Analgesic Medications in Pregnancy

Precautions for Pregnant Analgesics:

A. NSAIDs should generally be avoided in pregnancy (despite Category B before third trimester)
- Second trimester use is likely safe
- Miscarriage risk in first trimester
- Premature Ductus Arteriosus closure in third trimester.

B. Tramadol should be avoided in pregnancy
- Second trimester use may be safe
- Fetal toxicity in animals (highest risk in first trimester)
- Respiratory problems and withdrawal symptoms in newborn (avoid in third trimester)

C. Opioids should be avoided in pregnancy unless there is no viable alternative
- First trimester use is associated with heart defects and Spina bifida

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Class B: No risk in controlled animal studies

A. Acetaminophen (Tylenol)
- Analgesic of choice in pregnancy

B. Narcotics (Class D if prolonged use or high dose)
- Nalbuphine (Nubain)
- Meperidine (Demerol)
- Butorphanol (Stadol)
- Fentanyl (Duragesic)
- Hydromorphone (Dilaudid)
- Methadone (Dolophine)
- Morphine Sulfate
- Oxycodone (Percocet)

C. NSAIDs (first and second trimester only)
- Ibuprofen (Motrin)
- Indomethacin (Indocin)
- Ketoprofen (Orudis)
- Naproxen (Naprosyn)
- Piroxicam (Feldene)
- Sulindac (Clinoril)

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Class C: Small risk in controlled animal studies

A. Narcotics (Class D if prolonged use or high dose)
- Codeine (Tylenol with codeine)
- Hydrocodone (Vicodin)
- Tramadol (Ultram)
- Propoxyphene (Darvocet)

B. Barbiturates
- Butalbital (Fiorinal)
- Class D if prolonged use or high dose

C. NSAIDs (first or second trimester only)
- Aspirin
- Etodolac (Lodine)
- Ketorolac (Toradol)
- Nabumetone (Relafen)
- Oxaprozin (Daypro)

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Class D: Strong evidence of risk to the human fetus

A. Aspirin
Used only with specific indications in pregnancy
Risk of neonatal Hemorrhage, IUGR, perinatal death
Low dose Aspirin may be safer

B. All NSAIDs (Third Trimester)

C. Prolonged use or high dose of any Narcotic

D. Prolonged use or high dose Butalbital (Fiorinal)

E. General Anesthesia - not in Briggs (1998)

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Preparations: Lactation Safe Analgesic Medications

A. Acetaminophen (Tylenol)
B. Ibuprofen (Motrin)
C. Tramadol
- Small amount crosses into Breast milk

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Preparations: Avoid Opioids in Lactation

A. Opioids that are converted to active metabolites by CYP2D6
- Codeine
- Hydrocodone
- Oxycodone

B. Risk of overdose in babies if mother is a ultra-rapid CYP2D6 metabolizer
- Ultrarapid CYP2D6 metabolism occurs in 10% caucasians, 3% african americans, 1% chinese and hispanic 

C. Preacutions if these Opioids are used in Lactation
- Avoid use beyond 4 days of life when milk intake increasing substantially
1- Consider pumping and dumping while taking the Opioid
2- Transition to Acetaminophen or NSAID as soon as possible
- Use the lowest effective dose of the shortest acting agent
- Limit dosing to immediately after feeding

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Removal Of Separated Endodontic Files Inside Canal

- First of all: the file type controls the treatment plan.
- Then, We should know the area that the files has been separated in,

If Coronal Third then the file should be by-passed or removed by the manual H files that engage it from a side,
If middle third then the file should be removed or even by-passed and flared as manual filing,
If Apical third then the file should be removed ONLY, or even may be left in place ONLY if it is sealed with the apical foramen, otherwise should be removed.
It Beyond the apex or pushed after separation to pass beyond the apex then it must be removed through the canal or through the surgical apicectomy.

- Note: Manual K file should be removed by H files, Manual H files is easier to separate inside canals and is very difficult to be removed from the canals,
while the rotary file is not liable to fracture unless with inexperienced endodontists and removal of it is nearly impossible (especially it is one of the first files in the sequence ex: S1 and S2 of Protaper rotary files),
all the files mentioned above can be removed by ultrasonic scaller that hits the dentin debris next to the broken file causing vibration and elevation of the file toward the crown (but if it is very fitting inside the canal and broke due to excessive force applied into the canal then it will not be elevated by ultra-sonic scaler),
Finally, we can remove the separated file by using the Gates Glidden (GG), by applying GG size 2 or 3 next to the file, taking care not to perforate the root, causing a small hole to apply a small H file inside to remove or by-pass the separated file.

- In All Cases:
Recall the patient for check up every 1 week, 1 month, 3 months and 6 months,
Using the Sodium Hypocloride is very effective in by-passing and removal of the separated files,
Using the Glyde is very effective in by-passing the separated files,
Try to pre-curve the the tip end of the file before inserting inside the canal with gentle pressure and clock and  anti-clock wise directions to by-pass the file so that you can remove it or complete filing,
Try to start trying to deal with the separated file with manual files size 10 then 8 then 6, taking in consideration that liability of those files to separate increases as the size decreases.

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Caldwell-Luc Operation

Definition:

It is a radical operation in the maxillary sinus performed through the oral vestibule.

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Indications:

1. Inflammatory Condition: ex. Chronic Maxillary Sinusitis.

2. Cystic Condition: ex. Removal of Antral Polyps and Cysts & Antro-Choanal polyps

3. Neoplastic Condition: Benign and Malignant Lesions.
A. Benign lesion:
· Odontogenic: Ameloblastoma & Adenomatoid Odontogenic Tumor.
· Non-Odontogenic: Osteoma & Polyp.
B. Malignant Lesion:
· Squamous Cell Ca
· Minor salivary Gland Tumor
· Adenoid Cystic Ca

4. Miscellaneous:
· Removal of any root fragments or, Antrolith
· Zygomatico-maxillary fracture involving the floor of the orbit & anterior wall of maxillary sinus
· Management of hematoma in the maxillary sinus· Closure of mouth-sinus communications (oro-antral fistulæ)
· Removal of antral mucocœles
· A route to the ethmoid and sphenoid sinuses.
· Visualisation of the orbital floor for decompression.
· Vidian (nerve of the Pterygoid Canal) neurectomy.
· Access to the pterygo-maxillary fossa (the space behind the maxillary sinus).

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Contraindications:
1. Not performed in patients below 17 years of age as there may be damage developing tooth bud in that region.
2. Acute Infection.
3. Systemic Diseases.

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Technique / Procedure:

1. Anesthesia: GA preferred.
2. Incision of anterior wall of maxilla especially over the canine fossae, the incision should be semi lunar or, U shaped.
3. Removal of bone & window creation, the breadth of the window should be not less than the diameter of an index finger.
4. With the help of a periosteal elevator & curator, the whole lining of the antrum will be excised along with the lesion (depending upon the type of lesion, fresh bone may need to cut
5. Debridement.
6. Irrigation with normal saline.
7. Drainage by naso antral tube, this is called antrostomy
8. Sometimes ribbon gauze impregnated with antibiotic solution or, paste is placed & removed gradually (within -5 days) to facilitate healing.

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Another Technique: (Endoscopic Entry):

1- First an opening is punched from the mouth into the maxillary sinus with a special instrument.
2- The surgical instruments can then be passed through this opening.
3- Then the endoscope is passed into the maxillary sinus via the nose so that the operator can obtain a good overview of the sinus.
4- Altered mucosa is removed by means of the instrument which is inserted in the maxillary sinus via the opening in the mouth.
5- In addition the opening of the sinus to the nose is enlarged in order to allow for better ventilation since this promotes the postoperative healing of the sinus.

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Complications:

Common Complications:

1- Facial swelling
2- numbness of the face (infra-orbital neurapraxia). This is numbness of the cheek and not weakness, which always occurs temporarily but rarely persists.
3- numbness (temporary / permanent) of the upper teeth and the associated Gingivae.

Less Common Complications:
1- Oro-Antral Communication / Fistula)
2- Post-Operative Nosebleeds (Epistaxis)
3- Overflow of Tears (Epiphora) due to blockage of the tear duct.
4- Tooth root injury leading to tooth death (Devitalisation) & Tooth Discoloration

Rare Complications:
1- Facial asymmetry due to persistent facial swelling.
2- Prolonged Maxillary Sinusitis.
3- Post-Operative bleeding from the sinus / nose requiring packing of the sinus / nose or even a blood transfusion.
4- Infection of the Naso-Lacrimal Sac (Dacryocystitis)
5- Post-Operative hypersensitivity or 'Burning’ pain over the cheek, Gingivae or teeth. (hypæsthesia / dysæsthesia of the Infra-Orbital Nerve).
6- Blindness (if the eye socket is entered) & reduced sharpness of vision & movement of the eye (ocular dysfunction).

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Medication:

Analgesic, Antibiotic, Anti-Histamin and Corticosteriods.

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Denture Support, Retention and Stability

Denture Stability: It's the resistance of the denture against Any-Direction movement.
Denture Retention: It's the resistance of the denture against movement away from the tissues.
Denture Support: It's the resistance of the denture against movement toward the tissue.

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Denture Support:
- Periodontal Ligament around the natural teeth should be 2.5 times more than the complete denture bearing area on the mucosa.

- To achieve the best support for the denture, try to make a maximum area as much as possible.

- The Primary Support Areas are:
A- Mandible: Buccal Shelf of bone and Retromolar Pad.
B- Maxilla: Horizontal Portion of the hard palate.

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Denture Retention:
- The Primary Retention methods are:
A- Border Sealing of the Denture.
B- Neuromascular Control.
C- Physical (Adhesive) forces: Salive-Denture base and Saliva-Mucosa.

- The Criteria of the great retentive force are:
A- The Salive film covers the whole surface area of the denture.
B- The Denture Base extends the full length in the sulcus.
C- Border Seal prevent the ingress of the saliva and air.

- Elements of the great retentive force are:
A- Total Surface area. (More surface area=More retention)
B- Viscosity of the saliva. (More Saliva Viscosity=More retention)
C- Distance between the denture base and the mucosa. (More Distance=Less retention)

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Denture Stability:
- Factors affecting the Denture Stability:
A- Denture Base Adaptation.
B- Ridge Anatomy.
C- NeuroMascular Control.
D- Occlusal Harmony.

- Ridge Anatomy effect the Denture Stability By:
A- Large, Square and Broad Ridges.
B- Steep Palatal Vault.
C- Firm Vs. Flabby Ridges.

- NreuroMascular Control effect the Denture Stability By making the denture borders to be polished to allow the tongue, cheek and lips to seat the denture during function.

- Occlusal Harmony effect the Denture Stability By:
A- Bilateral, simultaneous posterior tooth contacts in retruded jaw relationship.
B- Free of the Occlusal interferences.
C- Acceptable level of the mandibular occlusal plane.
D- Teeth set close to the natural teeth position.

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Denture Stomatitis (Denture Sore Mouth)

Definition:
- Denture-related stomatitis indicates an inflammatory process of the mucosa that bears a complete or partial removable dental appliance, typically a denture.
- It was known as: “chronic denture palatitis”, “stomatitis prothetica”, “denture related candidiasis” “denture-induced stomatitis” and “denture stomatitis”.
- The denture stomatitis occurs with patients of partial denture less than patients of complete denture.
- No racial or sex predilection exists.
- It can affect as many as 35-50% of persons who wear complete dentures.
- Denture sore mouth is common, but rarely sore.
- Caused mainly by a yeast (Candida) that is a normal inhabitant in the oral cavity, and it's not a transmitted disease.
- It can predispose to angular chelitis.
- It has no serious long-term consequences

Clinical Picture:
- Occurs in the maxilla more than the mandible, where the washing affect of salive is greater in the mandible.
- The Denture-induced stomatitis is assymptomatic, but patients may complain of halitosis, slight bleeding and swelling in the involved area, or a burning sensation, xerostomia, or taste alterations (dysgeusia).

Classification (Stages):
suggested by Newton in 1962, and states:
- Newton´s type I: pin-point hyperaemic lesions (localized simple inflammation)
- Newton´s type II: diffuse erythema confined to the mucosa contacting the denture (generalized simple inflammation)
- Newton´s type III: granular surface (inflamatory papillary hyperplasia)

Related disorders:
May be accompanied with other disorders of the same origin (Fungal), ex:
- Angular cheilitis
- Median rhomboid glossitis
- Candidal leukoplakia.

Aiteology:
The aetiology is best considered Multifactorial, but wearing the denture in the night is the major causitiva factor.
Other factors are:
1. Prosthetic factors:
- No denture stomatitis can exist without a prosthesis.
- Prosthetic traumatism is favoured by denture functional deficiencies

2. Infectious factors:
- The dentures can accumulate bacteria and yeasts, that cause the ecological changes:
- Bacteria proliferate: Staphylococcus species, Streptococcus species, Neisseria species, Fusobacterium species. or Bacteroides species has been identified in patients with denture stomatitis.
- Candida species, particularly Candida albicans, have been identified in most patients. Patients with denture stomatitis show higher intraoral concentrations of fungi than individuals without this disorder.

Predisposing factors:

1. Systemic factors
a. Physiological. (advanced age)
b. Endocrine dysfunctions.
c. Nutritional deficiencies.
d. Neoplasias.
e. Immunosuppression.
f. Ample spectrum antibiotics.

2. Local factors
a. Antimicrobials and topical or inhaled corticosteroids
b. Carbohydrate rich diet
c. Tobacco and alcohol consumption
d. Hyposalivation
e. Deficient oral hygiene
f. Wearing dentures (especially through the night)

Diagnosis:
- Clinical presentation of erythema and oedema on the palatal mucosa covered by the denture base (but not beyond) is a diagnostic finding.
- Take a smear of the palate to check for presence of Candida species, by staining with KOH, periodic acid-Schiff or by imprint cultures.
- Blood tests, microbiological studies or biopsy may be required.

Prevention:
• A routine basis inspection of the oral cavity for screening for this disorder, even when the lesions are asymptomatic.
• Properly denture sanitization and perform good oral hygiene
• Appropriate denture-wearing habits, instructing the patient to take his/her denture out of the mouth for 6-8 hours each day
• Patients with partial dentures should undergo periodic professional plaque control

Treatment:
• Good oral hygiene is mandatory.
• Local factors which promote growth of yeasts, such as smoking or wearing the dentures throughout the night, must be discouraged.
• Dentures should be removed for as long as possible and definitely overnight.
• Dentures should be brushed in warm, soapy water and soaked overnight in an antiseptic solution such as bleach, chlorhexidine or in any solution suitable for sterilizing baby´s feeding bottles.
• Denture fitting and occlusal balance should be checked to avoid trauma. A new prosthesis should be made, if necessary.
• Newton`s type I and II denture stomatitis have been successfully treated with low energy lasers to reduce inflammation of the supporting mucosa, Inflammatory papillary hyperplasia usually needs to be surgically removed before the denture is placed, and mild cases may respond to antifungal treatment.

• Antifungal medications are recommended when yeasts have been isolated, or when lesions do not resolve with hygiene instructions.

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Trismus

Introduction:

Trismus is a common presentation by the patient in routine dental practice. This condition causes difficulty in opening mouth which in turn impairs eating, interferes with oral hygiene, restricts access for dental procedures, and may adversely affect speech and facial appearance.

Trismus has number of potential causes and it’s important to recognize the underlying cause for effective management of this condition

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Definition:

Trismus in greek is Tonic contraction of the muscles of mastication.

The Normal Mouth Opening Range:
Range- 40-60 mm (avg-35mm)
Males display greater mouth opening

The Normal Lateral movement is 8-12 mm

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Causes Of Trismus (Etiology)

Several conditions may cause or predispose an individual to develop Trismus.

1. Intra-Articular Causes:

A- Ankylosis
B- Arthiritis Synovitis
C- Meniscus Pathology

Ankylosis:
- True Bony Ankylosis: can result from trauma to chin, infections and from prolonged immobilization following condylar fracture
Treatment- several surgical procedures are used to treat bony ankylosis, Eg: Gap arthroplasty using interpositional materials between the cut segments.

- Fibrous Ankylosis: usually results due to trauma and infection
Treatment- trismus appliances in conjunction with physical therapy.

Trismus Appliances:

Indications:
A- Intracapsular (TMJ) pathosis
B- Bony interferences from styloid or coronoid process
C- The presence of foreign body
D- Muscle fibrosis or immature scar tissue

Types Of Trismus Appliances:

A- Externally activated appliances
- Dynamic bite opener
- Threaded, tapered screw
- Screw type mouth gag
- Fingers
- Tongue blades
- Continuous-dynamic jaw extension apparatus.

B- Internally activated appliances

- Tongue blades
- Plastic tapered cylinder

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2. Extra-Articular Causes:

A- Infection
B- Dental treatment
C- Trauma

D- TMJ Disorders
E- Tumors and Oral care
F- Drug Therapy:
G- Radiotherapy and Chemotherapy
H- Congenital / Developmental Causes:
I- Miscellaneous disorders

A- Infection
Odontogenic- Pulpal
- Periodontal
- Pericoronal

Non-Odontogenic- Peritonsillar abscess
- Tetanus
- Meningitis
- Brain abscess
- Parotid abscess

The hallmark of a masticatory space infection is trismus. Or infection in anterior compartment of lateral pharyngeal space results in trismus. If these infections are unchecked, can spread to various facial spaces of the head & neck and lead to serious complications such as cervical cellulitis/ mediastinitis.
Treatment- Elimination of etiologic agent along with antibiotic coverage

Trismus or lock jaw due to masseter muscle spasm, can be a primary presenting symptom in tetanus, Caused by clostridium tetani, where tetanospasmin (toxin) is responsible for muscle spasms.
Prevention- primary immunization (DPT)

B- Trismus Related To Dental Procedure:
Oral surgical procedures- extraction of lower molar teeth may cause trismus as a result either of inflammation involving muscles of mastication or direct trauma to the TMJ
Inaccurate positioning of the needle when giving inferior alveolar nerve block before extraction
Barbing of needles at the time of injection followed by tissue damage on withdrawal of the barbed needle causes post-injection persistent paresthesia, trismus and paresis
Treatment- in acute phase
Heat therapy
Analgesics
A soft diet
Muscle relaxants (if necessary)
When acute phase is over the patient should be advised to initiate physiotherapy for opening and closing mouth.

C- Trauma:
Fractures, particularly those of the mandible and Fractures of zygomatic arch and zygomatic arch complex,Accidental incorporation of foreign bodies due to external traumatic injury
Treatment- fracture reduction, removal of foreign bodies with antibiotic coverage

D- TMJ Disorders:
Extra capsular disorders – myofacial pain
Intra capsular problems – disc displacement, arthritis, fibrosis etc
Acute closed locked conditions – displaced meniscus

E- Tumors And Oral Malignancies:
Rarely, trismus is a symptom of nasopharyngeal or infra temporal tumors/ fibrosis of temporalis tendon, when patient has limited mouth opening, always pre malignant conditions like oral sub mucous fibrosis (OSMF) should also be considered in differential diagnosis

F. Drug Therapy:
Succinyl choline, phenothiazines and tricyclic antidepressants causes trismus as a secondary effect. Trismus can be seen as an extra-pyramidal side-effect of metaclopromide, phenothiazines and other medications.

G. Radiology / Chemotherapy:

- Complications of Radiotherapy:
1. Osteoradionecrosis may result in pain, trismus, suppuration and occasionally a foul smelling wound.
2. When muscles of mastication are within the field of radiation, it leads to fibrosis and result in decreased mouth opening.
- Complications of Chemotherapy:

Oral mucosal cells have high growth rate and are susceptible to the toxic effects of chemotherapy, which lead to stomatitis.

H. Congenital / Developmental Causes:
Hypertrophy of coronoid process causes interference of coronoid against the anteromedial margin of the zygomatic arch.
Treatment-Roronoidectomy
Trismus-pseudo-camtodactyly syndrome is a rare combination of hand, foot and mouth abnormalities and trismus.

I. Miscellaneous disorders
- Hysteric patients: Through the mechanisms of conversion, the emotional conflict are converted into a physical symptom. Eg: trismus

- Scleroderma: A condition marked by edema and induration of the skin involving facial region can cause trismus

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Camphorquinone (CQ)

 - It is a photo-initiator that triggers polymerization of light-curing materials such as dental adhesives and composites.
- CQ does not become a part of the polymer network, suggesting that CQ can be leached out into surrounding environment including dental pulp and exert adversary effects on tissues.
- CQ treatment increases the levels of proinflammatory cytokines (eg, interleukin 6, interleukin 8, and matrix metalloproteinase-3 [MMP3].
- CQ also inhibits odontogenic differentiation and mineralization capacities of DPSC and MC3T3-E1 cells.
- CQ may trigger pulpal inflammation.
- Yellow coloured CQ influences the colour of the composite.
- Amines (Part of the CQ structure) also form by-products during photoreaction and can tend to cause yellow or brownish discolourations under the influence of heat or light.
- The researchers tried to solve the CQ's aesthetics, biocompatibility and toxicity issues, so that they decided to substitute the "simple amines" with polymeric or macromolecular amines.
- CQ can be replaced by polymeric radical photoinitiators carrying the photosensitive CQ groups in the side chain.
- Acylphosphine oxides such as Lucirin TPO are the most common available used commercial products.

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Dental Abscess

Definition:
Abscess is a (semi) liquid collection of pus lined by granulation tissue (if acute) or granulation tissue and fibrosis (if chronic).

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Pathological features:
- Contain PMNs/macrophages, lymphocytes (live and dead), bacteria (dead and viable), and liquefied tissue substances.
- May lead to rupture (‘pointing’), discharge into another organ (fistula formation), or opening onto an epithelial surface (sinus) .
- Incomplete treatment due to resistant organisms (myocbacteria) or poor treatment may lead to a chronic abscess.
- Complete elimination of the organisms in a chronic abscess without drainage can lead to a ‘sterile’ abscess (‘anti-bioma’).

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Typical causes:
- Suppuration of tissue infection (e.g. renal abscess from pyelonephritis).
- Contained infected collections (e.g. subphrenic abscesses).
- Haematogenous spread during bacteraemias (e.g. cerebral abscesses).

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Diagnosis:
Deep abscesses are characterized by swinging fever, rigors, high WCC, and i CRP. Untreated they lead to catabolism, weight loss, and a falling serum albumin. Ultrasound, CT, MRI, or isotope studies may be necessary to confirm the diagnosis.

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Treatment:
- Drain the pus e.g. incision & drainage (perianal abscess), radiologically guided drain (renal abscess), closed surgical drainage (chest empyema), or surgical drainage and debridement (intra-abdominal abscess).
- IV antibiotics (course may be prolonged).

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Amelogenesis Imperfecta

Definition:
Amelogenesis imperfecta is a tooth development disorder in which the teeth are covered with thin, abnormally formed enamel.

Amelogenesis imperfecta presents with abnormal formation of the enamel.
Enamel is composed mostly of mineral, that is formed and regulated by the proteins in it.
Amelogenesis imperfecta is due to the malfunction of the proteins in the enamel: ameloblastin, enamelin, tuftelin and amelogenin.
People afflicted with amelogenesis imperfecta have teeth with abnormal color: yellow, brown or grey.
The teeth have a higher risk for dental cavities and are hypersensitive to temperature changes.
This disorder can affect any number of teeth.

Types:
1- Hypoplastic AI:
Inadequate deposition of enamel matrix.
Enamel matrix present is normal.
Enamel may be "Thin or Pitted".
The thin enamel may be "Smooth or Rough".
Generalized small pits scattered across surface of teeth or localized large area of hypoplastic enamel typically on the buccal middle third of the tooth.
Smooth enamel exhibits a smooth surface which is thin, hard and glossy or rough.
The enamel is more dense than that of smooth pattern.
Most commonly is autosomal dominant inheritance.

2- Hypmaturation AI:
Adequate deposition and mineralization of enamel matrix but inadequate maturation of crystal structure (mineral).
Soft enamel with similar radiodensity to underlying dentin .
Pigmented enamel has mottled , brown appearance .
Snow-Capped Teeth: Zone of opaque white enamel on the incisal / occlusal end of the teeth

3- Hypocalcified :
No mineralization occurs.
Enamel is soft and easily lost.
Enamel is dull, lustreless, opaque white, honey or browned colour.
Enamel and dentin appear radiographically indistinct.

4- hypomaturation hypoplastic:

Causes:
Amelogenesis imperfecta is a hereditary Disorder.

Symptoms:
The teeth enamel become soft and thin.
The teeth appear yellow.
The teeth become easily damaged.
Both baby teeth and permanent teeth are affected.

Differential Diagnosis:
The most common differential diagnosis with the Amelogenesis Imperfecta is the Dental Fluorosis.
- The variability of the fluorosis make it very difficult to differentiate.
- It varies from mild white "flecking" of the enamel to profoundly dense white colouration with random, disfiguring areas of staining and hypoplasia.
- Requires careful questioning to distinguish from Amelogenesis Imperfecta.
- Fluorosis may present with areas of horizontal white banding corresponding to periods of more intense fluoride intake and may show the premolars or second permanent molars to be spared (chronological distribution).
- The history will often reveal excessive fluoride intake either in terms of a habit such as eating toothpaste in childhood, or related to a local water supply.

Treatment:
The treatment depends on the severity of the problem.
The treatment starts from simple composite restorations until a Full crown restorations that will improve the appearance of the teeth and protect them from damage.
Treatment is often successful in protecting the teeth.
The teeth may have to be extracted and implants or dentures are required.
Generally, treatment is veneers , full coverage , overdenture, full denture or extraction and implant.

Complications:
The enamel is easily fractured and damaged, which affects the appearance of the teeth, especially if left untreated.

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Post-Operative Instructions Following Tooth Extraction

When the dentist perform an extraction, healing process after an extraction must be as comfortable as possible.

The removal of teeth is a surgical procedure, and post-operative care is imperative.
Your patient has to follow all instructions carefully to avoid any unnecessary pain and possible infection.
Inform your patient in case of any difficulties or concerns following the extraction, he/she has to call you or return to your clinic for a follow-up exam.

Immediately Following Surgery the instructions are:

1. Place gauze pad over the surgical area with slight pressure by biting down to stop bleeding.
2. Use the prescribed analgesics once the pain starts to raise up.
3. Do not suck on a straw, spit, or smoke.
4. Restrict your activities the day of surgery, and resume normal activity when you feel comfortable.
5. Place ice packs on the side of your face where surgery was performed.
6. For mild discomfort, use Ibuprofen (Advil, Motrin). DO NOT take more than 800mg every 4-6 hours.
7. Vigorous mouth rinsing or touching the affected area following surgery should be avoided. This may initiate bleeding caused by dislodging the blood clot that has formed.
8. Do not rinse your mouth for the first post-operative day or while there is bleeding.
9. After the first day, use a warm salt water rinse every 4 hours and after meals to flush out particles of food and debris that may lodge in the area.
10. Restrict your diet to liquids and soft foods which are comfortable for you to eat.
11- Tell the patient to start brushing teeth from next day, gently in the area of extraction and normally in the rest.

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Diagnostic Tests Of Dental Pain

There are several simple tests that may assist in diagnosis of dental pain.

- Pulp Sensitivity Test:
This test can be done by using cold or hot stimuli.
Cold Stimulus is done by using Dry ice, or an ordinary ice stick that is placed in the cervical region of the tooth to detect posibility of pulpal inflammation.
Hot Stimulus is done by heating an instrument and placing it to one of the tooth surfaces.
In both of them, if pain occured and faded away once removing the stimulus indicating healthy tooth, if pain occured and persisted for a few minutes indicating inflammed pulp that must be treated endodontically and if the pain didnt occure indicating a necrotic pulp.

- Percussion Test:
Using an instrument handle, the tooth is tapped in the longitudinal axis. A painful response suggests possible periapical inflammation. (ex: Apical Periodontitis)

- Probing:
Placing a fine, blunt probe (Periodontal Probe) gently into the gingival sulcus surrounding the tooth to check the health of the gingival tissues. Bleeding and/or sulcus depths greater than 3-4 mm indicate a periodontal disease and a pocket which then should be diagnosed to have periodontal treatment.

- Mobility Test:
Holding a tooth firmly on the buccal and lingual sides between a finger and a solid instrument enables mobility to be assessed.
All teeth have a small amount of mobility (<0.5 mm) (Normal Or Mild Movement),
The teeth with movement of (0.5-2 mm) should be splinted (Moderate Movement),
While the teeth with (Severe Movement) of (2-4 mm) should be treated surgically or to be extracted.

- Palpation:
Careful digital palpation around the area of concern may reveal tenderness and the type and extent of swelling. (Usefull in cases of Tumor or Abscess or Soft Tissue Abnormalities)

- Radiographic Examination:
Sometimes we need a radiographic X-ray to detect some underlying abnormalities and possible pain sources.
We use periapical radiographes to check 3 neighboring teeth together and it's usefull to detect the extent of caries, reccurent caries, periapical lesions, crown root ratio and fructures.
We use orthopantomograph (OPG) to check the upper and lower full teeth set and neighboring important structures for abnormalities and possible causes of pain and it's very usefull in cases of impacted teeth, relation between upper teeth and maxillary sinus and presence of oral lesions in bone.

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Oral Herpes Simplex

Etiology:
Herpes virus hominis, Most commoly type I virus, but approximately 10% are thought to be caused by Type II.

Clinical Forms:
- Oral Herpes Simplex occurs in three clinical forms:
1- Recurrent small blisters on the lips commonly referred to as fever blisters or secondary herpes labialis. (most common form).
2- Generalized oral infection called primary herpetic stomatitis.
3- Small ulcers usually localized on palatal mucosa. (least common form).

Treatment:
- Antiviral drugs such as Acyclovir, Famciclovir, Penciclovir, Valacyclovir and over-the-counter Abreva have all shown that they can decrease the time of disease as well as help with pain management.
- Treatments that suppress the immune system abnormalities may improve more severe lesions and lessen pain.

Prognosis:
- Primary infection usually resolves in 10-14 days. Once the virus has entered the body, it travels through nerve trunks to the nearest ganglion where it may lie dormant for the remainder of the patient’s life.
- The Recurrence occured by “reawakening” of the virus, not reinfection from the outside.
Patients should drink liquids to prevent dehydration, should take a broad-spectrum antibiotic to control secondary bacterial infection, but does not shorten the viral infection. Antiviral drugs may shorten the duration of the disease if they are started early. (once the symptoms appear).
Clinicians should be aware that the herpes virus may cause disseminated infection including encephalitis in which case the prognosis is extremely grave.

Differential Diagnosis:
- Primary herpetic stomatitis may resemble oral lesions of erythema multiforme, but herpes can be diagnosed by exfoliative cytology.
- Lesions of herpangina and hand, foot and mouth disease, both caused by Coxsackievirus, may clinically resemble oral herpes virus infections.
- Recurrent intraoral herpes may be confused with herpes zoster.
- Aphthous Ulcer can be differentiated since it usually does not occur over bone, does not form vesicles and is not accompanied by fever or gingivitis.

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Dental Numbering Systems

 1- Universal Numbering System:

((Primary Teeth))

---Beginning with the upper right "E" designated by letter A -----> J
---Beginning with the left lower "E" molar designated by letter K---->T

((Permenant Teeth))

---Starting with upper right third molar, starts with number 16 -----> 1 , since (1) resembles upper left third molar.
---Starting with lower left third molar Teeth are numbered 17 ----> till 32

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2- Palmer Natation System:

((Primary teeth))-Now used-
---For each quadrant, number teeth as (A, B, C, D, E)

((Permenant teeth))
---For each quadrant, Number teeth as (1, 2, 3, 4, 5, 6, 7, 8)

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3- Federation International "Two digit system" (FDI)

In this system ...
-1st digit indicates quadrant, where (1--->4) refers to permenant jaws, While (5--->8) refers to primary jaws.

-2nd digit refers to the tooth number from (1--->8) in permenant teeth, and (1--->5) in primary teeth.

So as for the first digit:
1 ----> Refers to upper right quadrant
2 ----> upper left quadrant
3 ----> lower left quadrant
4 ----> lower right quadrant
5 ----> upper right quadrant(In Primary teeth)
6 ----> upper left quadrant(Primary)
7 ----> lower left quadrant(primary)
8 ----> lower right quadrant(primary)

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How To Use ProTaper Endodontic Files

ProTaper geometries:

The Endodontic ProTaper files have a unique features, including:

- Changing percentage tapers over the length of its cutting blades.
- The progressively tapered design replicates the Schilderian Envelope of Motion technique and serves to significantly improve flexibility, cutting efficiency, and safety.
- They are convex, triangular cross-section, which enhances the cutting action while decreasing the rotational friction between the blade of the file and dentin.
- They have a changing helical angle and pitch over their cutting blades, which reduces the potential of an instrument from inadvertently screwing into the canal.
- The noncutting, modified guiding tip. This feature allows each instrument to safely follow the secured portion of a canal, while the small flat on its tip enhances its ability to find its way through soft tissue and debris.
- The ProTaper system is comprised of three Shaping and five Finishing files

Types Of Protaper Endodontic Files:

There are two types of files for the ProTaper Endodontic Files;
"The Shaping Files" and "The Finishing Files" ...

The Shaping Files:

- Shaping Files are Two: File No. 1 & File No. 2, Termed S1 & S2, Purple and White Respectively.
- The Auxiliary Shaping File, termed SX, has no identification ring on its gold-colored handle and, with a shorter overall length of 19 mm.
- The S1 and S2 files have D0 diameters of 0.17 mm and 0.20 mm, respectively, and their D14 maximal flute diameters approach 1.20 mm.
- SX File, provides excellent access when space is restrictive. The SX file has a D0 diameter of 0.19 mm and a D14 diameter approaching 1.20 mm.
- The Shaping files have increasingly larger percentage tapering, allowing each instrument to engage, cut, prepare and shape the canal, performing its own 'crown down' work.
- SX File has a much quicker rate of taper between D1 and D9 as compared to the other ProTaper "S files", it is primarily used after the S1 and S2 files to more fully shape canals in "coronally broken down" or "anatomically shorter" teeth.

The Finishing files:

- There are five "Finishing files" named F1, F2, F3, F4, and F5 have yellow, red, blue, double black, and double yellow colores corresponding to D0 diameters and apical tapers of 20/07, 25/08, 30/09, 40/06, and 50/05, respectively.
- From D4–D14 each instrument has a decreasing percentage taper which serves to improve flexibility, reduce the potential for dangerous taper-lock, and reduce the potential to needlessly overenlarge the coronal two-thirds.

ProTaper shaping technique:

- First, one should know that: The potential to consistently shape canals and clean root canal systems is significantly enhanced when the coronal two-thirds of the canal is first pre-enlarged, followed by preparing its apical one-third.

Scout the coronal two-thirds:

- "Hand files" sizes 10 and 15 are measured and precurved to match the anticipated full length and curvature of the root canal.
- The 10 and 15 hand files may be utilized within any portion of the canal until they are loose and a smooth reproducible glide path is confirmed.
- The loose depth of the 15 file is measured and this length transferred to the ProTaper S1 and S2 files.

Shape the coronal two-thirds:

- The secured portion of the canal can be optimally pre-enlarged by first utilizing S1, then S2. Prior to initiating shaping procedures,
- The pulp chamber is filled with a full strength solution of NaOCl.
- Without pressure, the ProTaper Shaping files are inserted into the canal and follow the glide path freely and easily.
- For more optimize safety and efficiency, the Shaping files are used, like a brush, creating lateral space, which will make the Shaping file’s larger, stronger, and of more active cutting blades.
- N.B: this brush-cutting action can be used to:
Eliminate cervically positioned triangles of dentin,
More effectively shape into fins, isthmuses, and canal irregularities, and
To relocate the coronal aspect of a canal away from furcal danger.
- N.B: If any ProTaper File ceases inside the secure Portion of the canal, then withdraw it and know that the debris blocked the intrablade spaces making the walls push the file away and decrease the cutting effeciency.
- N.B: Upon removing each Shaping file, visualize where the debris is located along its cutting blades to better appreciate the region within the canal that is being prepared.
- Following the use of each Shaping file, irrigate, recapitulate with a 10 file to break up debris, and move it into solution, then re-irrigate.

Scout the apical one-third:

- The apical one-third of the canal is fully negotiated and enlarged to at least a size 15 hand file, Working length confirmed, then the patency file is established.
- NOW, A decision must be made between whether to finish the apical one-third with rotary or hand instruments.
- If, a new size 15 hand file glide easily inside the canal without any interupption, this means that the canal if of normal shape and having no irrigularities and anatomical morphologies, then the Rotary ProTaper will be very good, easy and successfull.
- While If, a size 10 or 15 hand files must be precurved and necessitate a reciprocating handle motion, then the Manual ProTaper File is the best and most successful choice.

Shape the apical one-third:

- Vigorous irrigation with NaOCl is very important now, to remove the debris that may decrease the effect of the shaping files (discussed befor in "Shape the coronal two-thirds" section), to avoid blockage of canals and facilitate the shaping proccess.
- The ProTaper sequence is to carry the S1, then the S2, to the full working length.
- Float, follow, and brush (discussed befor in "Shape the coronal two-thirds" section) until the terminus of the canal (Apical Foramen) is reached.
- S1, then S2, will typically move to length in one or more passes depending on the length, diameter, and curvature of the canal.
- Following each ProTaper file, irrigate, recapitulate with a size 10 file, then re-irrigate.
- After using the Shaping files, particularly in more curved canals, working length should be reconfirmed, as a more direct path to the apical foramen has been established, leading to decrease working length.
- The preparation can be finished using one or more of the ProTaper Finishing files in a non-brushing manner.
- The F1 is selected and passively allowed to move deeper into the canal, in one or more passes, until the terminus is reached.
- Apical flutes are inspected, and if they are loaded with dentin, then visual evidence supports, the shape is cut.
- After using the F1 file, Irrigate with NaOCl, recapitulate, confirm patency, then re-irrigate to liberate debris from the canal.

ProTaper finishing criteria:

- Following the use of the Protaper File F1, the ProTaper Finishing Criteria is to gauge the size of the foramen with a Manuale file 20 to determine if this instrument is snug or loose at length, If the 20 hand file is snug at length, then the canal is fully shaped and, if irrigation protocols have been followed, ready to pack.
- if the 20 hand file is loose at length, then gauge the size of the foramen with a 25 tapered hand file. If the 25 file is snug at length, then the canal is fully shaped and ready to pack.
- If the 25 file is short of length, proceed to the Protaper File F2 and, when necessary, the Protaper File F3, the Protaper File F4, and the Protaper File F5, gauging after each ProTaper Finisher with the same D0 correspondingly sized hand file.
- If the 50 hand file is loose at length, then use alternative NiTi rotary or manual files to finish the apical extent of these larger, easier, and more straightforward canals.

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Medications Used In Dentistry

Introduction to dental medications.

Dental Work as other medical fields , requiring application of therapeutics to treat, control, prevent, .... etc conditions.

Here, we are going to talk about different medications, drug classifications, doses, side effects, Interactions, brand names, ... etc.

the dental field contains a lot of diseases, Syndromes, Conditions altering the treatment modality and requiring different drugs, so that there are a lot of drugs to the dentist that may prescribe, furthermore, there are a lot of drugs that the dentists should know as they cause conditions in oral cavity, leading to a diagnosis of medical condition in the patient Or even may have interactions with drugs you're welling to prescribe.

Drugs used in dentistry are a lot, simply, can be classified into:

• Medications used to control pain and anxiety
• Analgesics
• Antibiotics
• Anesthetics
• Medications used to treat dental infections
• Antifungals
• Other dental medications

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Chapter One: Medications used to control pain and anxiety

Dental treatment includes pain, In almost all the procedures ex: reduction, cavity preparation, surgery, sublingual scaling, … etc., then, the dentist should be care about this point, because, the dental Client (Patient) who comes to the dental office seeking treatment is almost nearly 90% afraids from what is called a dentist, then it becomes one of the most important success factors of the dentist in his work in the point of view of the patient is feeling comfortable in treatment without pain. AS one of the most reported Complication by clients is PAIN.

Dental Procedures is then accompanied with control of pain and sedation, with different procedures, including psychological control of pain, medication, anesthesia, sedation, Anxiety reduction protocol, and much more.

Here In this article we will discuss those drugs that include control of pain and anxiety, but NOW in this part of the article we will discuss the general view of the next chapters.

Several medications are available to help create more relaxed, comfortable dental visits. Some of the medications make the client feel no pain during the treatment, while the others can make him relax and others make him sleep completely.

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How can we choose the way to control pain and anxiety for the Client?

First of all, the dentist should discuss with the patient the procedures that will be done, the overall health of the client, history of allergies and your anxiety level befor any approach is to be chosen.

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Basics to follow when choosing drug for relieving pain.

Analgesics are the drugs that are used for relieving pain, the Minor dental procedures (Non-surgical) requires a little relieving drugs, so the Non-narcotic are the drugs of choice, while the more invasive surgical procedures including oral and maxillofacial surgeries requires the narcotic analgesics as it works in the CNS (will be discuss later in the Chapter Three).

Before the dental procedure is to take place, the dentist should decide to put the client in the status of “FREE OF PAIN” then the anesthesia should be taken in consideration. The Anesthesia is classified into local and general anesthesia, while most of dental procedures requires the local, then it be used in almost all the cases, but the general anesthesia will be used in Oral and Maxillofacial surgeries, in completely un-cooperative patients or for child patient where the cavity preparation is nearly impossible.

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What is the Anxiety and how it can be controlled?

Anxiety is a psychological and physiological state characterized by somatic, emotional, cognitive, and behavioral components.[2] It is the displeasing feeling of fear and concern. (Wikipedia)

Anxiety can be controlled by the anti-anxiety drugs, such as nitrous oxide, or by sedatives, tranquilizers, Or By Anxiety reduction Protocol And can be classified as:

1- Benzodiazepines
2- Sedatives – Hypnotics
3- Anti-histaminics

All act as Anti-anxiety, anti-convulsant, sedative-hypnotics and skeletal muscle relaxants.

1- Benzodiazepines are a lot: but what are used in dentistry are:

+Diazepam (Valium)
+Chordiazepoxide (Librium)
+Oxazepam (serax)
+Lorazepam (Ativan)
+Flurazepam (Dalman)

2- Sedatives and hypnotics are: Barbiturates and non-Barbiturates.

+Barbiturates are: Pentobarbital, secobarbital, phenobarbital, methohexital.

3- Anti-histaminics are: Benadryl, Phenergan, Atarax & Avil.

Anxiety Reduction Protocol (Most Commonly Used with Oral & Maxillofacial Surgeries):

- Before appointment

• Hypnotic agent to promote sleep on night before surgery (optional)
• Sedative agent to decrease anxiety on morning of surgery (optional)
• Morning appointment and schedule’s so the reception room time is minimized

- During appointment

• Non-pharmacological means of anxiety control
A- Frequent verbal reassurances
B- Distracting conversation
C- No surprises (Clinicians warns patients before doing anything that could cause anxiety)
D- No unnecessary noise
E- Surgical instruments out of patient’s sight
F- Relaxing background music

• Pharmacological means of anxiety control
A- Local anesthetics of sufficient intensity and duration
B- Nitrous oxide
C- Intravenous anxiolytics.

- After Surgery

• Succinct instructions for postoperative care
• patient information on expected postsurgical sequelae (e.g, swelling or minor oozing of blood)
• Further reassurance
• Effective analgesics
• Patient information on who can be contacted if any problem arise
• Telephone call to patient at home during evening after surgery to check whether any problems exist.

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Chapter Two: Analgesics

What are the Analgesics ... ?

The Analgesics are those drugs that elevate the pain threeshold above the subcortical level.
- Analgesics is a british word means painkilling.

What are the Classifications of analgesics:
Narcotics - Non-Narcotics.

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- Non-Narcotic Analgesics are:

A- NSAIDs
B- Anti-Pyretics

A- NSAIDs are :- analgesic, anti-pyretic, Anti-inflammation & Anti-Rheumatics

1- Aspirin( Acetyl Salicylic Acid) Works as Peripheral Vasodilatation and works on hypothalamus to decrease prostaglandin to decrease pain and inflammation.
2- Ibuprofen*
3- Zombirac*
4- Diflunisal* are: Derivative of salicylic Acid
5- Piroxicam*
6- Diclofinac*
* (( Such As NSAIDs in Properties ))

B- Anti-Pyretics is those drugs that acts as analgesics and Antipyretics such as ( Acetaminophen ) and it's an aspirin substitute.

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Narcotic Analgesics: Work on narcotic receptors on CNS.

- Morphine ia the drugs of choice in cases of: Post-operative pain, Accidental pain or traumatic pain.

Examples:

1- Methadone: Adult Dose 2.5-10 mg ( Not For Children under 18 years old )
2- Meperidine: Adult Dose 50-100 mg
3- HydroMorphine: Adult Dose 2 mg ( 8 times more potent than Morphine )
4- Codeine: Adult Dose 15-60 mg ( drug of choice used for cough suppression )

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Chapter Three: Antibiotics

1-Prophylactic antibiotics used before dental surgeries.
2-Commonly used antibiotics in dentistry.
3-Dental Concerns for uses of anti-infective agents

- Prophylactic Antibiotics Used Before Dental Surgeries-

* Only In the following conditions, Prophylactics antibiotics are recommended in order to avoid endocarditis

-- Prosthetic cardiac valves (High risk of endocarditis)
-- Surgically constructed pulmonary shunts (High Risk)
-- Previous Bacterial Endocarditis (High Risk)

-- Valvular Dysfunctions (Moderate Risk)
-- Hypertrophic Cardiomyopathy (Moderate Risk)
-- Mitral Valve Prolapse (Moderate Risk)

These Risks In these cases are in those dental procedures:

-- Dental Extractions.
-- Periodontal Surgeries.
-- Implant Procedures.
-- Re-implantaion Of avulsed teeth.
-- Endodontic instrumentation beyond the apex.
-- Subgingival Procedures.

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:: World Of Dentistry :: TEAM

Dental Caries

Index:

Part 1 = Introduction - Definition.
Part 2 = Classification Of Caries.
Part 3 = Factors Influencing Caries Etiology.
Part 4 = Histopathology Of Dental Caries.
Part 5 = Clinical Diagnosis Of Dental Caries.
Part 6 = Management of Deep Dental Caries.
Part 7 = Sequence of Dental Caries.

Introduction - Definition

What is Dental Caries:

It is a disease of microbial origin in which the dietary carbohydrates are fermented by the bacteria forming an acid which causes the demineralization of the inorganic part and disintegration of the organic part of the tooth.

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Classification Of Caries:

A. According to number of surfaces involved:

1) simple (1 surface involved)
2) compound (2 surfaces involved)
3) complex (2 surfaces involved)

B. According to anatomic site:
1) occlusal (pit-and-fissure) caries
2) smooth-surface caries (proximal and cervical caries)
3) root caries

C. According to histology:
1) enamel caries
2) dentinal caries
3) cemental caries

D) According to severity:
1) incipient caries
2) occult caries
3) cavitation caries

E) According to onset:
1) primary (virgin) caries
2) secondary (recurrent) caries
3) residual caries

F) According to duration:
1) acute (rampant)
2) chronic

G) According to chronology:
1) early childhood caries
2) adolescent caries
3) senile caries

H) According to progression:
1) arrested caries
2) recurrent caries
3) radiation caries

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Factors Influencing Caries Etiology.

A)Host factors:

1) tooth factors:
a. Composition surface enamel due to dense
mineralization and high F-
content more resistant to caries than
subsurface layers of enamel.

b. Morphology more chances of caries if deep ,
narrow occlusal fissures or buccal or lingual pits present

2) saliva factors:
a. composition
a1) inorganic less chances of caries if higher Ca2+
and PO43- concentration
a2) organic less chances of caries with higher
ammonia and urea content

b. pH decrease in pH of saliva below 5.5 (ka critical
pH) predispose to caries.
The remarkable buffering-capacity of saliva (due to HCO3-H2CO3 and phosphate buffer systems) controls the marked fall in pH, thus preventing caries formation.

c. Position more chances of caries if malaligned , rotated teeth.

d. quantity decreased amount or absence ( xerostomia)
increases the risk of caries.

e. viscosity

f. antibacterial properties: due to the presence of lysozyme (cleaves the N-acetyl glucosamine and N-acetyl muramic acid components of bacterial cell wall) and salivary peroxidase system ( salivary peroxidase and thiocyanateSCN- components of saliva interferes with glycolytic pathway of bacteria)

3) systemic factors:
a) heredity
even though no strong evidence has been found connecting caries-susceptibility with heredity, studies have shown
“high DMF” father and “high DMF” mother produced offspring with a “high DMF” rate
And “low DMF” parents produced offspring with “low DMF” rates.
b) Pregnancy and lactation
despite the popular belief, there is NO evidence suggesting increase in caries in pregnancy (unless the mother has neglected her general oral health care).

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B) Diet factors
a. physical nature of diet
person taking food with more fibre-content less
susceptible to caries than those taking soft, refined
(worse if sticky) food

b. local factors

b1) carbohydrate content
though all forms of fermentable sugar leads to caries , there is always a higher risk of caries with free sucrose than starches.
Because sucrose in addition to its acid- byproduct produced during fermentation also aids in plaque development and adherence of cariogenous microbes to the tooth surface.
However starches due to large molecular structure, shows limited diffusion and hence can not directly enter the plaque .

b2) vitamin content
vitamins like (vit.D, vit.K and vit.B6) have been found to decrease the incidence of caries,
vit. B-complex deficiency has shown decrease in the rate of caries
whereas even though it is well-established that vit C-deficiency causes severe periodonta land pulpal changes , no evidence of decrease in caries by Vit C-supplement has been reported.
however a more extensive study to confirm the link between vitamins and caries is still desireable.
b3) fluorine content
even though there is reduced incidence of caries with F-in drinking water, there is no significant caries reduction with dietary fluoride (because of its metabolic unavailabilty).

C) Cariogenic potential of the microorganism

Available data strongly suggest an active involvement of Streptococcus mutans in caries initiation (especially in pit and fissure caries, and smooth-surface caries; and to some extent the root surface caries)
On the other hand, oral actinomyces like
Actinomyces viscosus, and
Actinomyces neslundii, have a more important role in root surface caries.
Also A. neslundii, Lactobacillus spp. And other filamentous rods have been implicated in dep dentinal caries.

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Histopathology Of Dental Caries

Enamel is composed of tightly packed hydroxyapatite crystals, which are organized in long columnar rods (enamel rods), but during caries progression certain histological changes are seen in enamel .

The following 4 histological zones of an enamel lesion clearly explains the development of enamel caries

zone 1 translucent zone
zone 2 dark zone
zone 3 body zone
zone 4 surface zone

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Zone 1 translucent zone
Deepest zone representing the advancing front of enamel caries.
In this zone , pores or voids form along the enamel prism(rod) boundaries (due to easy H+ ion penetration)
It appears structureless when perfused with quinolone solution (having refractive index comparable to that of enamel) and seen with polarized light (hence translucent)

Zone 2 dark zone
Next deepest zone
Presence of many tiny pores block light transmission. These smaller air or vapor-filled pores make the regiion opaque.
Loss fo crystalline structure suggesting the process of demineralization and remineralization in this zone.

Zone 3 body zone
In demineralization phase, it is the largest portion of the lesion.
(whereas in remineralization phase, zone2dark zone is the largest portion which increases in the expense of the “body zone”)
Largest pores seen (pore volume 5 to 25%)
Presence of bacteria if pores large enough to permit their entry
Striae of Retzius well marked
(striae of Retzius is the primary point of entry of carious lesion into rodprism cores of enamel)

Zone 4 surface zone
Relatively unaffected by caries (only partial demineralization)
Because surface of enamel is relatively immune to caries (due to hypermineralization- because of saliva contact , and
higher surface F-content)
Also pore volume is lower than the body of lesion.

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After the involving the enamel, the carious lesion progresses to the dentinal structure.
Caries advancement in dentin proceeds through 3 stages:

1) demineralization of dentin (by weak organic acids)
2) degeneration and
dissolution of organic material of dentin , mainly collagen
fibers (type I)
3) bacterial invasion after the loss of structural integrity caused
due to 1) and 2).

During the development of dentinal caries, clinically 5 different zones of progression can be seen (ac to Sturdevant )
zone 1 normal dentin
zone 2 subtransparent dentin
zone 3 transparent dentin
zone 4 turbid dentin
zone 5 infected dentin

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Histologically , 5 zones of early dentinal caries progression can be seen (listed pulpally to occlusally)
zone 1 zone of fatty degeneration of Tomes’ fibers
zone 2 zone of dentinal sclerosis
zone 3 zone of decalcification of dentin
zone 4 zone of microbial invasion
zone 5 zone of decomposed dentin

Zone 1 zone of fatty degeneration of Tomes’ fibers
the most advancing front of dentinal caries characterized by the presence of a layer of fat globules ; hence stains red with the stain, sudan red.
significance

1) fat layer leads to impermiability of the dentinal tubules (DT) – trying to prevent further invasion of  carious lesion
2) favors sclerosis of dentin in zone 2.

Zone 2 zone of dentinal sclerosis
layer of sclerotic dentin which appears white in transmitted light
calcification of DT as a rxn of vital pulp and vital dentin to carious invasion , so as to prevent further penetration of microorganisms.
formation of this zone is minimal in rapidly progressing caries, and prominent in slow caries.

Zone 3 zone of decalcification of dentin
this zone lies above the zone of sclerotic dentin
initial decalcification of only the walls of the DT
presence of PIONEER BACTERIA- first of the microorganisms penetrating DT before there is any clinical evidence of caries.
bacteria present in individual DT are in pure form (i.e. either completely cocci or completely bacilli; not in mixed form)

Zone 4 zone of microbial invasion
in a layer above zone 3.
characterized by the presence of microorganisms in early stage of caries- acidogenic microorganisms in deeper layer- proteolytic microorganisms replace acidogenic bacteria supports the hypothesis that initiation (by acidogenic bacteria) and progression ( by proteolytic microorganisms ) are 2 distinct processes in caries development.

During initiation phase- in the early stage when caries is not deep , acidogenic bacteria predominant which utilizes carbohydrate for their metabolism
Later in progression phase – as the caries goes deeper , less and less of carbohydrate substrate available , hence acidogenic bacteria are replaced by proteolytic microorganisms which uses dentinal protein for their metabolism.

Zone 5 zone of decomposed dentin
Most superficial zone of early dentinal caries.
no recognizable structure in decomposed dentin

collagen and minerals seem to be absent
great number bacteria dispersed in this decomposed granular matter.

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Clinical Diagnosis Of Dental Caries

By one or all of the following:
1) Visual changes in tooth surface texture or color
2) Tactile sensation with judicious use of explorer
3) Radiographs
4) Transillumination
Aided by the knowledge of the probability of overall caries risk and patterns of susceptibility.

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A) Diagnosis of Pit and Fissure Caries:

Any one or more of the following:
1) Softening at the base of pit and fissure
2) Opacity surrounding the pit or fissure, indicating demineralization of enamel
3) Brown-gray discoloration radiating peripherally from the pit or fissure
4) Softened enamel that may be flaked away by explorer radiolucency beneath the occlusal enamel surface

B) Diagnosis of Proximal Surface Caries:

1) Visual – white chalky appearance or shadow under the marginal ridge
2) Tactile- probing with explorer on proximal surface may detect cavitation, which is defined as the break in the surface contour of enamel
3) Radiographic diagnosis- made with bitewing radiographs which show radiolucency beneath the enamel surface in the proximal area (should not be confused with cervical burnout!)

Arrested Lesions on Proximal Surface:
1) Appears as brown spots
2) On probing, surface is intact and hard
3) Radiograph shows decreased radiographic density in the affected region
4) Usually seen in old patients

Proximal Surface in Anterior Teeth:
1) Transillumination- in which light source directed through the tooth from the lingual side. Proximal surface caries, other than incipient caries, appear as a dark area along the marginal ridge
2) Tactile- exploration to detect any cavitation
3) Radiographs – may detect any small incipient lesion as well.

C) Diagnosis of Smooth Surface caries on the Facial and Lingual surfaces (Usually Gingival)

Initial phase :
1) CHALKY-WHITE, OPAQUE AREAS (“WHITE SPOTS”) over the smooth surface of the tooth, that is visually different from adjacent translucent enamel , which is revealed only when the tooth surface is clean and dry and disappears partially or totally when the tooth is wet . This initial phase of caries in enamel is k/a “incipient caries”.
The tooth at this stage appears to have lost its translucency because of extensive subsurface porosity due to demineralization.
2) Undetectable tectilely since surface is hard , intact and smooth.

Advanced Phase:
1) White to dark brown discoloration
2) Demineralized and softness to penetration

Arrested Lesion:
1) Dark, discolored areas mostly due to extrinsic staining
2) Hardening of lesion (due to remineralization)
3) Sclerotic or eburnated dentin

D) Diagnosis of Root Surface Caries:

1) Look for the following features at CEJ or more apically on cementum
early stage-
a) Well-defined discoloration adjacent to gingival margin,
typically near the CEJ
b) Softened cemental tissue compared with adjacent structure
advanced stage- softening on exploration
and cavitation.

2) Usually in older individuals , or in patients who has undergone perio- surgery , with the following predisposing factors
a) Cemental exposure
b) Dietary changes
c) Systemic diseases
d) Medications that affect amount and character of saliva.

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 Management of Deep Dental Caries

A) Chemical Measures For Caries Control:
Use of:

1) Substances which alter the tooth surface or tooth structure

a) Fluoride Exposure Application
Fluoridation of water supply ( with 1 ppm of F-)
Topical application of fluoride

i) Self-application
- Low dosehigh frequency rinses
(0.05% NaF daily)
- High potencylow frequency rinses
(0.2% NaF weekly)
- Fluoridated Dentifrices Toothpastes
(twice daily)
ii) Professional Application
- acidulated phosphate fluoride gel (APF gel)
(1.23% annually or semi-annually)
- NaF solution (2%)
- stannous fluoride (8%)

b) Bis-biguanides ( like chlorhexidine , alexidine)

c) Silver Nitrate

d) Zinc Chloride and Pottasium Ferrocyanide Solution

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2) Substances Which Interfere With Carbohydrate Degradation Through Enzymatic Alteration:

a) Vitamin K – Use of Synthetic Vit K (2-methyl-1,4-naphtoquinone)
b) Sarcoside - Na Lauroyl Sarcosinate,
Na Palmitoyl Sarcosinate,
Na Dehydro Acetate

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3) Substabces Which Interfere With Bacteria Growth And Metabolism:

a) Urea and Ammonium Compounds
b) Chlorophyll
c) Penicillin
d) Other antibiotics ( erythromycin, kanamycin, spiromycin, tetracycline, tyrothricin, vancomycin)
e) Caries vaccine
f) Nitrofurans – furacin, furadroxyl

B) Mechanical Measures For Caries Control:

1) Dental Prophylaxis (routine scaling and polishing)
2) Toothbrushing
3) Mouth Rinsing
4) Dental Floss
5) Oral Irrigators
6) Chewing Xylitol Gums (for 5 to 30 mints after meal)
7) Detergent Foods in Diet (hard, fibrous foods)
8) Pit and Fisure Sealants

C) Nutrietional Measures For Caries Control:

1) Diet Counselling
2) Restriction of Soft, Sticky Refined Carbohydrate Intake
3) Limiting in Between Meals.

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Sequence of Dental Caries

The Dental Caries can cause DEATH !!!

- First of all, We should know that the caries is the most common infectious disease for the humans.
- The Caries is a bacterial infection, which occurs briefly due to bacteria that ferment the carbohydrates to produce the Lactic acid which causes the demineralization of the enamel surfaces, causing the decay and cavities.
- The Caries may extend deeply into the tooth layers, to reach the dentin layer, which is sensitive, causing the tooth pain.
- Then the bacteria will penetrate the dentinal layers soon if neglected to reach the pulp chamber (or horns), causing the pulpitis, which will start as reversible OR irreversible.
- The Bacteria may drown deeply inside the pulp chamber to reach the orifices of the pulp causing pulp inflammation that would, if neglected, cause partial pulp necrosis that requires partial pulpectomy to manage.
- Then, the bacteria drown inside more deeply that will necrose the rest of the pulp canals causing complete pulp necrosis, then the patient will feel no pain.
- In this stage, the tooth is most commonly ( Badly Decayed ) and black in color, the patient may no seek dental help because he/she suffers of no pain, this neglection will cause the next serious step, which is the periapical abscess.
- The Periapical Abscess may be acute, because of the sudden increase of the pathogens strength or sudden decrease of the host immunity, causing pain specially during biting and percussion.
- And the periapical abscess may become chronic soon or after, if the immunity increased or the pathogens strength decreased, to wall of the infection.
- The chronic abscess may exacerbate to transform the chronic abscess into acute painful one again that leads the patient to seek dental help.
- The infection may then spread to the facial spaces, lower molars may spread infection to the submandibular and sublingual spaces, while the anterior teeth may spread this infection to the submental space.
- The neglected infection may spread to the spaces causing facial cellulitis and subsequent Ludwig's angina that may be fatal.

So, Caries may Lead to DEATH !!!

This Article Has Been Authored By :: World Of Dentistry :: TEAM