dentinal tubules - patent through no overlying cementum
• lateral canals, accessory canals
• developmental defects
• cracks or resorptive lesions
• DeDeus 1975
  • 1140 adult human teeth studied, 313 had lateral, secondary and accessory canals
  • molar and premolar mostly, incisor least ramifications
  • majority apical

Signs and symptoms

• deep periodontal pocket reaching or close to tooth apex
• negative or altered response to pulp vitality tests
• bone resorption in apical or furcation region
• spontaneous pain or pain on palpation and percussion
• purulent exudate
• tooth mobility
• sinus tract
• tooth and/or gingival colour alterations

Aetiology

• endodontic and or periodontal infections
• carious lesions that affects the pulp and secondarily affects the periodontium
  • 1st endo -> 2nd perio
• periodontal destruction that secondarily affects root canal
  • 1st perio -> 2nd endo
• or both eveny concomitantly
  • 1st endo and 1st perio (simultaneous but separate)
  • "true combined" simultaneous and connected
• trauma and or inatrogenic factors
  • perforations
  • root fracture
  • resorption

effect of endodontic pathology on the periodontium

• pathways of communication, apical foramen
• infected pulp leads to inflammatory response in PDL at apical foramen or small portals of exit
• inflammatory by-products permeate through apex or through smaller canals in apical third of the root canal system and exposed dentinal tubules
• can trigger an inflammatory vascular response in periodontium
• inflammatory by-products include living and non living pathogens

effect of periodontal disease on dental pulp

• conflicting evidence
• proposed that periodontal disease may have no effect on pulp until it involves apex
• other evidence suggest effect on pulp is degenerative including increase in calcification, fibrosis and collagen resorption, as well as direct inflammatory effect
• Czarneck and Schilder 1979
  • perio vs healthy teeth
  • histological study
  • pulps were all histologically within normal limits
• Bergenholtz and Lindhe 1978
  • 57% of teeth had mild pulp alterations
  • secondary dentine formation +- inflammatory cell infiltrates
  • SRD teeth, no increased incidence of pathologic pulp reaction
• Conclusion
  • unless perio extends to root apex, pulp capable of surviving significant injury

Historical classification

• simon 1972, Garguilo 1984
• primary endo
  • chronic apical lesion with necrotic pulp
• primary endo secondary perio
  • secondary involvement of periodontal breakdown due to plaque accumulation at gingival margin of sinus tract
• primary perio
  • pulp test indicates clinically normal pulpal reaction
• primary perio secondary endo
  • apical progression of periodontal pocket to invovle apical tissue
  • infection enters pulp through lateral canals and apical foramen
• true combined
  • endo lesion progression coronally joins with a periodontal pocket progressing apically
  • least common, poor prognosis
  • VRF may appear radio and clinically very similar, can be considered a true combined lesion
• 

Diagnosis

• pt histiroy
  • truma/iatrogenic factors
• radio and clinical
• FM perio assess
  • PPD
  • CAL
  • BOP/SOP
  • mobility
  • vitality/percussion
• endo perio lesions
  • presence of perio pocket reaching close to apex combined with negative pulp vitality
• 
• 

Prognosis

• hopeless, poor, favourable
• prognosticating factors:
  • extent of perio destruction
  • presence/severity of periodontal disease affecting patients overall oral health

Root fractures

• cementum dentine pulp
• horizontal or transverse
• VRF
  • longitudinal or transverse
  • originate in crown or root
  • common in RCT teeth
  • clinically deep narrow periodontal pocket
  • mild discomfort on function
  • radiographic image varies, might be missed
• Siskin 1980 VRF
  • N = 32
  • 84% occurred during lateral condensation of gutta perfcha
  • clinical signs
    • 30/32 Deep narrow probing depths
    • 9/32 recurrent periodontal abscesses
    • 21/32 mild discomfort,
    • 2/32 severe pain
    • Radiographic signs 75% - diffuse widening of PDL
  • treatment
    • 21/32 required extraction
    • 5/32 root amputation
    • 4/32 ARF and osseous recontouring to expose fracture
• 

Root perforations

• may manifest as inflammatory lesions in marginal periodontium
• Alhadainy 1994, causes or perfs
  • mainly iatrogenic
  • straightening of endo fil in curved canal
  • lessened with NiTi files
  • strip perforation, removal of dentine from danger zone within furcal area of coronal third
  • midroot
  • transporation or zip perforation, excessive cutting of outer dentinal wal lcompared to inner dentinal wall
• clinical signs
  • increased PPD
  • suppuration
  • increased tooth mobility
  • periodontal abscesses
• symptoms
  • sudden pain during endodontic treatment
  • taste of irrigant during treatment
• diagnosis
  • loos fit endo file
  • bleeding into canal
  • radiograph with endo file in situ
  • prognosis
  • coronal poorer, proximity to oral environment
  • time lapsed before correction
• treatment
  • nonsurgical
    • MTA with CaOH2
    • resto material to seal perforation
  • surgical
    • flap reflection to expose perforation
    • sealing with appropriate restorative material

Root resorption

• physiologic or pathologic process resulting in loss of dentine cementum bone
• external root resorption (initiated in periodontium)
  • progressive inflammatory (stimuli from pulpal infection and sulcular infection)
  • Invase cervical resorption (non inflammatory)
  • replacement resorption (non inflammatory)
    • occurs following extensive necrosis of PDL with formation of bone onto denuded area of root surface
    • complication of luxation injuries, especially in avulsed teeth
  • internal root resorption
    • chronic pulpal inflammation associated with an infected coronal pulp space
    • multinucleated giant cell activity
• Heithersay 1999
  • cervical root resorption
  • cervical location, invasive nature
  • pink discolouration of tooth crown
  • surface irregularity might be probed, filled with vascular soft tissue
  • pulp typically protected by a thin layer of predentine and dentine
    • invaded at a late stage of process
    • remains asymptomatic
    • vital pulp
  • fibrous tissue, numerous blood vessels and mononuclear clastic resorbing cells adjacent to the dentine surface
• Frank 1987
  • case report seriers
  • described treatment protocol
  • confirm pulp vitality
  • raise fla pto expose margins of defect
  • spoon excavate fibrous tissue from lesion
  • place hard setting CaOH
  • restore with appropriate material
  • suture flaps to desirable height to facilitate oral hygiene

Pericoronitis

pericoronitis

• localised suppurative infection within the tissue surrounding the crown of a partially erupted tooth
• most commonly lower wisdom teeth retromolar pad angle of mandible
• associated with pain swelling trismus, occasional fever
• management
  • exo
  • operculectomy
  • debridement and irrigation under la
  • antibiotics if systemic signs of infection present
  • review to ensure resolution of symptoms
• 
•