Orbital Cellulitis Diagnosis and Management

Orbit anatomy
Bones which make the orbit
Frontal
Zygoma
Maxillary
Nasal
Ethmoid
Lacrimal
Sphenoid

Orbital Cellulitis

Orbital cellulitis is a dangerous infection with potentially serious complications

It is usually caused by a bacterial infection from the sinuses (mainly ethmoid, accounting for more than 90% of all cases)

Other causes :a stye on the eyelid, recent trauma to the eyelid including bug bites, or a foreign object

Children

• In children, orbital cellulitis is usually from a sinus infection and due to the organism Hemophilus influenzae (decrease in incidence after vaccination program implentation). 
• Other organisms are Staphlococcus aureus, Streptococcus pneumoniae, and Beta hemolytic streptococci

Pathophysiology

• Extension of infection from the periorbital structures, most commonly from the paranasal sinuses, but also from the face, globe, and lacrimal sac
• Direct inoculation of the orbit from trauma or surgery (orbital decompression, dacryocystorhinostomy, eyelid surgery, strabismus surgery, retinal surgery, and intraocular surgery, have been reported as the precipitating cause of orbital cellulitis)
• Hematogenous spread from bacteremia

Orbital septum

• The orbit is separated from the soft tissue of the eyelid by the orbital septum. This is a fascial plane that is continuous with the periosteum of the facial bones.
• The orbital septum inserts into the tarsal plate of the upper and lower eyelids.
• The orbital septum usually proves to be an effective barrier that prevents the spread of infection from the eyelids posteriorly to the orbit.
• While preseptal cellulitis can occasionally spread to the orbital contents, it is generally a clinical entity that is distinct from orbital cellulitis

Orbital vs. Preseptal Cellulitis

• Orbital cellulitis is infection of the soft tissues of the orbit posterior to the orbital septum, differentiating it from preseptal cellulitis, which is infection of the soft tissue of the eyelids and periocular region anterior to the orbital septum
• Differential Diagnosis: orbital pseudotumor (inflammatory condition, responds to steroids)

Chandler Classification

• Stage I-Inflammatory edema-Preseptal
• Stage II-Orbital cellulitis  - Postseptal
• Stage III-Subperiostal abscess
• Stage IV-Orbital abscess
• Stage V-Complication due to posterior extension

Symptoms

• Fever, generally 102 degrees F or greater.
• Painful swelling of upper and lower lids (upper is usually greater).
• Eyelid appears shiny and is red or purple in color.
• Infant or child is acutely ill or toxic.
• Eye pain especially with movement.
• Decreased vision (because the lid is swollen over the eye).
• Eye bulging (forward displacement of the eye).
• Swelling of the eyelids
• General malaise.
• Restricted or painful eye movements

Complications

• Subperiostal/Orbital abscess (Chandler III-IV)
• Cavernous sinus thrombosis
• Hearing loss
• Septicemia or blood infection 
• Meningitis
• Optic nerve damage and blindeness

A male with orbital cellulitis with proptosis, ophthalmoplegia, and edema and erythema of the eyelids

Non-surgical treatment

• IV ABx
• Antifungals (if indicated)
• Nasal decongestants (open sinus ostia)
• Duretics – DIAMOX (carbonic anhydrase inhibitor), mannitol  (reduce IOP)

Surgical Treatment

• Surgical drainage if the response to appropriate antibiotic therapy is poor within 48-72 hours or if the CT scan shows the sinuses to be completely opacified.
• Consider orbital surgery, with or without sinusotomy, in every case of subperiosteal or intraorbital abscess formation.
• Surgical drainage of an orbital abscess is indicated if any of the following occurs:  decrease in vision, An afferent pupillary defect. proptosis progresses despite appropriate antibiotic therapy
• The size of the abscess does not reduce on CT scan within 48-72 hours after appropriate antibiotics have been administered.
• If brain abscesses develop and do not respond to antibiotic therapy, craniotomy is indicated.

How?

1. Superior orbit decompression   
2. Medial orbit decompression
3. Inferior orbit decompression
4. Lateral orbit decompression
5. Intranasal approach

Superior Orbit Decompression

• Frontal cranioitomy – unroofing of superior wall of orbit
• Titanium sheild placed to support the frontal lobe of the brain
• High morbidity, consider only for severe cases
• Medial Orbit Decompression
• External ethmoidectomy incision  or coronal forehead approach
• External ethmoidectomy- complete ethmoid sinus resection, then orbital fat herniates into sinus defect
• Coronal incision- ethmoidectomy via a superior approach, more risk for lacrimal sac and trochlea injury  

  

Inferior Orbit Decompression

• Orbital floor blow-out fracture , but spares infraorbital nerve
• Subcilliary eyelid incision or Caldwell-Luc incision
• Combined approach?
• Intraorbital fat herniates maxillary sinus

Lateral Orbit Decompression

• Lateral canthotomy
• Removal of lateral orbital bone posterior to the rim
• Orbital fat protrudes the newly created space
• An incision extending from the lateral canthus to the area just below the inferior punctum is created 4 mm to 5 mm below the lower border of the tarsal plate to avoid injury to the septum and the canaliculus

Intranasal approach

• Decompression of medial anf medioinferior floors of orbit
• Endoscopic sinus surgery technique
• Anterior Ethmoidectomy
• Maxillary antrostomy

Oral medicine-Aphthous and other common ulcers-Diagnosis and Management

Ulceration
Ulceration  is  a  breach  in  the  oral  epithelium,  which  typically  exposes  nerve endings  in  the underlying  lamina  propria,  resulting  in  pain  or  soreness,  especially when  eating  spicy  foods  or  citrus  fruits.  Patients  vary  enormously  in  the  degree  to which  they  suffer  and  complain  of soreness   in   relation   to   oral   ulceration.   It   is always  important  to  exclude  serious  disorders  such as oral cancer (Part 9) or other serious disease, but not all patients who complain of sore ness have discernible organic disease. Conversely,  some with serious disease have no pain. Even in  those  with detectable  lesions,  the  level  of  complaint can vary enormously. Some patients with large ulcers complain little; others with minimal  ulceration    complain    bitterly    of  discomfort.  Sometimes there is a psychogenic influence.

Terminology
Epithelial thinning or breaches may be seen in:  mucosal   atrophy   or   desquamation  — terms  often used for thinning of the epithelium which  assumes  a  red  appearance  as the  underlying  lamina propria containing blood vessels shows  through. Most commonly this is seen in desqua-  mative   gingivitis   (usually   related   to   lichen  planus, or less commonly to pemphigoid) and in  geographic  tongue  (erythema  migrans,  benign migratory glossitis). A similar process may also  be seen in systemic disorders such as deficiency  states (of iron, folic acid or B vitamins). 

Small Erosions and Minor aptheous ulcers

Chemical Burn-Above and Thermal burn-Below

Mucosal inflammation (mucositis, stomatitis)  which  can  cause  soreness.  Viral stomatitis,  candidosis, radiation mucositis, chemotherapy-  related  mucositis  and  graft-versus-host-disease are examples.  erosion which is the term used for superficial  breaches of the epithelium. These often have a red appearance initially as there is little damage to the underlying lamina propria, but they  typically become covered by a fibrinous exudate which  has  a  yellowish  appearance.  Erosions  are  common  in vesiculobullous disorders such as pemphigoid.  ulcer  which  is  the  term  usually  used  where  there is damage both to epithelium and lamina  propria. An inflammatory halo, if present, also highlights the ulcer with a red halo around the  yellow  or  grey  ulcer.  Most ulcers  are  due  to  local  causes  such  as  trauma  or  burns, but  recurrent  aphthous stomatitis  and  cancer  must  always be considered.

Main causes of oral ulceration

Local causes

• Aphthae
• Infections
• Drugs
• Malignant disease
• Systemic diseases
• Chemical burn, right
• maxillary tuberosity  
• Thermal burn, palate

Main causes of mouth ulcers
Local causes
Trauma

• Appliances
• Iatrogenic
• Non-accidental injury
• Self-inflicted
• Sharp teeth or restorations

Burns

• Chemical
• Cold
• Electric
• Heat
• Radiation

Recurrent aphthae

Infections

• Acute necrotising gingivitis
• Chickenpox
• Deep mycoses
• Hand, foot and mouth disease
• Herpangina
• Herpetic stomatitis
• HIV
• Infectious mononucleosis
• Syphilis
• Tuberculosis

Drugs

• Cytotoxic drugs,
• Nicorandil, NSAIDs
• Many others

Malignant neoplasms

• Oral
• Encroaching from antrum

Systemic disease

• Mucocutaneous disease
• Behcet's syndrome
• Chronic ulcerative stomatitis
• Epidermolysis bullosa
• Erythema multiforme
• Lichen planus
• Pemphigus vulgaris
• Sub-epithelial immune blistering diseases (Pemphigoid and variants, dermatitis  herpetiformis, linear IgA disease)

Haematological disorders

• Anaemia
• Gammopathies
• Haematinic deficiencies
• Leukaemia and myelodysplastic syndrome
• Neutropenia and other white cell dyscrasias

Gastrointestinal disease

• Coeliac disease
• Crohn's disease
• Ulcerative colitis

Miscellaneous uncommon diseases

• Eosinophilic ulcer
• Giant cell arteritis
• Hypereosinophilic syndrome
• Lupus erythematosus
• Necrotising sialometaplasia
• Periarteritis nodosa
• Reiters syndrome
• Sweet's syndrome
• Wegener's granulomatosis

Causes of oral ulceration
Ulcers and erosions can also be the final common  manifestation of a spectrum of conditions. These  range  from:  epithelial  damage  resulting  from  trauma;  an immunological  attack  as  in  lichen planus,    pemphigoid    or    pemphigus;    damage because  of  an  immune  defect  as  in HIV  disease  and leukaemia; infections such as herpesviruses,  tuberculosis and syphilis; cancer and nutritional  defects  such  as  vitamin  deficiencies  and  some  gastrointestinal diseases.

Ulcers of local causes
At any age, there may be burns from chemicals  of  various  kinds,  heat ,  cold,  or ionising radiation or factitious ulceration, especially of the maxillary gingivae or palate. Children may develop ulceration of the lower  lip  by  accidental biting  following  dental local  anaesthesia.    Ulceration    of    the    upper    labial fraenum,  especially  in  a child with  bruised  and  swollen lips, subluxed teeth or fractured jaw can  represent non-accidental injury. At any age, trauma,  hard  foods,  or appliances  may  also  cause ulceration. The lingual fraenum may be trauma-  tised  by repeated  rubbing  over  the lower  incisor  teeth in cunnilingus, in recurrent coughing as in  whooping cough, or in self-mutilating conditions.  Most  ulcers  of  local  cause  have an  obvious  aetiology,  are acute,  usually  single  ulcers,  last  less  than  three  weeks and  heal  spontaneously. Chronic  trauma  may  produce  an  ulcer  with  a  keratotic margin.

 

Minor aphthous ulceration

RAS  lesions  early  on,  along  with  some  natural  killer (NK) cells. Cytotoxic cells then appear in the  lesions  and  there  is  evidence  for  an  antibody  dependent cellular cytotoxicity (ADCC) reaction. It now seems likely therefore that a minor degree of immunological dysregulation underlies aphthae. RAS may be a group of disorders of different  pathogeneses.  Cross-reacting  antigens  between  the oral mucosa and microorganisms may be the  initiators, but attempts to implicate a variety of  bacteria or viruses have failed.

Predisposing factors
Most   people   who   suffer   RAS   are   otherwise  apparently completely well. In a few, predisposing  factors  may  be  identifiable,  or  suspected.
These include:
1. Stress: underlies RAS in many cases. RAS are typically worse at examination times.
2. Trauma: biting the mucosa, and dental appliances may lead to some aphthae.
3. Haematinic deficiency (deficiencies of iron, folic acid (folate) or vitamin B  12) in up to 20% of patients.
4. Sodium lauryl sulphate (SLS), a detergent in some oral healthcare products may produce oral ulceration.
5. Cessation of smoking: may precipitate or aggravate RAS.
6. Gastrointestinal disorders particularly coeliac disease (gluten-sensitive enteropathy) and Crohn's disease in about 3% of patients.
7. Endocrine factors in some women whose RAS are clearly related to the fall in progestogen level in the luteal phase of their menstrual cycle.
8. Immune deficiency: ulcers similar to RAS may be seen in HIV and other immune defects.
9. Food allergies: underlie RAS rarely.

Drugs may produce aphthous-like lesions.

Key points for dentists: 

Aphthous ulcers They are so common that all dentists will see them
It is important to rule out predisposing causes (sodium lauryl sulphate, certain foods/drinks, stopping smoking or vitamin or other deficiencies) or conditions such as

Behcet's syndrome
Enquire about eye, genital, gastrointestinal or skin lesions
Topical corticosteroids are the main treatment

Traumatic ulceration, lateral tongue Recurrent aphthous stomatitis (RAS; aphthae; canker sores)

RAS is a very common condition which typically starts  in  childhood  or  adolescence  and presents with  multiple  recurrent  small,  round  or  ovoid ulcers with circumscribed margins, erythematous haloes, and yellow or grey floors. RAS  affects  at  least 20%  of the  population, with the highest prevalence in higher socio-economic   classes.  Virtually  all   dentists   will   see patients with aphthae.

Aetiopathogenesis
Immune  mechanisms  appear  at  play  in  a  person with a genetic predisposition to oral ulceration. A genetic  predisposition  is  present,  and  there  is  a positive   family  history  in   about   one   third   of
patients with RAS. Immunological factors are also involved, with T helper cells predominating in the


Clinical features
There   are   three   main   clinical   types   of   RAS, though  the  significance  of  these distinctions  is
unclear and it is conceivable that they may rep- resent three different diseases:

1. Minor aphthous ulcers (MiAU; Mikulicz Ulcer) occur  mainly  in  the  10  to 40-year-old age group, often cause minimal symptoms, and are small   round   or   ovoid   ulcers   2-4  mm  in diameter. The ulcer floor is initially yellowish but  assumes  a  greyish  hue  as healing and epithelialisation proceeds. They are surrounded by  an  erythematous  halo and some  oedema, and  are  found  mainly  on  the  non-keratinised mobile mucosa of the lips, cheeks, floor of the mouth,  sulci  or  ventrum  of  the tongue.  They are only uncommonly seen on the keratinised mucosa of the palate or dorsum of the tongue and occur in groups of only a few ulcers (one to six) at a time. They heal in seven to 10 days, and  recur at  intervals  of  one  to  four  months leaving little or no evidence of scarring. are  found  on  any  area  of  the  oral  mucosa, including    the    keratinised    dorsum of   the tongue or palate, occur in groups of only a few ulcers (one to six) at one time and heal slowly over 10 to 40 days. They recur extremely frequently may heal with scarring and are occasionally found with a raised erythrocyte sedimentation rate or plasma viscosity.

3. Herpetiform  Ulceration  (HU)  is  found  in  a slightly older age group than the other forms of RAS and are found mainly in females. They begin with vesiculation which passes rapidly into  multiple  minute  pinhead-sized  discrete ulcers  (Fig.  10),  which involve  any  oral  site including    the    keratinised    mucosa.    They increase  in  size and  coalesce  to  leave  large round ragged ulcers, which heal in 10 days or longer, are often extremely painful and recur so frequently that ulceration may be virtually continuous.

2. Major aphthous ulcers (MjAU; Sutton's Ulcers; periadenitis     mucosa     necrotica recurrens (PMNR))  (Figs  8  and  9)  are  larger,  of  longer duration,  of  more  frequent recurrence,  and often  more  painful  than  minor  ulcers.  MjAU are round or ovoid like minor ulcers, but they are  larger  and  associated  with  surrounding oedema  and  can reach  a  large  size,  usually about  1  cm  in  diameter  or  even  larger.  They

Major Aptheous Ulceration

Diagnosis
Specific  tests  are  unavailable,  so  the  diagnosis must  be  made  on  history  and clinical  features alone.  However,  to  exclude  the  systemic  disorders discussed above, it is often useful to undertake the investigations shown in Table 3. Biopsy is  rarely indicated,  and  only  when  a  different diagnosis is suspected.

Investigation of aphthae

1. Full blood count
2. Haematinics
3. Ferritin
4. Folate
5. Vitamin B12
6. Screen for coeliac disease

Management
Other  similar  disorders  such  as  Behcet's  syndrome must be ruled out (see below). Predisposing factors should then be corrected. Fortunately, the natural history of RAS is one of eventual remission  in  most  cases.  However,  few  patients do  not  have spontaneous  remission  for  several years   and  although  there  is  no  curative treatment, measures should be taken to relieve symptoms,  correct  reversible  causes (haematological disorder, trauma) and reduce ulcer duration.

Maintain good oral hygiene Chlorhexidine or triclosan mouthwashes may help.

Examples of readily available topical corticosteroids
Steroid                                         Dosage every six hours
Low potency
Hydrocortisone
hemisuccinate pellets                             2.5 mg pellet dissolved in mouth close to ulcers

Medium potency
Triamcinolone acetonide 0.1% in           Apply paste to dried lesions
carmellosegelatinpaste
Betamethasone
phosphate tablets

High potency
Beclometasone                             0.5 mg; use as mouthwash Becotide 100 1 puff to lesions (100micrograms)

(Beclomethasone)
dipropionate spray

Topical corticosteroids can usually control symptoms
There is a spectrum of topical anti-inflammatory agents  that  may  help  in  the management  of RAS.  Common  preparations  used  include  the following, four times daily:
•  Weak potency corticosteroids topical hydrocortisone hemisuccinate pellets (Corlan), 2.5mg
or
Medium potency steroids - topical triamcinolone acetonide in carboxymethyl cellulose paste (Adcortyl in orabase), or betamethasone
or
Higher   potency   topical   corticosteroids   (eg beclometasone).

The  major  concern  is  adrenal  suppression with   long-term   and/or   repeated  application, but  there  is  evidence  that  0.05%  fluocinonide in    adhesive    paste    and  betamethasone-17- valerate mouthrinse do not cause this problem. Topical   tetracycline  (eg   doxycycline),   or tetracycline   plus nicotinamide   may   provide relief and reduce ulcer duration, but should be avoided in children under 12 who might ingest the tetracycline  and  develop  tooth  staining.  If RAS  fails  to  respond  to  these  measures, systemic   immunomodulators   may   be   required, under specialist supervision.

Key points for patients: aphthous ulcers These are common
They are not thought to be infectious Children may inherit ulcers from parents The cause is not known but some follow use of toothpaste with sodium lauryl sulphate, certain foods/drinks, or stopping smoking
Some vitamin or other deficiencies or conditions may predispose to ulcers
Ulcers can be controlled but rarely cured No long-term consequences are known

Infections
Infections  that  cause  mouth  ulcers  are  mainly viral,  especially  the  herpesviruses, Coxsackie, ECHO   and   HIV   viruses.   Bacterial   causes   of mouth   ulcers,   apart  from   acute   necrotising ulcerative gingivitis, are less common. Syphilis and tuberculosis are uncommon but increasing, especially   in   people   with   HIV/AIDS.   Fungal and protozoal causes of ulcers are also uncommon but increasingly seen in immunocompromised persons, and travellers from the developing world.

Herpes simplex virus (HSV)
The term 'herpes' is often used loosely to refer to infections with herpes simplex virus (HSV). This is a ubiquitous virus which commonly produces lesions  in  the  mouth  and oropharynx.  HSV  is contracted  by  close  contact  with  infected  individuals from infected saliva or other body fluids after an incubation period of approximately four to seven days. Primary    infection    is    often    subclinical between the ages of 2-4 years but may present with   stomatitis   (gingivostomatitis).   This   is usually  caused  by HSV-1  and  is  commonly attributed to 'teething' particularly if there is a fever. In teenagers or older people, this may be due  to  HSV-2  transmitted  sexually.  Generally speaking,  HSV  infections  above  the  belt  (oral or  oropharyngeal)  are  caused  by HSV-1  but below  the  belt  (genital  or  anal)  are  caused  by HSV-2.
The  mouth  or  oropharynx  is  sore  (herpetic stomatitis or gingivostomatitis): there is a single   episode   of   oral   vesicles   which   may   be widespread,  and  which  break down to  leave oral ulcers that are initially pin-point but fuse to  produce  irregular painful ulcers. Gingival oedema,  erythema  and  ulceration  are  prominent,    the   cervical   lymph  nodes    may    be enlarged  and  tender,  and  there  is  sometimes fever  and/or malaise. Patients  with  immune defects  are  liable  to  severe  and/or protracted infections.
HSV  is  neuroinvasive  and  neurotoxic  and infects  neurones  of  the  dorsal  root  and autonomic ganglia. HSV remains latent thereafter in those  ganglia,  usually  the trigeminal  ganglion, but   can   be   reactivated   to   result   in   clinical recrudescence (see below).

Diagnosis
Diagnosis  is  largely  clinical.  Viral  studies  are used occasionally and can include: culture; this takes days to give a result electron microscopy; this is not always available
polymerase chain reaction (PCR) detection of HSV-DNA; this is sensitive but expensive
immunodetection; detection of HSV antigens is of some value.
Management
Although  patients  have  spontaneous  healing within  10-14  days,  treatment  is indicated  particularly to reduce fever and control pain. Adequate  fluid  intake  is important,  especially  in children,  and antipyretics/analgesics  such  as paracetamol/acetoaminophen    elixir    help.    A soft  bland  diet  may be  needed,  as  the mouth can be very sore. Aciclovir orally or parenterally is    useful    mainly    in   immunocompromised patients or in the otherwise apparently healthy patient if seen early in the course of the disease  but  does  not  reduce  the  frequency  of  subsequent recurrences.

Recurrent HSV infections
Up  to  15%  of  the  population  have  recurrent HSV-1  infections,  typically  on  the  lips (herpes labialis:  cold  sores)  from  reactivation  of  HSV latent  in  the  trigeminal ganglion.  The  virus  is shed   into   saliva,   and   there   may   be   clinical recrudescence.    Reactivating    factors    include fever  such  as  caused  by  upper respiratory  tract infection  (hence  herpes  labialis  is  often  termed 'cold' sores), sunlight, menstruation, trauma and immunosuppression.
Lip  lesions  at  the  mucocutaneous  junction may  be  preceded  by  pain,  burning, tingling  or itching.  Lesions  begin  as  macules  that  rapidly become  papular,  then vesicular  for  about  48 hours, then pustular, and finally scab within 72- 96 hours and heal without scarring (Fig. 11). treatment  is  indicated.  Antivirals  will  achieve maximum benefit only if given early in the disease but may be indicated in patients who have severe,  widespread  or  persistent  lesions  and  in immunocompromised   persons.  Lip   lesions   in healthy patients may be minimised with penciclovir  1%  cream  or aciclovir  5%  cream  applied in    the    prodrome.    In    immunocompromised patients, systemic  aciclovir  or  other  antivirals such   as   valaciclovir   (the   precursor   of  penciclovir) may be needed.

Key points for patients: cold sores
These are common
They are caused by a virus (Herpes simplex) which lives in nerves forever They are infectious and the virus can be transmitted by kissing
They may be precipitated by sun-exposure, stress, injury or immune problems
They have no long-term consequences They may be controlled by antiviral creams or tablets, best used early on

Drug-induced ulceration
Drugs   may   induce   ulcers   by   producing   a local  burn,  or  by  a  variety  of mechanisms such   as   the   induction   of   lichenoid   lesions.  Cytotoxic  drugs (eg  methotrexate) commonly  produce  ulcers,  but  non-steroidal anti-inflammatory   drugs    (NSAIDs),    alendronate   (a   bisphosphonate),   nicorandil   (a cardiac drug) and a range of other drugs may also cause ulcers.

Herpes labialis

Recurrent   intraoral   herpes   in   apparently healthy  patients  tends  to  affect  the hard  palate or gingivae  with  a  small  crop  of  ulcers  which heals within one to two weeks. Lesions are usually over the greater palatine foramen, following a palatal local anaesthetic injection, presumably because of the trauma. Recurrent  intraoral  herpes  in immunocompromised patients may appear as chronic, often dendritic, ulcers, often on the tongue.

Diagnosis
Diagnosis  is  largely  clinical;  viral  studies  are used occasionally.

Management
Most  patients  will  have  spontaneous  remission within one week to 10 days but the condition is both   uncomfortable   and   unsightly,   and   thus

Lichenoid reaction to propranolol

A  drug  history  is  important  to  elicit  such uncommon  reactions,  and  then  the offending drug should be avoided. Patients to refer:

• Severe aphthae
• Malignancy
• HIV-related ulceration
• TB or syphilis
• Drug-related ulceration
• Systemic disease
• Mucocutaneous disorders.

Purpose of Root Canal Obturation and method of root canal obturation

Introduction

Root canal obturation involves the three-dimensional filling of the entire root canal system and is a critical step in endodontic therapy. There are two purposes to obturation: the elimination of all avenues of leakage from the oral cavity or the periradicular tissues into the root canal system; and the sealing within the root canal system of any irritants that remain after appropriate shaping and cleaning of the canals, thereby isolating these irritants. Pulpal demise and subsequent periradicular infection result from the presence of microorganisms, microbial toxins and metabolites, and the products of pulp tissue degradation. Failure to eliminate these etiologic factors and to prevent further irritation as a result of continued contamination of the root canal system are the prime reasons for failure of nonsurgical and surgical root canal therapy.

The importance of three-dimensional obturation of the root canal system cannot be overstated, with the ability to achieve this goal primarily dependent on the quality of canal cleaning and shaping as well as clinical skill. Other factors that influence the ultimate success or failure of each case include the materials used and how they are used. The ultimate coronal restoration of the tooth following canal obturation may loom as the most important goal, for there is reasonable evidence that coronal leakage through improperly placed restorations after root canal treatment and failure of the restorative treatment or lack of health of the supporting periodontium are the final determinants of success or failure in treatment.

Factors influencing complete obturation

• Quality of the cleaning and shaping of the canal system
• Skill and experience of the clinician
• Materials and their usage
• Restoration of the tooth
• Health of the supporting periodontium

Characteristics of an Ideal Root Canal Filling

An ideal root canal filling three-dimensionally fills the entire root canal system as close to the cemento-dentinal junction as possible. Minimal amounts of root canal sealers, most of which have been shown to be biocompatible or tolerated by the tissues in their set state, are used in conjunction with the core filling material to establish an adequate seal. Radiographically, the root canal filling should have the appearance of a dense, three-dimensional filling that extends as close as possible to the cemento-dentinal junction. These standards should serve as the benchmark for all clinicians performing root canal therapy, and it is only through a knowledgeable approach to root canal treatment that quality assurance can be continually demonstrated in the obturation of root canal systems.

The ideal root canal filling

3-D filling of the entire root canal space as close as possible to the cemento-dentinal junction

Radiographically dense fill with absence of voids

 

Shape reflecting a continuously tapered funnel that is approximately the same as the external root morphology

While a plethora of materials has been advocated over the last 150 years for root canal obturation, historically, gutta-percha has proven to be the material of choice for successful filling of root canals from their coronal to apical extent. Although it is not the ideal filling material, gutta-percha has satisfied the majority of criteria for an ideal root filling material. The disadvantages of gutta-percha – specifically, its adhesiveness, lack of rigidity, and ease of displacement under pressure – do not overshadow its advantages. In light of its shortcomings, a sealer/cement is always used with gutta-percha. However, regardless of the delivery system or technique used, neither gutta-percha nor sealer/cement alone enables standard-ofcare canal obturation. In addition, the available materials and techniques do not routinely provide for an impervious seal of the canal system; all canals leak to a greater or lesser extent.

It is recommended that clinicians master multiple obturation techniques and become competent with various root canal sealers/cements, to be able to manage the diversity of anatomical scenarios that may be encountered.

Contemporary Sealers/Cements

The use of a sealer during root canal obturation is essential for success. Not only does it enhance the possible attainment of an impervious seal, it also serves as a filler for canal irregularities and minor discrepancies between the root canal wall and core filling material. Sealers are often expressed through lateral or accessory canals and can assist in microbial control should there be microorganisms left on the root canal walls or in the tubules.Sealers can also serve as lubricants, enabling thorough seating of the core filling material during compaction. In canals in which the smear layer has been removed, many sealers demonstrate increased adhesive properties to dentin in addition to flowing into the patent tubules. A good sealer should be biocompatible and well tolerated by the periradicular tissues, and although all sealers exhibit toxicity when freshly mixed, their toxicity is greatly reduced on setting and all are absorbable when exposed to tissues and tissue fluids. Subsequent tissue healing or repair generally appears unaffected by most sealers, provided there are no adverse breakdown products of the sealer over time. In particular, the breakdown products may have an adverse action on the proliferative capability of periradicular cell populations. Some clinicians consider that a small puff of root canal filler extending beyond the working length is indicative of a fully obturated canal space with a well-sealed apical constriction. Excessive sealer should not be routinely placed in the periradicular tissues as part of an obturation technique.

Sealers/cements can be grouped based on their prime constituent or structure, such as zinc oxide-eugenol, polyketone, epoxy, calcium hydroxide, silicone, resin, glass ionomer, or resin-modified glass ionomer. However, many of the sealers/ cements are combinations of components, such as zinc oxideeugenol and calcium hydroxide,43 with the addition of calcium hydroxide claimed to create a therapeutic material that can be inductive of hard tissue formation.Epoxy-based and methacrylate-based resin sealers that can be bonded to the root canal dentin (but not to gutta-percha) are also now available.

Sealers should be mixed to a creamy consistency, allowing them to adhere to the master cone and not ball up at the shaft of the cone, leaving the gutta-percha exposed. The sealer should adhere to the cone evenly along its length and at the end of the cone. Clinicians should read the product insert and material safety data sheet for each product chosen before using it.

Contemporary Core Filling Materials

Gutta-percha is the standard material of choice as a solid core filling material for canal obturation. It demonstrates minimal toxicity and minimal tissue irritability, is the least allergenic material available when retained within the canal system,and in cases of inadvertent gutta-percha cone overextension into the periradicular tissues, is well tolerated provided the canal is clean and sealed. Chemical solvents have been used for almost 100 years to soften gutta-percha, with methods ranging from merely dipping the gutta-percha cones into the solvent for one second for better canal adaptation, to creating a completely softened paste of gutta-percha with the solvent. Solvents used have included chloroform, halothane, rectified white turpentine, and eucalyptol. Periradicular tissues may be irritated if the solvent is expressed beyond the canal or significant amounts of softened gutta-percha are inadvertently placed into the periradicular tissues. Failure to allow for dissipation of chemical solvents, if volatile, or the removal of excess solvent with alcohol can result in significant shrinkage and possible loss of the apical seal. The use of chemical solvents has been both praised and questioned, but with the advent of thermoplasticized gutta-percha, the need to consider the use of solvents at any time must be questioned. The use of solvents, however, may still be considered for a number of challenges the clinician may face in daily practice, such as the custom fitting of master cones in irregular apical preparations or following apexification.

Gutta-percha Cones

The composition of gutta-percha cones is approximately 19% to 22% Balata and 59% to 75% zinc oxide, with the remainder a combination of various waxes, coloring agents, antioxidants, and metallic salts.58 The specific percentages for components varies by manufacturer, with resulting variations in the brittleness, stiffness, tensile strength, and radiopacity of the individual cones attributable primarily to the percentages of gutta-percha and zinc oxide. The antimicrobial activity of gutta-percha is also primarily due to the zinc oxide.

The cones are manufactured in both standardized and nonstandardized sizes. The standardized sizes coordinate with the ISO root canal files sizes 15 through 140 and are used primarily as the main core material for obturation. They generally have a 2% taper, but can have a 4 or 6% taper or more. The non-standardized sizes are more tapered from the tip or point to the top. With some obturation techniques these cones have been used primarily as accessory or auxiliary cones during compaction, being matched with the shape of the prepared canal space or the compaction instrument.

Non-standardized cones began to assume a greater role as the primary core material in the more contemporary obturation techniques, and with the development of more predictable shapes with current nickel titanium (NiTi) rotary and hand instruments, cones tapered from 4% to 10% have gained use.

Tapered gutta-percha cones

In particular, for techniques that use vertical compaction of heat-softened gutta-percha, both the non-standardized and more tapered cones have become quite acceptable. Custom cones can also be developed for canals with irregular or large apical anatomy, Over time, numerous methods have been advocated for obturating the prepared root canal system, each with their own claims of ease, efficiency, or superiority. Most contemporary techniques still rely on gutta-percha and sealer to achieve their goal. Four basic techniques exist for the obturation of the root canal system with gutta-percha and sealer

(1) the cold compaction of gutta-percha; (2) the compaction of heat-softened gutta-percha with cold instruments

Cold compaction carrier              Heated compaction              Presoftened core

until it has cooled; (3) the compaction of gutta-percha that has been thermoplasticized, injected into the system, and compacted with cold instruments; and (4) the compaction of gutta-percha that has been placed in the canal and softened through the continuous wave technique (Calamus). A multitude of variations on these four basic themes exists. For injectable thermoplastic obturation techniques, gutta-percha may come in either pellet forms or in cannulae.

Cold compaction carrier Heated compaction Presoftened core

No single technique has proven to have statistically significant superiority when considering both in vitro and in vivo studies, as the success of all techniques is highly dependent on the cleaning and shaping of the canals and the clinician’s expertise in the use of a particular technique.While many have advocated the use of the lateral compaction technique or a single cone fill (monocone) to achieve a quality apical seal, the technique in itself does not necessarily favor the filling of canal irregularities.63 Recognizing this, use of a softened gutta-percha technique with heat or chemical softening is required to achieve a thorough obturation.

In addition, while filling the entire root canal system is the major goal of canal obturation, a major controversy exists as to what constitutes the apical termination of the root canal filling material. Working length determination guidelines often cite the cemento-dentinal junction or apical constriction as the ideal position for terminating canal cleaning and shaping procedures and placing the filling material. However, the cemento-dentinal junction is a histologic and not a clinical position in the root canal system and, in addition, the cemento-dentinal junction is not always the most constricted portion of the canal (yellow arrows) in the apical portion of the root

Contemporary practices of obturation favor material softening even this does not guarantee that an impervious seal of the root canal system will be established. Also, with softened gutta-percha obturation techniques there has been a greater incidence of material extrusion beyond the confines of the canal. While softening of gutta-percha may be viewed as routinely desirable, the selective use of this technique solely or in combination with a solid core of gutta-percha must be at the discretion of the competent clinician when anatomy dictates this approach.

Apical constriction of root canal

Recent research conducted at Nova Southeast University using micro CT scanning technology has shown the effectiveness of scanning for imagery and the greater precision observed compared to standard radiographs. In one example, a mesiobuccal canal was filled using GT® Series X™ obturator and the mesiolingual canal was filled using a single cone technique (ActiV GP). It appeared from one angle that all canals were equally filled.

Radiograph of filled canals

However, closer examination subsequent to filling showed voids using the single cone technique throughout the length of the root filled using this technique. The single cone technique did not produce a monoblock obturation. The gutta-percha from the GT obturator flowed into the canal isthmus and filled it.

Voids using single cone technique

Cross-section with ActiV GP and GT Series X obturation

                                          

                                Activ V GP             GT Series X obturator

Canal isthmus filled with GT obturator gutta-percha

Differences in obturation techniques and results are also more observable using CT scanning than using traditional radiographs.Contemporary techniques include the use of bonded root canal filling materials. Recent developments in resin-bonding have led to the availability of resin cones and pellets similar in shape and size to gutta-percha materials.

Resin-based cones containing methacrylate resin, fillers, bioactive glass, and polymers are available that can be handled similarly to gutta-percha and can be used with a lateral or vertical compaction technique. Resin-based materials can also be delivered via a heated syringe (Obtura gun, Spartan Obtura). Since resin-based materials require a slightly moist environment, it is important to avoid using any dessicating solutions, such as alcohol, during root canal preparation. Further, if sodium hypochlorite or peroxide was used during root canal preparation, this must be thoroughly removed prior to using a resin-based material as it would reduce the ability of the resin material to bond. Similarly, the smear layer must also be thoroughly removed.

Prefabricated Obturators

Gutta-percha can also be formed on a plastic carrier or corecarrier. Prefabricated obturators were first described in 1978 by William Ben Johnson.79 The prototype for the obturator had been prenotched K-files wrapped in gutta-percha (hand formed) that were then heated over a flame until the surface glistened and expanded. These prenotched “obturators” were inserted into the canal and apical pressure applied while the handle was twisted off.

Prototype obturator

Prefabricated obturators were introduced in 1988 (Thermafil) using first a stainless steel and subsequently a titanium core, coated with gutta-percha. Plastic obturators were first offered in 1992. Since then, a number of prefabricated obturator systems have been introduced, including one that does not involve thermosoftening of the gutta-percha (SimpliFil, Discus Dental) but instead is used cold with only the apical area coated in gutta-percha, and after placement the carrier itself is removed.

A recently developed prefabricated obturator utilizes a resin-based system (RealSeal One, Sybron Endo) and is used with, and bonded to, methacrylate resin-based sealer material and is first held in its custom oven and thermosoftened. Other systems use thermosoftened gutta-percha, including Calamus® (Tulsa Dental, Dentsply) , Successfil® (Hygienic-Coltene-Whaledent, Inc.), Gutta- Flow®, System B Obturation System, Thermafil, Thermafil Plus, ProTaper® Universal and ProSystem GT® Obturators (Dentsply, Tulsa Dental), and Soft-Core® (Soft-Core® Texas, Inc.).

Current plastic obturators are available in a nonvented shape with a taper of around 0.04 (Densfil) and a vented shape with the same taper (Thermafil Plus). Both are biologically inert. The carrier is thick with a thinner outer coating of gutta-percha, which helps to reduce material shrinkage as the gutta-percha cools in the canal. A vented prefabricated obturator helps the flow of gutta-percha during placement and also aids in retrieval of the obturator should retreatment be necessary.

For sizes 40 and below in the Thermafil series, an insoluble liquid crystal plastic is used. For size 45 and above soluble polysulfone polymer is used. All of these use a size verifier to help select the correct size obturator, as do ProTaper Universal carriers, which start at a .04 taper. Systems that do not use a size verifier include the ProSystem GT carriers and GT Series X carriers, which are made in a variety of tapers between 0.04 and 0.12.