Pulp Capping (Direct and Indirect)

- Pulp Capping Procedure:

- Pulp capping:It is a term is derived from the name pulp cap which means trying to sterilize the damaged tooth area as well as one can, followed by stopping the bleeding and placing the right filling material on it.

- The precaution being that teeth that are already abscessed should never be pulp-capped – this is done to those teeth where the nerve is irritated but still alive and healthy enough to repair themselves given a chance to do so.

- Pulp capping gives it a chance by getting out the decayed portions and the bacteria then putting a clean dressing on it with the filling.

- After eliminating the wounded dental tissues of a carious tooth, the next step is usually filing the cavity with a suitable restoring material. When pulpal tissue is exposed it gets contaminated by bacteria and mostly these are the conditions that warrant the clinician to perform pulp capping. When performing this procedure, the degree of the pain and the pulpal size exposure are considered.

- Capping Materials:

- Calcium Hydroxide is the best possible capping material known till now.

- Advantages of Calcium Hydroxide:
1-It's alkaline PH (11) ... Giving more chances to healing of inflamed tissues.
2-Amazing bio-compatibility with pulpal tissues.
3-It's antibacterial Abilities (Bacterio-static).
4-It's ease of application.
5-Availability.
6-It's proven Abilities to dentine bridging for regeneration of healing dentinal tubules in the pathosed dentine pulp complex.

- Disadvantages of Calcium Hydroxide:
1- Associated with primary tooth resorption
2- May dissolve after one year with cavo-surface dissolution.
3- May degrade during acid etching
4- Degrades upon tooth flexure
5- Marginal failure with amalgam condensation
6- Does not adhere to dentin or resin restoration.

- NOTE:
Calcium hydroxide was originally introduced to the field of endodontics by Hermannin:: 1920 as a pulp-capping agent.

- Many studies have showed that direct pulp capping with MTA Is as successful ...

- Placing the restoration directly without capping on a pinpoint exposed pulp:
1- Severe sensitivity the patient will suffer.
2- Failure of restoration.
3- Irreversible pulpal tissue damage that will require endodontic treatment.

- The Pulp Capping is two Types: Direct and Indirect Pulp Capping:

- Direct Pulp Capping:

- The exposed pulp is directly covered. This works best when the exposure is not infected - for example a traumatic exposure caused by slipping with the drill.

- If the pulp becomes exposed while removing soft infected dentine, the chances are that the pulp will be infected also, and a direct pulp cap will fail (that is, an irreversible pulpitis will develop).

- Although Calcium Hydoxide has been proven successful for many years, MTA (Mineral Trioxide Aggregate) is fast becoming the material of choice for direct pulp caps. MTA is however very expensive.

- Indirect Pulp Capping:

- The pulp is not exposed - a layer of infected dentine is deliberately left, rather than expose the pulp.

- Indirect pulp caps, when done correctly, are more successful at maintaining long-term vitality than direct ones.

- It is not currently (2010) known whether it is necessary to "go in again" after a couple of months for further caries removal.

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Basics Of Paedodontics

In Branch Of Paedodontics:
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* If You're going to deal with children in your dental clinic, After studying different behaviors you shall meet, After gaining the talent of how to prepare for anaesthesia, And Different ART & SCIENCES regarding Children in dental clinic, Now You're ready to know These Nomenclature ..

(( PULPOTOMY , PULPECTOMY, Apexogenesis, Apexification, EXTRACTION, Stainless Steel Crowns, Orthodontics, Orthognathic Surgeries ))

*Let's start With Pulpotomy -&- Pulpectomy ..

- PULPOTOMY:

Is the process of extirpation of the diseased coronal pulp tissues after placement of medication that will allow Fixation Or Mummification of the remaining healthy pulp structure.

Materials Used:-High&Low speed contra angle hand piece, Large round carbide or diamond burs, fissure burs, Excavator, Cotton, Formocresol (Or Calcium hydroxide).
------------------------------------------------------------
- {{Indication}}

1-In Permenant teeth only in first visit of root canal treatment procedure.

2- In Deciduous teeth As a temporary management till eruption of permenant successors.

3-Minimally Inflamed pulp Of deciduous teeth.

4-Absence of any evidence of pulp necrosis.
------------------------------------------------------------
-{{Procedure}} ...

1-Use round burs to access into the primary pulp.

2-Use Spoon Excavators Or Low speed round burs to remove inflamed coronal pulp tissues.

3-Be Sure that all inflamed pulp tissues are removed and use the sign of (No More bleeding from pulp chamber).

4- Use Piece of Cotton with 5% Formocresol to (FIX) Or (MUMMIFY) exposed pulp tissues.

5-After few minutes(If you're going to make single visit pulpotomy) remove that piece of cotton, be sure that there's no bleeding,Put a layer of non Re-Inforced Zinc-Oxide Eugenol, use a good base material (Glass ionomer, Zinc phosphate) Followed by a proper Permenant Restoration. (Composite, Amalgam, Some Dentists use ketac Silver).

-------------------------------------------------------------------------

- Pulpectomy:

* Very similar to pulpotomy except that part of radicular pulp tissue is being removed .. This is performed when

*There is irreversable pulpitis, Pulp Necrosis, hyperemic pulp.

*{{Procedure}}

1- Remove coronal pulp tissues as mentioned in pulpotomy procedure

2- Use hand files to remove the inflamed pulp inside the canal.

3- Fill the canals with Zinc-oxide Eugenol, Then Use a good base material, Followed by permenant restoration.

4- Use Stainless Steel Crown if required.

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---->To Be Continued<----

Authored, Published, Edited By; World Of Dentistry TEAM

Picture Taken From .. A-CaMERON Handbook Pf Pediatric Dentistry

Healing Of Extraction Socket

Healing of an extraction socket is an example of healing by secondary intention.

Immediately after removal of tooth, the blood fills the extraction site and both extrinsic and intrinsic pathways of clotting are activated. This results in formation of fibrin meshwork that contains entrapped RBCs and helps seal of the torn blood vessels and reduces the size of extraction wound.

Clot organization begin 24-48 hours after extraction with:

-          Engorgement and dilatation of blood vessels within PDL remnants

-          Followed by  leukocytic migration and

-          Formation of a fibrin layer.

1^st Week:

-          The clot forms a temporary scaffold upon which inflammatory cells migrate.

-          Epithelium at the wound periphery grows over the surface of the organizing clot.

-          Osteoclasts accumulate along the alveolar bone crest setting the stage for active crestal resorption.

-          Angiogenesis proceeds in the remnants of the periodontal ligaments.

2^nd Week:

-          The clot continues to get organized through fibroplasia and new blood vessels that begin to penetrate towards the center of the clot.

-          Trabeculae of osteoid slowly extend into the clot from the alveolus, and osteoclastic resorption of the cortical margin of the alveolar socket is more distinct.

3^rd Week:

-          The extraction socket is filled with granulation tissue and poorly calcified bone forms at the wound perimeter.

-          The surface of the wound is completely reepithelialized with minimal or no scar formation.

Active bone remodeling by deposition and resorption continues for several more weeks.

Radiographic evidence of bone formation does not become apparent until the sixth to eighth weeks following tooth extraction. Due to the ongoing process of bone remodeling the final healing product of the extraction site may not be discernible on radiographs after 4 to 6 months.

REFERENCE: Peterson’s Principle Of Oral And Maxillofacial Surgery, 2^nd Edition

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Bonding To Dentine

- The main problems encounter in "Bonding To Dentine" procedure are:
1- High Water Content of Dentinal Tubules.
2- High Organic Content of Dentinal Tubules.
3- Presence of Smear Layer.

- Indications of "Bonding To Dentine"

1- Marginal Seal where preparations margins are on dentine or cementum.
2- Retention and Seal of direct resin composite restorations.
3- Retention and Seal of indirect porcelain and composite inlays.
4- Repairing Teeth.
5- Veneers.
6- Cementing Ceramic Crowns
7- As An Endodontic Sealer.

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Aphthous Stomatitis

Description:
- This is one of the most common oral diseases.
- It's a painful lesion that size from less than 1 mm to 2 cm, single or multiple.
- There is three types: The small lesions are less than 0.5 cm and called the "Minor Aphthae", The large lesions are more than 0.5 cm and called the "Major Aphthae", while they may be Multiple and pinpoint seldom exceeding 1 mm and are called "Herpetiform Aphthae".
- The exact incidence is unknown, but estimates range from 20% to 60% of the population.
- The Lesion begins as a red macule, less often papule, but not blisted. Then it ulcerates and the ulcer become covered by pyogenic membrane producing the characteristic yellow-white center with surrounding erythematous flare.
- It's usually round to oval but may be elongated in natural folds such as the vestibule.
- The lips, cheeks, soft palate, floor of mouth, ventral and lateral tongue are often involved but attached gingival, hard palate and dorsal tongue are seldom affected.
(Occurs on freely movable mucosa that does not overlie bone).
- Aphthous lesions affect all age groups from young to old but young adults and females are more affected.
- Also Known as: Canker sores, recurrent aphthous stomatitis, RAS.

Etiology:
- The cause is unknown.
- There are too many theories for them all to be correct. Aphthous stomatitis may not be a single disease with a single cause but instead a variety of diseases all manifested by painful mouth sores.
- The concept that canker sores are caused by a microbiologic agent has been superceded by theories revolving around an immunopathogenesis. The deposition of antibodies and complement within epithelium and basement membrane during the early stages of the disease suggests a humoral immune response, and the influx of lymphocytes rather than neutrophils in early lesions points to a cellular immune reaction as well. It is yet to be learned if the immune response is directed against self (autoimmunity) or against an extrinsic antigen such as bacteria or viruses. To further cloud the issue, a variety of other factors have been implicated. Withdrawal of certain foods such as cheese, tomato products and gluten, as well as sodium lauryl sulfate-containing toothpastes, has been claimed to help some patients whereas in others, correction of iron, B12 and folate deficiencies have brought about a cure. Improvement of aphthous lesions during the last stages of pregnancy with exacerbation after delivery suggests that gonadal hormones may lay a role. The occurrence of canker sores during menstruation also suggests a hormonal basis. To add a final element of mystery, aphthous stomatitis has been reported to worsen when cigarette smoking is discontinued.

Treatment:
- To reduce pain, patients with few lesions may be treated with topical medications such as Orabase® with Benzocaine, Zilactin®, or Soothe-N-Seal®.
- Anti-inflammatory agents such as topical steroids or Aphthasol® have also been shown to be effective.
- For severe or widespread disease, systemic prednisone such as a Medrol 4 mg Dosepak® is helpful.
- Long-term systemic steroid therapy may be associated with numerous adverse effects, including osteoporosis, asceptic necrosis, cataracts, depression, fluid retention and exacerbation of diabetes.

Prognosis:
- Cure is seldom achieved but palliation and long-term remission may be achieved by above mentioned treatment.
- Without treatment, healing time varies from 4 days for a small lesion to a month or more for major aphthae.
- Major aphthae may also cause scarring.

Differential Diagnosis:
- Aphthous stomatitis must be differentiated from herpetic stomatitis, the disease with which it is most often confused.
- Recurrent intraoral herpes occurs almost exclusively on mucosa overlying bone. The hard palate is the most common site.
- Lesions indistinguishable from aphthous stomatitis have been reported in Behcet’s syndrome, Reiter’s syndrome, Crohn’s disease and celiac disease.

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Epulis fissuratum

 
- Description:
A Lesion that appears in the buccal vestibule of the anterior maxilla or the lingual aspect. (most commonly in anterior aspect)
Where the body of the dental prosthetic appliance flanges contact with for a long time, causing a two or more folds of soft tissue that is separated by a cental groove.
The excess tissue is firm and fibrous, and ulcerations may be present.
The size of the affected tissue varies widely, since almost the entire length of tissue around a denture can be affected.
Most of the patients are females (64% of cases study) in the fifth and sixth decade of like.
The lesion's duration is from one week to 10 days, but 40% of the patients reported a duration of 6 months to two years.
No symptoms are associated with the lesion except some pain with ulcerated types.
Also Known As: Granuloma fissuratum, inflammatory fibrous hyperplasia, denture epulis and denture induced fibrous hyperplasia.

- Etiology:
This is an inflammatory fibrous hyperplasia or oral mucosa caused by ill-fitting or over-extended denture borders.

- Histologically:
The excessive tissue is composed of cellular, inflamed fibrous connective tissue.

- Microscopic Appearance:
The appearance of an epulis fissuratum microscopically is an overgrowth of cells from the fibrous connective tissue. The epithelial cells are usually hyperkeratotic and irregular, hyperplastic rete ridges are often seen.

- Treatment:
Surgical excision of the lesion and reduction of the denture border.

- Prognosis:
Good

- Differential Diagnosis:
The lesion has such a characteristic clinical appearance that differential diagnosis is not a problem.
Persistent ulcerated areas in epulis fissuratum should be biopsied to rule out squamous carcinoma.
Folds similar to epulis fissuratum may be seen in Crohn’s disease.
Epulis fissuratum can also appear around dental implants. occurred because the Broken implant denture clasp with poor oral hygiene.

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Leukoedema

Definition:
It's a normal variation of the buccal mucosa, or inside surface of the cheek. It presents as a white-bluish tinge of the buccal mucosa but the color disappears when the cheek is stretched. This aids to differentiate this lesion from other similar looking conditions which could be premalignant, such as leukoplakia. It is more prevalent in people who have dark skin and can be more intense in smokers.

Etiology:
Intracellular edema of the superficial epithelial cells coupled with retention of superficial parakeratin is thought to account for the white appearance. Microscopic examination reveals superficial squamous cells have a clear, seemingly empty cytoplasm but it has not been shown that there is an increase in intracellular water. Thus, the term edema is questionable.

Histology:
The white appearance is caused by water within the spinous cells causing the light to reflect back as whitish.

Treatment:
None required.

Differential Diagnosis:
- White sponge nevus
- hereditary benign intraepithelial dyskeratosis
- dyskeratosis congenital...
All are extremely rare.

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Bacteria and Oral Odontogenic Infections

1- Caused by the oral normal inhabitant bacteria.

2- The bacteria are primarily: gram positive aerobic cocci, gram-positive anaerobic and gram-negative anaerobic.

3- The Odontogenic infections most commonly caused by polymicrobial origin.

4- The Odontogenic infections are caused mainly by:
Anaerobic 44%
Aerobic 6%
Mixed 50%

5- The Anaerobic gram-positive rods and anaerobic gram-negative cocci have little or no role in oral odontogenic infections.

6- The facultative S. Milleri group organisms can synthesize hyalurunidase, that allow spreading of infection the deeper connective tissue, initiating the cellulitis infections, the streptococci then produce the by-products that make a good environment, lowered tissue PH and release of essential nutrients, All make the anaerobic bacteria to grow there, and as the local oxidation reduction potential is lowered, the anaerobic bacteria predominate causing liquefaction necrosis of tissue by the collagenase the release, while the collagen break down and the invading WBC’s necrose & lyse, they form micro abscesses that may coalesce to form the clinical recognizable abscess.
So That: Each Oral Infection starts by cellulitis, is aerobic, whereas each one ends with chronic infection, is anaerobic.

7- Odontogenic infections includes 4 stages:
- Inoculation Stage: characterized by a soft mildly tender, doughy swelling, where the invaded streptococcus starts to colonize the host (in first 3 days).
- Cellulitis Stage: the swelling becomes harder, tenderer and red as the mixed flora starts to promote the inflammatory response. (3-5 days).
- Abscess Stage: when the anaerobic bacteria starts to predominate, causing the liquefied abscess.
- Resolution Stage: when the abscess drain through skin or mucosa of by surgery.

-----------------------------

Principle 1: Determine the severity of the infection:

This is done by the good complete history and physical examination.

- Complete History:
1- The patient chief complain should be recorded in patient's own words, ex: swelling, boiling gum or toothache.
2- Duration, onsite, time and rapidity of the infection.
3- Electing the patient's symptoms of infection, which are: pain, swelling(tumor), warmth(Salor), Redness(rubor) and loss of function(functio laesa)
4- The Patient then is asked about how does he feel in general, ex: fatigued, feverish, sick, weak and malaised.
5- Dentist should be aware of some cases that are refered from other physicians and cases of patients having self-treatment in home, that may cause unfavourable unexpected results.
6- The dentist must take the complete medical history of the patient.

- Physical Examination:
1- First of all the dentist should obtain the patient's vital signs, including tempreture, blood pressure, pulse rate and respiratory rate.
- The tempreture should be elevated slightly in cases of infection up to 38.3 C (101 F).
- The blood pressure should be elevated. in cases of pain and anxiety there is increased systolic blood pressure while there may be hypotention in cases of severe septic shock.
- The patients pulse rate should be slightly elevated, uncommonly up to 100 beat/min, but if elevated more than that, so aggressive treatment should be held for such a severe infection.
- Patients respiratory rate should be carefully observed to detect any partial or complete upper airway obstructions, the normal is 14-16 breath/min, while in mild to mederate infections in may reach 18 breath/min.
2- physical examination of the patients general appearance, if there is more than minor localized infection, there may be fatigue, feverishness and malaise. (Toxic Appearance).
3- physical Examination of the head and neck region for any swelling the underlying erythema.
4- open the patients mouth widely, as the patient to swallow and having deap breaths, to check for trismus 73%, dysphagia 78% and dyspnea 14%.
5- The dentist should have a good oral examination to detect the cause of infection.
6- Having A good Radiographic Image( intraoral periapical or extraoral panoramic ).
7- Complete the physical Examination by palpation of the swelling.
- If it's very soft, mildy tender, edematous swelling then it's in inoculation (Edema) stage. but,
- If it's slighter broadlike consistensy with reddish color, diffuse tender pain and diffuse borders then it's in cellulitis stage. but,
- If it's localized slightly tender swelling of flactuant consistensy and well-defined margins of swelling then it's in Abscess stage, where the body immune system has locally walled off infection.

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