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Pulpal Histology/Pathology Overview
What the cellular elements of the pulp?
- 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
How far do the odontoblastic processes extend into the tubules?
Pashley – 1/3 the length of the tubule
What types of collagen are found in the dental tissues & what cells synthesize collegen?
- Pulp – type I & III; Dentin – type I (90% of organic component)
- Synthesized by mainly fibroblasts, but also odontoblasts, osteoblasts & cementoblasts
Are lymphatics found in the pulp?
Bernick – demonstrated lymphatics in the pulp
Discuss the pulp vasculature and regulation of blood flow?
- 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
Describe the ‘strangulation theory’ & does it occur?
- 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
Discuss calcific metamorphosis? Is RCT indicated?
- 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
Discuss the pulpal rxn to caries?
- 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
What is the effect of restorative dentistry on 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
How does age affect the pulp?
Bernick – decreased vascularity, nerves & pulp chamber size; increased calcifications
Describe the hydrodynamic theory of dentinal hypersensitivity. Any solutions?
- 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
How does vital bleaching affect the pulp?
Ritter – safe for the pulp up to 10 yrs post-op; bleaching effectiveness may decline
Periapical Pathology Overview
healing tissue with fibroblasts, collagen, proliferating capillaries and leukocytes
chronic inflammatory tissue primarily infiltrated with lymphocytes, plasma cells & macrophages
True cyst (bay cyst – Simon):
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
Is it possible to differentiate between a granuloma or cyst?
Priebe – No, can’t determine from a radiograph
What is the incidence of a granuloma, cyst & abscess?
- Nair – 50% granuloma; 35% abscess; 15% cyst (distinguishes 9%pocket / 6% true)
- Rubenstein & Kim – 85% granuloma; 15% cyst
What are the theories of cyst formation?
- 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
Do cysts heal following RCT?
Nair – pocket cysts should heal; true cysts, particularly large ones with cholesterol crystals are less likely to resolve following RCT
What are the histologic features of a sinus tract?
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
Is condensing osteitis a LEO?
Eliasson, Halvarsson & Ljungheimer – tx successfully and resolved with RCT 85%
Provide a differential diagnosis for the following:
Unilocular Periradicular Radiolucency:
- 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
Mutiloculary Periapical Radiolucency:
- 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
- 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
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