Pulp pathology: Definition, Etiologies, Pathogenesis and Histopathology
I-INTRODUCTION
The pulp is normally protected from aggressors present in the external environment and in particular from batteries. The destruction of the hard tissues that protect it exposes it to exogenous irritants that can be biological, chemical or physical agents.
The pulp, like all connective tissue, responds to physical, chemical or bacterial attacks with a pathology whose characteristics depend on the high specificity of this highly differentiated connective tissue and its particular environment.
II- Definitions
The term pulpopathy is defined as the main element of Endodontopathies which can best be applied to all pulp disorders.
Inflammation is the set of phenomena of defense of the organism against an aggression (trauma, infection etc.) which can manifest itself by different signs (pain, swelling, heat, redness etc.).
III-etiologies:
1-Infectious origins:
A-Local causes:
- Dental caries: is the most common cause of pulp disease, bacteria progress to the pulp and send their toxins and enzymes through which diffuse through the dentinal tubules to cause pulp inflammation
- Coronal fracture: Bacteria can penetrate through the fracture and diffuse their degradation products through the dentinal tubules to result in pulp inflammation.
- Periodontal pocket: bacteria from the periodontal pocket can reach the endodontium by hiding through the lateral canals, secondary accessory canals or even through the apical foramen to give rise to a pulpitis called retro pulpitis.
- B-General causes:
- septic inoculation of the pulp by blood in subjects suffering from general infection (such as tuberculosis, typhoid fever, etc.). This phenomenon will give rise to pulp disorders called hematogenous pulpitis
2-Physical origins:
- A-Local causes:
- Mechanics :
Trauma, erosion, abrasion, attrition and abfraction are lesions that can lead to exposure of the dentin, making it vulnerable to any infection of origin, subsequently resulting in pulp inflammation. It can also be noted
- An over-occluded restoration can cause pulpitis due to accumulation of occlusal forces
- Very fast orthodontic movement
- Untimely root planing
- Untimely apical curettage
- Thermals
- heat developed by friction of rotating instruments
- exothermic setting reactions during the setting of certain filling cements (silicate)
- Thermal conductivity of restoration materials.
Pulp pathology: Definition, Etiologies, Pathogenesis and Histopathology
- Electric:
Misuse of certain electrical instruments such as the pulp tester could result in pulp damage.
- Radiographic:
Irradiation of malignant cervicofacial tumors causes constant damage to odontoblasts.
- B-General causes:
- These are the variations in altitude (between 1500 and 8000m), and the variations in atmospheric pressure (during the climb).
- These variations are sources of violent pain especially in the maxillary teeth, rarely in healthy teeth. This pain is called Aerodontalgia, caused by barotrauma
3-Chemical origins
| Local causes | General causes |
| * Dental medications: formalin, arsenic anhydride, phenol, etc. * dental products : silicate without protective base, resin monomers, composite, varnish, etc. (by diffusion), | Poisoning – endogenous (diabetes) – exogenous (mercury, lead) |
IV- pathogenesis
The pulp reaction varies depending on the nature , intensity and duration of the irritant factor.
- Short-term irritation (sudden trauma, untimely surgical maneuvers) : the pulp response is generally a partial, primary, acute inflammation at the site of the injury.
- Repeated irritation (occlusal trauma); pulp response is chronic
- Active caries: no formation of reaction dentin and the vessels dilate and inflammatory cells appear in increasing numbers as the caries approaches the pulp
- Passive caries: the reaction of the pulp is fibrosis and degeneration, most often calcic; reaction dentin forms at the level of the caries, which reduces the volume of the pulp cavity.
- But in the long run we can note: the transition from the chronic form to the secondary acute form and towards that (cooling and warming) and even the spontaneous healing of pulpitis, and this if can result:
- either a change in the etiological character (treated or not)
- of the appearance of additional factor (open or closed)
- from the failure or strengthening of the body’s defense elements.
- – Chronic inflammation can persist for a long time, quietly, and then be followed by total necrosis.
V- Histopathology of pulp inflammation
- 1-specificity of pulp inflammation:
Unfavorable factors: The fact that the pulp is enclosed in a cavity with inextensible walls, and that the collateral circulation is reduced explains the frequent extension of the inflammatory process of the pulp tissue when the aggression is violent or continuous.
Favorable factors:
– The ability of the pulp to develop a barrier to the formation of sclerotic dentin and reactional dentin in response to caries aggression
-The arteriovenous plexus on the periphery of the pulp allows the regulation of the inflammatory process:
- remains localized in the pulp area opposite the site of the attack, an increase in lymphatic drainage and the absorption of exudates by the capillaries of the neighboring healthy pulp.
- If the irritation ceases, healing of the local inflammation occurs.
- If bacterial invasion continues, the inflammatory reaction produces irreversible lesions of the coronary pulp
- 2-Dynamics of pulp inflammation
- Neurovascular phase; injured cells release arachidonic acid (prostaglandin) which will cause vasodilation, increased diapedesis and vascular permeability
- The injured vascular wall releases highly algogenic bradykinin
- Histamine released by peripheral mast cells increases vascular permeability and causes localized vasodilation.
- Nerve fibers stimulated by bradykinin and prostaglandins release different neuropeptides (substance P and calcitonin-gene retarted (CGRP)) involved in pulp inflammation.
- Cell phase:
Polymorphonuclear cells : are the first white cells to cross the vascular walls and accumulate in the tissues at the level of the attack in the form of clusters which phagocytose foreign bodies
Lymphocytes appear later in chronic lesions in varying proportions of neutrophils and eosinophils, macrophages, T and B lymphocytes, mast cells
An innate immune response is produced by the action of macrophages in phagocytosing bacteria, but also by stimulating lymphocytes through interleukin and also derived from blood monocytes that enter inflamed tissues where they differentiate into macrophages
A specific acquired immune response may occur if the antigen agent persists through T and B lymphocyte intervention and antibody formation.
Pulp pathology: Definition, Etiologies, Pathogenesis and Histopathology
3-Inflammatory manifestations of the pulp
A) Acute pulpitis:
- Primary or secondary, these are closed pulpitis , or indirectly opened or closed fortuitously.
- Hence the painful consequences and the tendency towards necrosis.
- A-1- Initial pulp inflammation (pulp hyperemia):
- – marked vasodilation and increased capillary permeability, responsible for significant serous exudation causing intra-tissue edema
- – vascular slowing or stasis.
Local irritation can cause venous congestion in the apical region on which drainage of the pulp will depend.
- A-2- Acute serous pulp inflammation:
- It is characterized by massive migration and a predominance of polymorphonuclear neutrophils
- the odontoblastic layer is often completely destroyed with a phenomenon of projection of the odontoblastic nuclei into the dentinal tubules.
A-3-Abscessive pulp inflammation
The polymorphonuclear cells degrade after phagocytosis, and release proteolytic enzymes that liquefy the surrounding tissue, giving rise to pus.
- B) Chronic pulpitis:
- a- Chronic closed pulpitis:
- A sort of balance is created (between a proliferative tendency towards repair and the persistence of exudative islands of acute inflammation) which can be broken
- the presence of lymphocytes and plasma cells which have an immunological role and will synthesize the proteins necessary for cell growth and differentiation.
- b- Chronic open pulpitis:
- Ulcerative pulpitis : Characterized by tissue ulceration that is lined by a layer of granulation tissue beneath which there are signs of pulpal inflammation
- Hyperplastic pulpitis: This is an outgrowth of the pulp tissue, consisting of thick connective tissue, with very dilated blood vessels, poor in nerves.
| Senescence (physiological ) | Senility (pathological) |
| -advanced age of the individual -aging phenomenon | -no contribution with age -premature phenomenon |
| -slow and progressive phenomenon | -accelerated phenomenon |
| -phenomenon generalized to the whole pulp -Ordered phenomenon | – phenomenon localized at the level of the irritated pulp area – disordered, anarchic phenomenon |
4-senility and senescence
Pulp pathology: Definition, Etiologies, Pathogenesis and Histopathology
Wisdom teeth can be painful if they are misplaced.
Composite fillings are aesthetic and durable.
Bleeding gums can be a sign of gingivitis.
Orthodontic treatments correct misaligned teeth.
Dental implants provide a permanent solution for missing teeth.
Scaling removes tartar and prevents gum disease.
Good dental hygiene starts with brushing twice a day.