Histology/Pathology

• TenCate – Odontoblasts, fibroblasts, undifferentiated mesenchymal cells, macrophages, Lymphocytes & Dendritic cells
• Farnoush – found mast cells in both inflamed and normal pulps
• Reader – mylenated A-delta fibers 28%; unmylenated C fibers 72% of total

Pashley – 1/3 the length of the tubule

• Pulp – type I & III; Dentin – type I (90% of organic component)
• Synthesized by mainly fibroblasts, but also odontoblasts, osteoblasts & cementoblasts

Bernick – demonstrated lymphatics in the pulp

• Takahashi & Kim – SEM showed AV anastomosis, VVanastomosis, U-shaped arterioles
• Kim – PBF increased with C-fiber activation (A-delta insignificant); C-fibers release substance P which increases PBF; the increase in tissue pressure excites both A-delta & C fibers

• As pulpal inflammation ↑, pulpal pressure ↑. With this increased pressure, veins and lymphatics collapse at the apex and strangle the pulp – necrosis results
• Tonder – cat study disproved this theory; localized increase in pressure with no strangulation

• Pathways - Pulp canal obliteration due to trauma – resembles cememtum or bone
• Andreasen – 22% of traumatized teeth undergo CM; only 8.5% developed pulp necrosis
• Walton – canal present histologically, although absent radiographically
• Holcomb & Gregory – RCT if PARL develops; only 7% require RCT

• Reeves & Stanley – if caries is < .5mm from the pulp or if it invades reparative dentin, there is irreversible damage; if >1.1mm then little pathosis is seen
• Trowbridge – chronic inflammation occurs long before bacteria penetrates the pulp

• Stanley, White & McCray – tertiary dentin begins to form @ 19 days at 1.49 um/day
• Abou-Rass – consider RCT for teeth with stressed pulps
• Zach – heat is capable of causing pulp necrosis
• Felton & Madison – 13% incidence of pulp necrosis following FCC

Bernick – decreased vascularity, nerves & pulp chamber size; increased calcifications

• Brannstrom – heat causes inward fluid movement; cold – outward; distortion of odontoblastic processes stimulates nerve response
• Pashley – occlude tubules with unfilled resins or oxalate salts
• Kim – K+ ions desensitize nerve ending

Ritter – safe for the pulp up to 10 yrs post-op; bleaching effectiveness may decline

healing tissue with fibroblasts, collagen, proliferating capillaries and leukocytes

chronic inflammatory tissue primarily infiltrated with lymphocytes, plasma cells & macrophages

inflammatory lesion with a distinct pathological cavity completely enclosed in an epithelial lining

lined with epithelium, but communicates with the root canal

acute inflammation consisting primarily of PMNs

Priebe – No, can’t determine from a radiograph

• Nair – 50% granuloma; 35% abscess; 15% cyst (distinguishes 9%pocket / 6% true)
• Rubenstein & Kim – 85% granuloma; 15% cyst

• Breakdown theory – (Toller): Osmotic pressure buildup due to semi-permeable membrane (remnants of cellular debris inside lumen leads to increased osmotic pressure due to Starling’s law)
• Cavitational Breakdown theory – (Ten Cate): Continuous growth of epithelial cells (rests of Malassez) removes central cells from their nutrition; innermost cells die & cyst cavity forms
• Epithelial Proliferation theory – (Seltzer): epithelial cells proliferate to line the abscess cavity
• Immunologic theory – (Torabinejad): Immune rxn (to antigens-bacteria in infected RC) responsible for proliferation of epithelium

Nair – pocket cysts should heal; true cysts, particularly large ones with cholesterol crystals are less likely to resolve following RCT

Baumgartner – lined with either epithelium or granulomatous tissue; 67% lined with epithelium to level of rete ridges; 33% were completely lined with epithelium to the PA lesion

Eliasson, Halvarsson & Ljungheimer – tx successfully and resolved with RCT 85%

• PA Granuloma
• PA Cyst
• PA Abscess
• PA Fibrous Scar – more frequent with thru & thru lesions or S RCT
• Nasopalatine Duct Cyst – max midline; > 6mm between central incisor roots
• Traumatic Bone Cyst – not a true cyst; trauma etiology; mand teeth
• Benign Fibro-osseous lesions (early stages) – periapical cemental dysplasia
• Lateral Periodontal Cyst – mand and max canine & premolar area

• Myxoma
• Ameloblastoma – aggressive neoplasm; any tooth-bearing area, but mand most common; peak age 30-40
• Central Giant Cell Granuloma – multinucleated giant cells; rule out hyperparathyroidism
• Hemangioma
• Odontogenic Keratocyst – post mand most common but may occur in any tooth bearing area; multiple OKCs associated with Basal cell nevus syndrome

• Condensing Osteitis - LEO
• Idiopathic Osteosclerosis – idiopathic dense bone; vital pulps
• Benign Fibro-osseous lensions – mixed radiolucent/radiopue; ossifying fibroma, cemento-osseous dysplasia, PCD; vital pulps
• Cementoblastoma – attached to root with radiolucent rim; neoplasm of cementoblasts
• Osteoblastoma – neoplasm of osteoblasts; may occur in any bone; not attached to root
• Odontoma - compound (tooth like) or complex