Diseases of the pulp

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 Pulpitis is an inflammation of pulp tissue, a response

to surrounding environment The vitality of the tooth depends on defence response of pulp dentine complex by: - Sclerotic dentin - Tertiary dentin - Calcified bridge of dentinal tubules

ETIOLOGY
1.
2.

MECHANICAL: Trauma, iatrogenic damage and barometric changes.

THERMAL: uninsulated metallic restorations and dental procedures like cavity preparation, exothermic chemical reactions of dental materials etc. CHEMICAL: Irritation from certain dental materials or from erosion. caries

3.

4. BACTERIAL: Through toxins or from direct extension of

1. 2. 3. 4. 5. 6.

Severity and duration of irritant. Nature of irritant. Health condition of the pulp or pre-existing state of the pulp Apical blood flow Local anatomy of the pulp chamber Host defence

Mediators of pulpal inflammation

Locally produced mediators of inflammation including

eicosanoides , cytokines and neuropeptides, support the inflammatory process and the subsequent repair phase.
Both CGRP and SP exert chemotactic attraction on

leukocytes,including expression of adhesion molecule on vessel wall necessary for exit of these cell to the tissue and modulate T-lymphocyte activity.

 In many animal models,increased plasticity of pulpal

innervation has been obseved.within 48hr after experimental exposure of the pulp to the oral enviroment, neuropeptides,including SP and CGRP are increased in the nerve terminals close to the inflammatory zone. In addition there is extensive branching and sprouting of the peptide containing nerve terminal in the border zone of inflammatory process. This outgrowth of peptide containing nerve is part of an acute defense response that is fully developed within 48h after injury and last for as long as the irritation persists.

 These local phenomena are governed by trigeminal

cell bodies via peripheral influences. The activating signal is conveyed by a neurotrophin -nerve growth factor (NGF).this factor is normally found at a low level in pulpal fibroblast and serves to maintain the integrity of the peripheral nerve ending and to accelerate tissue repair. Consequently the increased local innervations increased level of neuropeptides support the mobilization and activation of cells necessary for an optimal defense reaction.

Following a bacterial challenge of exposed dentine,neutrophils May entre the tubules of the affected dentine at the pulpal end (encircled &prevent the dissemination of bacteria element to the pulp.

CHRONIC PULPITIS
It is a chronic inflammation of pulp tissue

characterized by specific clinical features. CLINICAL FEATURES: Signs and symptoms: - mild to moderate pain

Duration: - long duration (few days to months).

Precipitating factors of pain: - hot, cold agents and during biting. Nature of pain: Mild and intermittent pain The pain stops when precipitating factors are relieved.

The pain depends on: The size of exposed pulp (size of dental caries)

Severity of pulp inflammation

Age of patient Nature of covering dentin

HISTOPATHOLOGICAL FEATURES: The pulp tissue contains dilated blood

vessels with varying sizes.

Degenerated odontoblasts seen.
Areas of chronic inflammatory cells and

fibrosis can be seen around inflamed areas

A The advanced dentin caries reaches the pulpal tissues, there is accumulation of inflammatory cells.

B Within the coronal pulp, there is massive inflammatory cell infiltration with small areas of tissue disintegration.
C The bacteria within the dentinal tubules attract neutrophilic granulocytes. D Granulocytes dominate both perivascularly as well as intravascularly

Larger empty spaces represent initial tissue necrosis. Plasma cells and macrophages, which produce cytokines and chemokines, leading to chemo attraction of leukocytes. These mobilize monocytes, neutrophilic granulocytes, and other effectors cells, attracting them to the focus of infection.

Pulpitis and formation of a calcific barrier.

High power view shows barrier in more detail,in particular its irregulr structure and failur to hold back infection

As part of the pulp ageing process there is also a considerable decrease in the number of cells (fibroblasts, odontoblasts and mesenchymal cells), with the cell density decreasing by half from 20 to 70 years.

At the same time, fibrous tissue accumulation occurs to the point where almost nothing exists except the fibrous tissue. This is termed fibrous degeneration or pulp atrophy.

Pulp polyp
The pulp polyp is a proliferative soft tissue response to

infection or inflammation of pulp tissue remaining in a tooth with severe and rapid destruction of its crown by caries. It is essentially a pyogenic granuloma and looks like a hemorrhagic dome-shaped mass arising from the floor of the pulp chamber of the destroyed tooth.
It is not true pulp tissue and has few if any nerves, hence,

is not painful. It enlarges over several weeks but seldom attains a size larger than 1 cm in diameter. Treatment is surgical removal and endodontic therapy of the remaining tooth roots, or extraction of the affected tooth.

Clinical Features
The pulp polyp is typically found in the primary second molar or

permanent first molar, because these teeth are more likely than others to be greatly destroyed by caries at an age when the apical blood flow into the tooth is still very good. It is rarely seen after 20 years of age. The lesion presents as a pedunculated hemorrhagic mass of granulation tissue arising from the chamber floor in a tooth with much or all of its crown destroyed. Seldom is a polyp more than 0.7 cm in size. Surface ulceration may appear as gray/white change or the surface could be the same color and appearance as the surrounding mucosa. Palpation often induces mild hemorrhage and there is no pain associated with it. Vitality testing of residual tooth parts will often show reduced responses, if there is a response at all. Occasional cases show polypoid granulation tissue bulging outward from a much smaller carious destruction. Bilateral cases have been reported.

Microscopic Features
The pulp polyp presents as a mass of edematous or fibrosing

granulation tissue, admixed with a variable number of chronic inflammatory cells. Plup fibroblasts and endothelial cells are characteristic except in older lesions and blood vessels may be seen to radiate peripherally from a deep central location.
The surface is usually ulcerated and covered by fibrinoid necrotic

debris, but one third of the cases are covered by a relatively normal appearing stratified squamous epithelium.
Presumably the epithelium creeps in from the surrounding mucosa or

develops from sloughed keratinocytes which settle on the rich vascular environment of the polyp surface.
The mass is by nature pedunculated, extending up from normal or

slightly inflamed pulpal tissue in the root canals. Focal calcifications reminiscent of cementum or dentin may be seen as an aberrant repair attempt, especially toward the margins of the lesion.

Treatment and Prognosis The pulp polyp is treated by curetting the granulation tissue from the pulp chamber and performing endodontic procedures on the residual root structures, presuming the inter-radicular floor is still intact. Extraction is also a common treatment option. There is no malignant transformation potential and the lesion does not spontaneously regress.

PULP CALCIFICATION
(Pulp Stone or Denticles

It is a localized / generalized condition of pulp tissue characterized by formation of pulp stone in the form of calcified bodies

CLINICAL FEATURES : Site: coronal or radicular pulp Size: variable Signs and symptoms : painless

 RADIOGRAPHIC

FEATURES: Radiopaque mass / masses with variable sizes inside the pulp chamber or pulp canals.

HISTOLOGICAL TYPES: True pulp stone - consists of dentinal tubules. False pulp stone - consists of concentric calcified rings Free pulp stone - is freely located within the pulp tissue Attached pulp stone - is adherent to dentin wall Embedded pulp stone - is surrounded by secondary dentin

Pulp stones, like other types of stones, are formed from clearly concentric or diffuse layers of calcified tissue on a matrix that seems to consist primarily of collagen.
Their structure may help explain their origin; it has been shown that potential nidi of pulp stones may occur in the sheaths associated with blood vessels and nerves. Other potential nidi are calcifications of thrombi in vessels or calcification of clumps of necrotic cells. Whatever the nidus, growth is by incremental layering of a matrix that quickly acquires mineral salts.

COMPLICATIONS: It interferes with root canal treatment. Can cause pain if it impinges on major pulp nerves.

Uninflamed pulp. Typical pattern of calcifications. Larger pulp stones in the chamber blend into linear diffuse calcifications in the canal.

EVALUATION OF HISTOPATHOLOGIC CHANGES OF DENTAL PULP IN ADVANCED PERIODONTAL DISEASES

M. S. Sheykhrezaee1*, N. Eshghyar2, A. A. Khoshkhounejad3 and M. Khoshkhounejad4 1) Department of Endodontics, Faculty of Dentistry, Tehran University of Medical Science, Tehran, Iran 2) Department of Oral and Maxillofacial Pathology, Faculty of Dentistry, Tehran University of Medical Science, Tehran, Iran 3) Department of Periodontics, Faculty of Dentistry, Tehran University of Medical Science,

 This case- control study was performed to assess the possible

effects of advanced periodontal disease on the structure of dental pulp. MATERIALS AND METHODS Fifty-two permanent teeth extracted because of advanced periodontitis with 5mm attachment loss and grade III mobility were compared to fifty-two control teeth, obtained from systemically healthy adults. Teeth should Have at least one of these criteria: Advanced bone resorption to of root length, proved by radiography. Grade II or III furcation involvement Inaccessible areas Non maintainable areas

Decalcification was performed with immersion of teeth in 10% formic Acid for 3 months. Crowns were cut at the CEJ 2mm transverse sections of roots were performed. Totally 548 slides (276 and 272 in the study and control groups respectively) were examined. In the case group, teeth (roots) were then subcategorized according to depth of the adjacent periodontal pocket: 1) Group 1: coronal third of the root. 2) Group 2: Middle third of the root 3) Group 3: Apical third of the root

Inflammation, fibrosis, calcification and necrosis were observed in the (27.8- 40%), (0-59.4%), (0-26.4%) and (020.9%) of the different sections of the study group, and (0%), (9.7-50%), (0-11.6%) and (0%) of the control group . Abnormal pulp tissue was observed in the (33.3-88.1%) and (12.9-50.5%) of different sections of the study and control groups respectively. Complete necrosis of dental pulp occurred only when depth of adjacent periodontal pocket reached the apical third of the root. There was an increase in frequency of pathologic changes as the depth of periodontal pocket increased.

Result
Inflammation was observed in the (27.8-40%, mean: 33%) of different sections of study group and none of sections of the control group (Table 1). Inflammation was mild in most sections and always chronic. Fibrosis was seen in the (0-59.4%, mean: 45.3%) of the study group sections and (9.7-50%, mean 30.3%) of the control group in 4 to 12 mm sections from the apex). Calcification was seen in the (0-26.4%, mean: 18.4) of the study group sections and (0-11.6%, mean: 5.65%) of the control group sections in 2 to 12 mm sections from the apex.

Uninflammed

MILD

Moderate

Severe

During evaluation of 2mm level sections of both study and control groups, they found fibrosis in nearly half of sections. This can be explained by high collagen fiber density in apical pulp . In 4 to 12mm sections, there was a significant difference in prevalence of fibrosis between two groups. Diffuse or multiple calcifications were more prevalent in their study group and can be considered as the result of chronic hypoxia and cell death not only a normal histological finding or an aging Phenomenon. Necrosis was an infrequent (less than 30%) finding and seen only in patients with deep pockets (middle and apical) . Complete necrosis was seen only in the sections of roots adjacent to deep apical pockets. This finding shows that the entire pulp will not succumb despite that one or more lateral canals, or a number of dentinal tubules are involved as long as the main canal is not seriously Involved.

They showed that fibrosis and calcification (multiple and diffuse) are the most prevalent changes of the pulp; but inflammation and complete necrosis are infrequent and sometimes the result of apical involvement with periodontal disease. They found that in superficial (coronal) pockets, fibrosis is more prevalent than deep (apical) pockets. It can be explained that pulp reaction to superficial pockets is increased collagen production; and as the pocket deepens, the pulp reaction changes into dystrophic calcification and even complete necrosis.

In conclusion, advanced periodontal disease can affect pulp tissue. Fibrosis and calcification are the most prevalent changes. Necrosis of the pulp occurs infrequently and only in teeth with deep apical pockets. Pulp changes can jeopardize root canal therapy of these teeth. Careful consideration of diagnostic and treatment planning in patients with endodontic- periodontal involvement is recommended.

Angiogenic Signaling Triggered by Cariogenic Bacteria in Pulp Cells.

R.I. Soden1, T.M. Botero1, C.T. Hanks2*, and J.E. Nr1,3,4 1Department of Cariology, Restorative Sciences, and Endodontics, University of Michigan School of Dentistry,
J Dent Res 88(9):835-840, 2009

The inflammation observed in the dental pulp is characterized by a significant increase in blood vessel density. Lipoteichoic acid (LTA) Gram positive bacteria expression of
(VEGF) vascular endothelial growth factor in dental pulp cells. The hypothesis underlying this study was that LTA induces VEGF expression in dental pulp cells through TLR2 and PI3k/Akt signaling.

Vascular endothelial growth factor (VEGF) was initially characterized as a key regulator of vascular permeability. VEGF is considered the major inducer of angiogenesis in humans. Increase in vascular permeability and in vascular density tissue edema increase in tissue volume. In the brain, it was demonstrated that VEGF antagonism reduces edema formation and tissue damage after ischemia/reperfusion injuries.

Similarly to the brain, the pulp tissue is enclosed within rigid, non-expandable walls. Therefore, the vasodilation and the enhanced vascular permeability observed in pulpitis can be associated with an increase in intra-pulpal pressure. It is demonstrated that endotoxins expressed by cariogenic bacteria induce VEGF expression by dental pulp cells. Furthermore, VEGFR2 is expressed in the dental pulp of permanent and primary teeth in vivo, which suggests that these cells are capable of responding to VEGF-initiated signals.

Lipoteichoic acid (LTA) is a cell wall component of Grampositive bacteria and can induce the expression of several inflammatory mediators, including the CXCL2 and CXCL10 chemokines. The functional receptor in LTA-induced cell activation of several cell lines is the Toll-like receptor 2 (TLR2). Lipoteichoic acid (LTA) has been found to upregulate the expression of TLR2 in human odontoblasts. They have shown that LTA induces VEGF expression in MDPC-23 (an odontoblast-like cell line), OD-21 (undifferentiated pulp cells), and macrophages, suggesting that these cells may play a role in angiogenesis during pulpitis.

The purpose of this study was to examine the function of the cell membrane receptor TLR2, and the signaling kinases PI3K-Akt and I-B kinase (IKK), on LTA induced VEGF expression in dental pulp cells

MATERIALS & METHODS Cell Culture Four murine cell lines were used in this study: odontoblast-like cells (MDPC-23) undifferentiated dental pulp cells (OD-21), macrophages and gingival fibroblasts Cells were cultured in Dulbeccos Modified Eagles Medium

Test used for analysis

Immunocytochemistry

Flow Cytometry Enzyme-linked Immunosorbent Assay (ELISA)

Immunocytochemistry
As a positive control for TLR2 staining, they used RAW 264.7 macrophages. As negative controls for the immunocytochemistry, they used an isotype-matched non-specific immunoglobulin G.

Flow Cytometry
Samples were incubated in the dark for 30 min at 4C, and the proportion of cells expressing TLR2 was quantified by flow cytometry.

RESULTS
Quantitative evaluation by flow cytometry revealed that expression of TLR2 protein was highest in macrophages, followed by MDPC23, fibroblasts, and OD-21.

Immunohistochemistry revealed strong immunoreactivity for TLR2 in macrophages, fibroblasts, and MDPC-23, while the staining of OD-21 appeared somewhat weaker.

Analysis of these data, taken together, demonstrated that both odontoblast-like cells and undifferentiated pulp cells expressed TLR2, but its levels were consistently higher in the more differentiated MDPC-23 cells.

Immunohistochemical analysis of expression of TLR2 in macrophages, gingival fibroblasts, MDPC-23, and OD-21 cells. Cells were deposited onto a glass slide by means of a cytospin centrifuge and incubated with anti-mouse TLR2 antibody or isotype-matched non-specific Ig G. Expression of TLR2 was demonstrated by the presence of the red reaction product from the AEC stain.

Notably, PI3K and Akt are involved in TLR-mediated cell signaling and in angiogenesis They observed that, upon stimulation with LTA, the expression of VEGF was mediated via the PI3K-Akt pathway in MDPC-23 and OD-21 cells, and it was independent of I-B Kinase (IKK). Small-molecule inhibitors of the PI3K-Akt pathway are currently in clinical trials for the treatment of cancer. They speculate that inhibitors of these kinases might be useful locally for the treatment of incipient pulpitis.

DISCUSSION
VEGF up-regulation is unquestionably correlated with inflammation and with increases in tissue micro vessel density and in vascular permeability . It is known that bacterial endotoxins induce VEGF expression in dental pulp cells and that VEGF is expressed in teeth with pulpitis . Increases in vascular density and permeability typically result in an overall increase in tissue volume..

However, the fact that the dental pulp tissue is enclosed within rigid walls does not allow for tissue expansion. Instead, what happens in the inflamed pulp is a measurable increase in pressure. Such increases in interstitial pressures might result in irreversible tissue damage and pulp necrosis. They reasoned that the understanding of signaling pathways triggered by VEGF in the dental pulp might lead to the characterization of novel therapeutic targets for pulpitis.

Model depicting presumptive LTA-induced signaling in dental pulp cells.

Bacterial LTA induces VEGF expression in odontoblasts, undifferentiated pulp cells, and macrophages via activation of TLR2 and signaling through the PI3K-Akt pathway.

It is hypothesized that VEGF secreted by odontoblasts and undifferentiated pulp cells binds to endothelial VEGFR2, leading to increased microvessel density (MVD) and edema in the dental pulp

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