History of Endodontics aae/abe



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What are the current theories of cyst formation?


STTT = Seltzer, Ten Cate, Toller, Torabinejad


  1. Epithelial proliferation (Seltzer) - Epithelial rest cells of Malassez activated by inflamm. mediators to proliferate and line cavity




  1. Cavitational Breakdown Theory (Ten Cate / Cohen) - Continuous growth of epithelial cells removes central cells from nutrition – innermost cells die and cyst cavity forms




  1. Osmotic Expansion of Cyst Lining (Toller) - Osmotic pressure buildup due to semi-permiable membrane (Starlings Law)




  1. Immunological Theory (Torabinejad) - Continued immune reaction to antigens – bacteria in infected root canal system. Immune complex reaction (Type III) responsible for proliferation of epithelium.

Cyst Formation


  1. Lin/Huang/Rosenberg 2007 – Proliferation of epithelial cell rests, formation of apical cysts, and regression of apical cysts after PA wound healing




  1. Ten Cate 1965: Epithelial rest cells of Malassez remain dormant until activated to proliferate by inflammatory mediators




  1. Shear 1963: Proliferating epithelial cells rely on surrounding CT for nutrients, innermost cells necrose, forming epithelial lined cystic cavity


Do Cysts resolve following NSRCT?
Only Pocket Cysts:

  1. Nair 1998Pocket Cysts heal, True Cysts do NOT heal due to self-sustaining nature

  2. Simon 1980 – Pocket Cysts may heal due to the continuity with the root canal space, True Cysts would not heal due to the independence from the root canal space and their self-sustaining nature


All Cysts:

  1. Lin 2009 – Apical true cysts may heal by apoptosis mechanism similar to pocket cyst when removal of inflammatory microbial etiology is satisfactory during NSRCT; All cysts are inflammatory in origin.

  2. Caliskan 2004 – Healing of large cyst-like lesions (7-18 mm diameter); + cholesterol crystals periapically; CaOH2 used- 74% complete/10% incomplete healing; Size of lesion is not major determining factor in NSRCT vs. EMS





Pulpal & Periapical Microbiology






Cause of Apical Periodontitis


Microorganisms colonizing the root canal system play an essential role in the pathogenesis of periradicular lesions:
Miller 1894 – Light microscopy, detected bacteria species in teeth with AP
Kakehashi 1965 – Germ free vs conventional rats – germ free rats: vital/hard tissue repair; conventional rats: pulp necrosis/AP - directly linked AP to bacteria
Sundqvist 1976 Human study, evaluated necrotic traumatized teeth – w/o AP – no bacteria; w/ AP – Bacteria present (90% Anaerobes)
Moller/Fabricius 1981– Monkey study, Devitalized pulps/sealed 6-7 months: Sterile necrotic pulps – no AP changes; Infected necrotic pulps – AP inflammation/destruction
Ricucci/Siqueira – AP is an intraradicular biofilm disease – CAGE %: 95/83/71/6

Bacteria involved in initial necrotic case – Mixed anaerobes


PPTTDF (“Two Ps, Two Ts, a D and a F”):
Gram -: Gram +:

Prevotella (intermedia) Lactobacillus

Porphyromonas (endodontalis/gingivalis) Streptococcus

Treponema (denticola) Peptostreptococci

Tannerella (forsythia) Proprionibacterium (proprionicum)

Dialister (invisus) Actinomyces (israeli)

Fusobacterium (nucleatum) Eubacterium
*Mixed, polymicrobial 3-20 species, symbiotic relationship
Siqueira/Rocas 2006 – 55% of bacterial species yet to be cultivated

polymicrobial, anaerobic community – initial invaders and late-comers
Bacteria involved in initial necrotic case – Mixed anaerobes
Rocas/Siqueira 2008 – Bacterial species: AP: <5mm: 12.0, 5-10 mm: 16, >10 mm: 20, Sinus tracts: 17; Larger the PARL = Greater Bacterial Diversity
Sundqvist 1975– Redirected understanding of canal flora – predominantly obligate anaerobic (91.4%) but mixed with facultative anaerobes
Baumgartner/Falkler 1991 – Carious pulp exp/AP teeth, extracted, cultured - Apical 5 mm, predominantly Obligate anaerobes (68%). Most prevalent species: P. intermedia/nigrescens (BPB), Peptostreptococcus, Veilonella
Fabricius 1982 – Monkey study, obligate anaerobes  w/ time and apical position within the canal; Early Pulpal Infection– More Facultative Bacteria
Siqueira – 400+ species poss. – 45% Molecular (qPCR), 32% Culture, 23% Both

Bacteria involved in previously treated cases – Gram +, facultative anaerobes – treatment resistant
E. faecalis:

Rocas 2004 – E. faecalis 9x more likely in Persistent than Primary Infections

Sedgley 2006 – E. faecalis 90% Persistent Infections (vs. 67% Primary) - qPCR

Sundqvist 1998– 1st to find E. faecalis in persistent endo failures, frequently as a single species microorganism (9/24 cases); Retreatment success rate ~74%

Moller – high incidence of Enterococcus faecalis (Gr+, facultative) – few or mono species infection

Haapasalo – unsealed cases during treatment or multiple appts reveal higher frequency of E. Faecalis

Zolleti/Siqueira 2006 – E. faecalis present in Retx cases with and without AP – possibly may be present

Fungi and AP:
Candida albicans – most prevalent fungi involved in AP
Siqueira 2004 – Review on Fungi and AP:

  1. C. albicans most commonly identified fungi in primary/persistent AP

  2. More commonly isolated from Persistent infections

  3. Multiple virulence factors

  4. Resistant to CaOH2 (Waltimo/Orstavik/Haapasalo)


Nair – found yeast-like microorganisms, therapy resistant
Waltimo/Orstavik/Haapasalo 1999 – Candida (resistant to many medicaments), resistant to CaOH2, dentinal tubule infection
Sen – Candida – Most common fungi in Persistent Infections
Bacterial species associated with Refractory cases

PACES:
Pseudomonas aeurginosa

Pseudorambacter alactolyticus

Proprionibacterium Proprionicum

Actinomyces

Candida Albicans (yeast)

Enterococcus faecalis

Streptococcus
Prevotella, Fusobacterium, Lactobacilli – Persitent infection (@ obturation)
Siqueira/Rocas 2009

Persistent infections: 1-5 species, Gram + facultative anaerobes (adequate RCT), 2-30 species, Gram + facultative anaerobes (inadequate RCT)

Persistent/Secondary Intraradicular Infections

Secondary infection= Microorganisms not present in the primary infection but introduced in the root canal at some time after intervention

Persistent infection= Microorgansims that were members of primary or secondary infections that resisted intracanal procedures and survived post-treatment
Sjogren 2003 – Prospective Human study, PA healing (5 years post-op), At time of root filling (1 visit): Negative culture: 94%, Positive culture: 68%; Bacterial presence at time of root filling  success of NSRCT; 2 visit necessary  infection

Fabricius 2006 – Monkey study (175 root canals), PA healing (2.5 years post-op), At time of root filling: Negative culture: 72%, Positive culture: 21%; Bacterial presence at the time of root canal filling decreased periapical tissue healing
Lin – Failed NSRCT teeth harbored intraradicular infection

Siquiera/Rocas 2004 – PCR analysis of non-healed NSRCT demonstrated intraradicular infection

Sakamoto/Siqueira/Rocas 2008 – Long term surviving bacteria = failure

Nutrient Source, Oxygen Tension, and Bacterial Gradients

  1. Nutrients Source: Carbohydrates vs. Peptides/AAs

  1. Saccharolytic: Digest carbohydrates

  2. Asaccharolytic: Digest proteins, amino acids (degradation products)

  3. Later pulpal infection (more apical), More Asaccharolytic dominant




  1. Oxygen Tension: Redox Potential of Canal

  1. Initial infection (Coronal): Facultative ( O2), Higher Oxygen Tension

  2. Later infection (Apical): Obligate Anaerobe ( O2), Lower Oxygen Tension




  1. Bacterial Gradient/Interactions

  1. Early colonizers – Facultative anaerobes

  2. Latecomers – Obligate anaerobes


Fabricius/Moller 1982 – Monkey study: devitalize/infect pulp space/seal canals, Clinical, Radiographic, Histo examination: Initial pulp infection (day 7): Facultative bacteria predominate; Later pulp infection (day 90, 180, 1060): Obligate bacteria
Sundqvist 1979 – Saccharolytic (initial invaders) vs. Assacharoltyic (late comers)

Virulence Factors

Sakamoto/Siqueira/Rocas 2007


  1. LPS - Gram – outer membrane, Lipid A moeity responsible for virulence




  1. LTA - Gram + outer membrane




  1. Peptidoglycans - Outer sheets of bacterial cell wall (Gram +: 80-100, Gram -: 2-3)




  1. Secretory Products (Proteolytic Enzymes) - Collagenases, Hyaluronidases, Chondroitin sulfatases




  1. Metabolic Byproducts - Polyamines, Sulfur




  1. Coaggregation/Biofilms


Biofilms vs Planktonic Bacteria

Biofilm = community of microorganisms embedded in exopolysaccharide matrix

Planktonic = free-floating single microbial cells


  1. Socransky – Dental biofilms can be up to 300 or more cell layers thick

  2. Mah – Antibiotic concentration to kill biofilm bacteria is 100-1000x greater than concentration need to kill planktonic bacteria

  3. Ricucci/Siqueira 2010– 106 roots w/ AP (42 treated) Intraradicular biofilms present: Cysts 95%, Abscesses 83%, Granulomas 70%; Extraradicular biofilms 6% (CAGE)

    1. No correlation between biofilm presence and clinical symptoms or sinus tracts. Larger lesions had greater % of biofilm presence.

    2. Intraradicular biofilms are responsible for AP

    3. Extraradicular infections in form of biofilms are not common, typically planktonic bacteria in form of abscess with PMNs




  1. Tronstad/Barnett 1990 – Extraradicular Biofilms in persistent apical lesions

Dentinal Tubule Infection

  1. Love – E.faecalis may invade dentinal tubules and remain viable by adhering to Type I collagen in the presence of human serum (Pathogenicity for persistent AP)




  1. Pashley – Dentinal tubule infection




  1. Peters/Wesselink/Walton 1995– Review – 70-80% teeth w/ AP have dentinal tubule infection; Failure of RCT appears to be unrelated to bacteria left within tubules after proper RCT




  1. Haapasalo/Orstavik 1987 – E. Faecalis survived w/in tubules 10 days w/out nutrients




  1. Sen – Bacteria penetrate 10-150 m into the tubules




  1. Siqueira – Bacteria invade dentinal tubules up to 300 m




  1. Nagoaka 1995 – Dentinal tubules:  Bacterial invasion rate in Non-Vital teeth (No dentinal fluid/odontoblast processes/immune cells to slow infection)

Causes of E. faecalis Resistance

Stuart 2006 – Review of E. faecalis and mechanisms of resistance


  1. Love 2001 – E. faecalis invades dentinal tubules/remains viable by adhering to Type I unmineralized collagen in the presence of human serum




  1. Distel – E. faecalis form biofilms




  1. Evans – E. faecalis have a proton pump – pulls H+ ions into cell – lowers pH within cell – survive CaOH2 (high pH)




  1. Sundqvist 1998 – E. faecalis can survive as single infection without dependence of nutrients from other microorganisms




  1. Sedgley 2005 – E. faecalis can survive long periods of nutrient starvation in obturated canals (gutta percha/ZOE) – 12 months Ex Vivo




  1. Orstavik/HaapasaloCa(OH)2does not kill E. faecalis in dentinal tubules
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