Dens in Dente

Dens invaginatus, dens in dente or tooth with in a tooth is a rare developmental anomaly. In it, the lingual pit is extended deep in to the crown or root, in later instance causing pulpitis. It is mostly seen in the maxillary lateral incisors but may be found in any anterior tooth.

Dens in Dente-lateral incisors

The cause of dens in dente in not known but role of genetic factor can not be established. In early stage, it can be treated by filling or endodontic treatment, if pulp is involved.

A. showing Type I Dens Invaginatus in lateral incisors. Note- periapical cyst. B. Type II dens invaginatus in second premolar and C. Type III dens invaginatus in mandibular canine. [1]

Ref: 

1. https://www.omicsonline.org/scientific-reports/srep147.php

Hypertension

The 2017 ACC/AHA guideline for high BP in adults provides four BP categories based on the average of two or more in-office readings on 2 or more occasions:

• Normal: Lower than 120 mm Hg systolic BP (SBP) and 80 mm Hg diastolic BP (DBP).
• Elevated: 120–129 mm Hg SBP and lower than 80 mm Hg DBP.
• Stage 1 hypertension: 130–139 mm Hg SBP or 80–89 mm Hg DBP.
• Stage 2 hypertension: Higher than or equal to 140 mm Hg SBP or 90 mm Hg DBP.

Ameloblastoma

Ameloblastoma is a rare head and neck tumor with an estimated annual incidence of 0.5 per million population. They constitute 1% of tumors and cysts involving the jaws and accounts for approximately 10% of the odontogenic tumors. Ameloblastomas are originated from the epithelial lining of odontogenic cysts, enamel organ or dental lamina, stratified epithelium of oral cavity or displaced epithelial remnants. They are primarily seen in adults during the third and fourth decade of life with no gender preference and more frequently located in the mandible (80%), especially in the angle and ascending ramus [1].

Even though they are benign and slow-growing lesions, ameloblastomas exhibit locally destructive behavior with a high recurrence rate. Thus, most relapses (50% and even over 80%) occur during the first 5 years after the primary surgery. The major contributing factor for recurrence seems to be the inadequate initial surgical procedure rather than the histological type [1].

Radiographic Features

Radiographically, ameloblastoma typically forms round, cyst-like, radiolucent area with well-defined margins. The smallest lesions appear unilocular; whereas larger ameloblastoma may comprise a few large clustered cysts, giving 'soap-bubble’ or 'multilocular appearance' or  ‘honeycomb’ appearance (Fig 1) Expansion of the lesion may be on both, lingual and buccal side.

Fig. 1. Ameloblastoma: multilocular appearance

Differential Diagnosis

Other multilocular lesions that may mimic ameloblastoma radiologically include odontogenic keratocyst, giant-cell granuloma and odontogenic myxoma. Ameloblastoma with a single bony cavity simulate many types of cyst and tumour radiographically.

Treatment

The surgical options for ameloblastoma vary from simple enucleation (with or without bony curettage) to radical excision.

Ref: 

1. Medina A, Velasco Martinez I, McIntyre B, Chandran R. Ameloblastoma: clinical presentation, multidisciplinary management and outcome. Case Reports Plast Surg Hand Surg. 2021;8(1):27-36. Published 2021 Feb 22. doi:10.1080/23320885.2021.1886854

Supernumerary Teeth

Extra numbers of teeth are known as supernumerary teeth. When they are present in the anterior maxilla in midline, they are known as mesiodens. When the extra teeth are present in the molar region as fourth molar, they are known as paramolar teeth. The anterior midline of the maxilla is the most common site whereas the maxillary molar area is the second most common site for supernumerary teeth.

Supernumerary tooth-mesiodens in anterior mandible in midline [1]

Radiograph showing mesiodens in anterior maxilla [1]

The investigation involves routine blood examination and IOPA or OPG radiographs. Depending on the anticipated level of difficulty of the surgery, additional investigations may be advised.

Treatment involves surgical extraction.

Ref:

1. Oral pathology clinical pathologic correlation, Regezi, Sciubba, Jordan 4th Ed Saunders

Oral Candidiasis

Oral candidiasis is a fungal disease that is caused by Candida albicans. It looks like a white  or creamy plaque or patch that can be wiped off with the help of a cotton swab or a tooth brush leaving a red base.

Gingival thrush

It occurs due to disturbance in the oral microflora due to antibiotics, corticosteroid, Xerostomia , immune defects especially in HIV infection, immunosuppressant, leukaemia or lymphomas and diabetes. It rarely occurs in a healthy individuals except in neonates.

Chronic mucocutaneous candidosis: note the wide adherent plaque.

Gram stain smear shows the Candida albicans hyphae. It should be differentiated from Koplik's spot or Fordyce's granules.

The treatment involves treating the cause. Antifungal agents, for example, nystatin oral suspension or pastilles, amphotericin lozenges, or miconazole gel or tablets or fluconazole tablets can be given.

Ref:

1. Oral diseases 2nd Ed. Crispian Scully, Roderick A. Cawson Churchill Livingstone

Malocclusion

MALOCCLUSION

Proposed by Edward H. Angle in 1890, the Angle Classifications are based on the relationship of the buccal groove of the mandibular first permanent molar and the mesiobuccal cusp of the maxillary first permanent molar. This classification is considered to be one of the most commonly used as its easy to use.

Bleeding Disorder

 Bleeding disorders: dental considerations

Acquired or congenital bleeding disorders of dental treatment concern include haemophilia, von Willebrand disease, other factor deficiencies and thrombocytopenia. Some systemic conditions also interfere with haemostasis, such as kidney, liver and bone marrow disorders.

Patients with bleeding disorders should be managed in a specialist setting, with appropriate consultation with the patient’s specialist or multidisciplinary team.

Bleeding Disorders

1. haemophilia

2. von Willebrand disease

3. Other factor deficiencies 

4. thrombocytopenia

Causes

Bleeding disorder may be due to defect in platelet activation, function and contact activation.  It may also be due to defect in clotting proteins or antithrombin function. 

The commonest caused of bleeding disorder are 

1. warfarin
2. von Willebrand disease

3. aspirin

Warfarin is the commonest anticoagulant that interferes by preventing the production of clotting factors by blocking vitamin K.

von Willebrand disease is the most common inherited bleeding disorder.

Aspirin is the less commonly used drug for pain and more used in long term for its impairing ability for platelet function. One tablet of aspirin renders the platelet non-functional for almost one week. It is to be noted that it rarely causes significant post-operative bleeding.

How to confirm bleeding disorder of a patient

The single most important evaluation part is an adequate history since screening tests for bleeding disorders do not always detect mild defects. A history suggestive of a bleeding tendency must be taken seriously. History of previous dental extraction or tonsillectomy provide a useful guide. Physical examination is also necessary and for conformation of diagnosis, laboratory test are needed.

An accurate diagnosis is essential for replacement therapy, if needed and enable other management protocols to be followed.

The dentist must place special emphasis on the following that are suggestive of bleeding disorder:

1. deep haemorrhage into  muscles, joints or skin (bruising)-suggests a clotting defect
2. bleeding from or into skin or mucosae-suggests purpura
3. most congenital bleeding disorders of significance become apparent in childhood
4. however, mild haemophilia might escape the history part until the adult life if the child and the parents have managed well and avoided the injuries. A mild haemophiliac might give a history of mild oozing from an extraction socket for 2-3 weeks despite all local measures such as pressure pack and suturing etc
5. history of blood transfusion or hospitalization might clearly give the idea of bleeding disorder in the same as a history of bleeding in a blood relative
6. history of drugs such as anticoagulant, certain herbal products, systemic disease, for example, cirrhosis, HIV and kidney diseases can also impair platelet function 

Congestive Heart Failure

Congestive heart failure or heart failure occurs when the heart muscle weakens and doesn't pump enough blood as it should. When this happens, blood often backs up and fluid can build up in the lungs, causing shortness of breath.

Certain heart conditions, for example, coronary artery disease or high blood pressure, gradually leave the heart too weak or stiff to fill and pump blood properly. 

Signs and symptoms of congestive heart failure 

• Shortness of breath with activity or when lying down
• Fatigue and weakness
• Swelling in the legs, ankles and feet
• Rapid or irregular heartbeat
• Reduced ability to exercise
• Persistent cough or wheezing with white or pink blood-tinged mucus
• Swelling of the belly area (abdomen)
• Very rapid weight gain from fluid build-up
• Nausea and lack of appetite
• Difficulty concentrating or decreased alertness
• Chest pain if heart failure is caused by a heart attack

Prophylactic antibiotic regimen for infective endocarditis in dental procedures

Antibiotic prophylaxis is recommended for invasive dental procedures that involve the manipulation of gingival tissue or periapical region or perforation of the mucosa when performed on high-risk individuals. Australian guidelines have provided a list of dental procedures that are likely to cause a high incidence of bacteraemia that always require prophylaxis. These are as follows:

• Tooth extraction.
• Periodontal surgery, subgingival scaling and root planning.
• Replantation of avulsed teeth.
• Other surgical procedures such as implant placement or apicoectomy.

Procedures that cause a moderate incidence of bacteraemia might be considered for prophylaxis if multiple procedures are being conducted, in cases where the procedure is prolonged, or in the setting of periodontal disease.

Antibiotic prophylaxis is not recommended for procedures with a low possibility of bacteraemia such as:

• Local anaesthetic injections.
• Dental X-rays.
• Treatment of superficial caries.
• Orthodontic appliance placement and adjustment.
• Following shedding of deciduous teeth.
• After lip or oral trauma.

Patient Selection

The current infective endocarditis/valvular heart disease guidelines [2] state that use of preventive antibiotics before certain dental procedures is reasonable for patients with:

1. prosthetic cardiac valves, including transcatheter-implanted prostheses and homografts;
2. prosthetic material used for cardiac valve repair, such as annuloplasty rings and chords;
3. a history of infective endocarditis;
4. a cardiac transplant with valve regurgitation due to a structurally abnormal valve;
5. the following congenital (present from birth) heart disease:

• unrepaired cyanotic congenital heart disease, including palliative shunts and conduits
• any repaired congenital heart defect with residual shunts or valvular regurgitation at the site of or adjacent to the site of a prosthetic patch or a prosthetic device

AP for a dental procedure not suggested [3]

• Implantable electronic devices such as a pacemaker or similar devices 
• Septal defect closure devices when complete closure is achieved 
• Peripheral vascular grafts and patches, including those used for hemodialysis 
• Coronary artery stents or other vascular stents 
• CNS ventriculoatrial shunts 
• Vena cava filters 
• Pledgets 

Paediatric Patients

Congenital heart disease can indicate that prescription of prophylactic antibiotics may be appropriate for children. It is important to note, however, that when antibiotic prophylaxis is called for due to congenital heart concerns, they should only be considered when the patient has:

• Cyanotic congenital heart disease (birth defects with oxygen levels lower than normal), that has not been fully repaired, including children who have had a surgical shunts and conduits.
• A congenital heart defect that's been completely repaired with prosthetic material or a device for the first six months after the repair procedure.
• Repaired congenital heart disease with residual defects, such as persisting leaks or abnormal flow at or adjacent to a prosthetic patch or prosthetic device[2].

The prophylactic antibiotic should be effective against viridans group streptococci. The guidelines recommend 2 grams of amoxicillin given orally as a single dose 30-60 minutes before the procedure as the drug of choice for infective endocarditis prophylaxis. It has bactericidal activity against streptococci and enterococci. It reaches peak concentrations within one to two hours of oral administration, it has a short half-life of 1.5 hours, but therapeutic levels are maintained for nearly six hours. It has high oral bioavailability. The usual paediatric dosage is 50 mg/kg, with a maximum up to 2 gr. If the patient is unable to take oral medications, parenteral administration of 2 gr amoxicillin or ampicillin is considered as an alternative.

Oral or parenteral administration of cephalexin 2 gr for adults or 50 mg/kg for children, or parenteral administration of cefazolin or ceftriaxone 1 gr i.m./i.v. for adults or 50 mg/kg i.m./i.v for children are other alternatives. Cephalexin can be replaced by another first- or second-generation oral cephalosporin of equivalent dosage.

In patients hypersensitive to penicillin, guidelines are in agreement that the alternative drug of choice is clindamycin 600 mg (15-20 mg/kg up to 600 mg for children). It can be administered orally or intravenously 30-60 minutes before the procedure (as per European association of cardiologist [2], not as per ADA or AHA-see table). Clindamycin is a bacteriostatic protein synthesis inhibitor. Peak serum concentrations are achieved within 45 to 60 minutes after oral administration. Clindamycin is effective against streptococci and methicillin-sensitive staphylococci. However, some studies have questioned the potency of clindamycin prophylaxis. While ESC guidelines recommend solely clindamycin in penicillin-allergic patients, the AHA and Australian guidelines provide a variety of alternatives in this group of patients. The AHA guidelines recommend macrolides, 500 mg of azithromycin or clarithromycin (15 mg/kg for children). The Australian guidelines recommend glycopeptides; however, the ESC guidelines do not recommend glycopeptides and fluoroquinolones due to the lack of evidence on their efficacy. Cephalosporins should be refrained from use in patients who have encountered anaphylaxis, angioedema or urticaria related to penicillins.

It is important to administer prophylaxis before the procedure so that minimal inhibitory concentrations of the drugs will be present from the beginning of the procedure. If the patient cannot receive a prophylactic antibiotic before the procedure, it can be administered up to two hours after the procedure; however, delay in the treatment might lead to increased bacteraemia. If the patient needs multiple interventions, prophylaxis should be repeated with each. It is advised to finish necessary interventions in one or two sessions if possible. Given that consecutive exposures to the same antibiotic increase resistance rates, the healthcare provider might opt to choose different antibiotics for subsequent sessions. These might be the second-line alternative therapies mentioned in the guidelines or administering the patient a combination beta lactamase inhibitor such as amoxicillin-clavulanate or sulbactam-ampicillin. If the patient is already on antibiotic therapy with penicillins, the operation could be delayed until after the cessation of the antibiotic and restoration of the oral flora. If this is not possible, an alternative group of antibiotics could be preferred.

Ref:

1. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-16/vol16no33#:~:text=The%20prophylactic%20antibiotic%20should%20be,choice%20for%20infective%20endocarditis%20prophylaxis.

2. https://www.ada.org/resources/research/science-and-research-institute/oral-health-topics/antibiotic-prophylaxis

3.https://www.ahajournals.org/doi/pdf/10.1161/CIR.0000000000000969

Haemophilia

The laboratory findings in haemophilia will be as follows.

APTT (activated partial prothrombin time) -prolonged

PT (prothrombin time)-normal

BT (bleeding time)-normal [1] or increased [2]

Factor VIII-C- low

Factor VIIIR:Ag [von Willebrand factor] and factor VIIIR:RCo [Ristocetin cofactor]-normal

Ref:

1. Crispian Scully, Roderick A. Cawson Medical problems in dentistry page 142 5th Ed. 
2. https://www.cdc.gov/ncbddd/hemophilia/diagnosis.html