EPIDEMIOLOGY OF DENTAL CARIES 9M*****

  • Dental caries is defined as a chronic infectious disease which results from the demineralization of the inorganic portion and destruction of the organic portion of the tooth. 
  • Epidemiology of dental caries can be studied under the following heading: Host, agent and environment All these factors should react over a period of time for dental caries to occur. 
  • CARIES FORMATION 
    • Substrate (sugar) + microorganism (s.mutans in plaque) = lactic acid = causing demineralization
    • Remineralization = fluoride, calcium, phosphate
      1. Fl = dentifrice
      2. Ca and PO4 = teeth and saliva
  • HOST FACTORS
    • TEETH 
      1. 80% of caries occur on occlusal surfaces
      2. Lower incisors are the least affected teeth 
      3. Malaligned rotated = bristles cannot reach and clean leading to increased caries 
      4. Dentinogenesis and amelogenesis imperfecta = hypoplastic teeth and pitts = more prone to caries
      5. Caries is considered to be bilateral 
    • SALIVA 
      1. COMPOSITION
        1. rich in calcium phosphate and fluoride = decrease in caries
        2. Rich in carbonate = increase in caries attack
      2. pH = 
        1. unstimulated pH is slightly acidic 
        2. High flow rate = pH increases
        3. pH of saliva = main is bicarbonate content 
        4. Sialin, phosphate and ammonia = also determines pH of saliva
      3. QUANTITY 
        1. Normal secretion = 700-800 ml/day 
        2. Aplasia of glands and xerostomia = increase in rampant caries
      4. VISCOSITY 
        1. Mucin responsible for viscous saliva  
        2. Viscosity does not influence caries 
      5. ANTIBACTERIAL PROPERTIES 
        1. Lactoperoxidase = this prevents early microbial colonization of tooth 
        2. Lysozyme = it is a positive enzyme that catalyzed the degradation of negatively charged peptidoglycans matrix of microbial cells 
        3. Lactoferrin = iron binding protein = needed for microbial growth
        4. IgA = inhibits adherence and thereby prevents colonization on mucosal surfaces and teeth by organisms, facilitating their removal of swallowing 
    • AGE = 3 peaks for caries development
      1. 4-8 years = manual dexterity is less
      2. 11 – 19 years = adolescents
      3. 55 – 65 years = root caries
    • Gender = Reasons 
      1. Early eruption of teeth 
      2. More fondness of sweets
      3. Hormonal variations
      4. Morphological differences
    • Familial hereditary 
      1. Good or bad teeth seen in the family 
      2. Morphology, occlusion, salivary flow
    • Emotional disturbances 
      1. Increase stress = decrease salivary flow = increased caries in oral hygiene is not followed 
    • Socio-economic status 
      1. Low SES = increases decayed and increased missing 
      2. High SES = increased filling 
      3. Overall low SES = increase dental caries
      4. Reason = affordability for prevention and treatment 
      5. Caries is considered as disease of poverty
    • TIME FACTOR FOR DEVELOPMENT OF CARIES
      1. Peak susceptibility = 2-4 years after eruption 
  • Agent factors
    • Diet 
    • Organisms = S.mutans = pioneer = acidogenic, aciouric, eat/consume sugar 
      1. Extracellular = dextrans and fructans. Responsible for adhesion on tooth
      2. intracellular polysaccharide = glycogen
    • Lactobacilli = secondary organisms, when caries have reached dentin. It kills all S.Mutans creates an environment of very low pH
    • Veillonella = anti caries organism = consumes acid as food = produced by S.Mutans for demineralization

DIET OF DENTAL CARIES

  1. Diet = it is defined as type and amount of food eaten daily by an individual
  2. Nutrition = defined as seen of the processes by which an individual takes in and utilizes food
  3. Carbohydrates
  1. Organic compound containing carbon, hydrogen and oxygen 
  2. Physical nature of diet = form, clearance, time, retention, oral hygiene
  3. Frequency of carbohydrate diet  
  4. Types 
    1. Monosaccharides = glucose, galactose, fructose
    2. Disaccharides = sucrose [ glucose+fructose]
    3. Polysaccharides = starch, glycogen 
    4. Polyols of alcohol = xylitol, mannitol and sorbitol

Classification of sugars 

Total sugars 

  1. Intrinsic sugar
    1. Sugar molecules inside the cell
  1. Fruit and vegetable
  2. Extrinsic sugar 
    1. Sugar molecules outsides the cell 
    2. Milk sugar = found in dairy products = lactose
    3. Non milk sugar = honey, fruit juices, table sugar = responsible for the caries

PURIFICATION OF WATER at household 4m*

  1. Boiling: 
    1. Very effective method of purification
    2. Boiled or rolled over for 10-20 mins
    3. Taste is slightly altered but harmless
    4. Care should be taken for vessels during storage as there is chance of contamination
    5.  It kills bacteria spores, cysts, ova and also removes temporary hardness by removing carbon dioxide and precipitating calcium carbonate.
  2. Bleaching powder
    1. It contains about 33% of “ active chlorine”
    2. It’s a unstable product
    3. To make it stable = excessive alum is added = chlorinated lime 
    4. On exposure to environment leads to loss of active chlorine
    5. It should be stored in dark and dry place 
    6. It gives pungent smell = hence not routinely used
  3. Chlorine solution:
    1. Prepared from 4 kgs bleaching powder in 20 liters of water
    2. 25% of activate chlorine
    3. But evaporates in the environement = stored in dark, dry and cold place
  4. High test hypochlorite
    1. Calcium compound containing 60 to 70% active chlorine. 
    2. It is stable than bleaching powder and less deterioration 
  5. Chlorine tablets
    1. Available readily in the market
    2. under various trade names like halazone tablets. 
    3. Very economical = formulation used currently was developed by NEERI, nagpur 
    4. 0.5 gm of chlorine tablet for 20 liters of water
  6. Iodine
    1. It is used for emergency disinfection of water. Why?
      1. highly expensive
      2. physiological activity with respect to thyroid
    2. Two drops of 2% ethanol solution of iodine will be sufficient for one liter of clear water 
    3. for a contact period of 20 to 30 min for effective disinfection.
    4. Remains active for longer time 
  7. Potassium permanganate:
    1. This was widely used,but now no longer recommended for water disinfection.
    2. Effective against vibrio cholera but not against other pathogens 
    3. It also alters the color, taste and smell of water.
  8. Filtration
    1. On a small scale, water can be purified by using THREE TYPES OF filters
    2. PASTEUR CHAMBERLAND FILTER = made up of percelian 
    3. BERKEFELD FILTER = made up of kieselguhr or infusorial earth. 
    4. KATADYN FILTERS = silver coating on filters = when bacteria touch silver- it dies due to oligodynamic effect
    5. Heart of the filter is = candle = ONCE PER WEEK 
    6. Wash it under running water using hard brush followed by boiling = to remove impurities clogging the filters 

AUGMENTATION CORONAL TO RECESSION 4m*

  1. Free gingival autograft = give by miller
  2. Free connective tissue autograft = LEVINE
  3. Laterally positioned flap = GRUPE AND WARREN
  4. Semilunar coronally positioned flap = TARNOW
  5. Subepithelial CTG = LANGER
  6. GTR = PINE AND PRETO
  7. Pouch and tunnel technique = AZZI 

Laterally positioned flap

  1. TO COVER isolated areas of recession around a single tooth 
  2. Adequate vestibular depth 
  3. Variant = double papilla flap
  4. Disadv = compromised blood supply 

Coronally positioned flap 

  1. To cover 2-3 mm of recession 
  2. Done on multiple teeth 
  3. Best for maxillary anterior teeth
  4. Pt who have Thick gingival biotype = Good prognosis 

Semilunar coronally positioned flap

  1. Used to cover recession of 1 mm 
  2. Slight recessions in anterior regions 

Subepithelial CTG 

  1. Large and multiple areas of recessions 
  2. NELSON graft = better blood supply = bilaminar or subpedicle CTG 

GTR

  1. Maxillary area only 
  2. 5mm recessions = more than 4.98 mm 

POUCH AND TUNNEL = It allows for CREEPING REATTACHMENT of marginal gingiva.

LASER 

  1. Light amplified stimulated emission of radiation 
  2. RESTING state to emission state. Now it give energy to go back to resting state from emission = CIRCLE FLOWCHART
  3. CO2 and Nd:Yag = mc used
  4. TYPES = soft tissue and hard tissue
Soft tissue Hard tissue
gingiva, tongue, mucosaAffinity towards water and pigmentPrimary effect is heating Diode, Nd:YAG and C02 lasersDiode = 655 – 980Nd;yag = 1064CO2 = 10600enamel and boneAffinity for water and hydroxyapatite’Erbium lasers with wavelength 2780, 2790, 2740
  1. Donot requires LA because laser seals terminal nerve endings 
  2. Less bleeding = because coagulation of blood vessels 
  3. Healing by laser is by secondary intention = scar formation as we dont close wound and no sutures needed 
  4. Hence, For large wounds = less aesthetic 
  5. Healing is slower but less postoperative pain 
  6. Less requirements of medications 
  7. AREAS WHERE LASERS CAN BE USED
    1. Incisions and Excisions = 
      1. disimpaction of third molar = mucopain or benzocaine is applied on mucosa with laser. 
      2. Application of mucoseal = for biopsy 
    2. Dipigemenations 
      1. Gingiva = brownish and blackish 
      2. Melanin = epithelium or superficial layer of connective tissue
      3. Painless procedure 
      4. Heals within 2 weeks and gingiva appears pink 
      5. No bleeding
    3. Pain management
      1. Tmj pain 
      2. Trigeminal neuralgia 
    4. PHOTODYNAMIC THERAPY 
      1. Special use = deep pockets not accessible with instruments and bacteria is still remaining 
      2. Methylene blue or toluidine blue = taken by bacterial cells but not by healthy cells
      3. Laser will generate free radicals = will kill the bacterial cells deep in the pocket 
    5. Low level laser therapy = Triple L 
      1. Fixed wavelength but you can increase the energy source 
      2. More power= more energy = cut faster in thicker tissue. If thin tissue = it leads to charring of tissue 
      3. LLL is used for healing of 
        1. recurrent aphthous stomatitis
        2. herpetic ulcers
        3. Mucositis
        4. lichen planus
        5. pemphigus lesions 
      4. LLL stimulate fibroblasts and collagen fibers = healing potential is increased 

SPLINTS 4m ***** 2m***

  1. Splinting is the process by which you join two or more than two teeth and convert them into rigid and fixed units. 
  2. Hence, this heals the periodontal tissue around the tooth
  3. Objective = Create an environment where tooth movement is restricted within physiological limits = hence improves the function and comfort of the patient 
  4. Rationale = 
    1. to control the forces on teeth and redirect forces on long axis of tooth = most damaging is torsional and horizontal forces 
    2. To establish physiological occlusion 
    3. To serve as stabilizing force
    4. To increase patient comfort when teeth are mobile
    5. To evaluate state of teeth 
  5. INDICATIONS 
    1. To prevent migration of teeth that have been repositioned 
    2. In severe periodontal cases 
    3. In surgical and nonsurgical procedure where teeth are difficult to stabilize 
    4. During orthodontic treatment when you are migrating teeth 
    5. TFO in lower anterior teeth 
    6. Grade 1 and 2 = check and evaluate the mobility status 
  6. CONTRAINDICATIONS
    1. Grade III mobility without eliminating causes such as inflammation
  7. Disadvantage 
    1. Maintenance of oral hygiene is compromised
    2. Phonetics 
    3. Tooth structure loss 
    4. Interproximal wear 
    5. Gingiva and perodontium can be damaged 
  8. BIOMECHANICS 
    1. Convert many mobile teeth into multirooted rigid unit 
    2. Hence, increases area of root resistance 
    3. It alters the center of rotation 
    4. Intrusive forces are tolerated better 
  9. REQUIREMENT 
    1. Have as many firm teeth as possible 
    2. It must not interfere with occlusion 
    3. It must not irritate the pulp 
    4. It must not compromise oral hygiene maintenance 
    5. Interdental embrasure must not be blocked by splint 
    6. Esthetically acceptable 
    7. Must not cause trauma to periodontium 
    8. Easy to fabricate 
  10. CLASSIFICATION 
    1. Temporary = 6 weeks
    2. Provisional = few months -6 months
    3. Permanent 
    4. Intracoronal = Into the enamel = remove the enamel and place the splint 
    5. Extracoronal = over the enamel
    6. According to material
      1. Bonded = with stainless steel wire and composite 
      2. Braided = like sutures

IMPLANTS

  1. Its threaded titanium structure = cover screw
  2. Above it we place abutment and over it we place crown 
  3. We use implant to replace missing teeth 
  4. No PDL around the implant = directly connected to tooth
  5. Biological width around tooth = 2mm 
  6. Biological width around implant = 4 mm 
  7. Implant is made up of bio titanium and alloys like aluminum and validium 
  8. Large surface area of implant is MUST = better connection with bone aka osseointegration = given by BRANEMARK 
  9. Time required for osseointegration = less time in mandible = less than 4-6 months = this time is called Loading time 
  10. Sandblasting or acid etching the surface area = better connection 
  11. Earlier we use plane surface = less surface area than threaded surface 
  12. FACTORS 
    1. Density of bone = less density = Primary stability of implant is less and mobile 
    2. Location of bone and anatomical structures
      1. Posterior mandible = inferior alveolar nerve
      2. Posterior maxilla = maxillary sinus 
      3. Inferior mandible = mental nerve
      4. These structures needs to be avoided when placing the implant 
  13. DRILLING 
    1. First instrument used is PILOT drill of 2 mm  
    2. Minimum diameter of implant = 3.3 mm 
    3. Minimum Length of implant = 8 mm 
    4. Different dimensions based on available bone available by manufactures 
    5. Bone must not overheat = must increase beyond 47*c 
    6. Motor revolutions = 800 -1200 rpm must = below this RPM = heating of bone happens
    7. We also used coolant and irrigant so bone doesn’t overheat 
    8. If bone is overheated = causes necrosis and connection with bone will be impossible 
    9. Bacterial infections and debris must be absent 
  14. 0.5 mm of bone around the implant 
  15. From adjacent tooth = 1.15 mm
  16. Distance between two implants = 3 mm 
  17. 2gm of amoxicillin before 30 mins of implant placing 
  18. If implant is of 4mm size = drill site must be less than 4 mm for tight fit of implant into bone

PERI IMPLANTITIS

  1. Inflammation around loaded implant when its on function and prosthesis attached to it aka crown
  2. Types =
    1. peri mucositis = soft tissues around implant is involved = reversible
    2. Peri Implantitis = hard tissues aka bone around implant is involved = irreversible 
  3. CAUSES
    1. Poor oral hygiene 
    2. Uneven forces
    3. Smoking 
    4. Osteoporosis 
    5. Residual cement 
  4. Signs and symptoms 
    1. Bleeding and redness 
    2. Bone loss around implant 
    3. Probing depth = greater than 5 mm
    4. Pus formation 
    5. Crown is mobile = because abutment is loosening 
  5. If less than 5 mm probing depth, no bone loss and implant made up of titanium = the treatment is 
    1. Scaling 
    2. Antibiotics
    3. 0.2% CHX mouthrinse
    4. If bone loss is 2 mm = we will not open the flap. Same treatment as above
    5. If bone loss = 3-5 mm = crestal bone loss around implant = regenerative surgery needed

What is the prognosis for a cracked tooth?

  1. The prognosis for a cracked tooth is always going to be questionable (Rivera & Walton 2008).
  2. The prognosis is always better if the crack does not extend to the pulp chamber floor (Turp & Gobetti 1996; Sim et al. 2016).
  3. Vital is better than necrotic (Turp & Gobetti 1996).
  4. The quality of the restoration and whether a full coverage crown may cover the crack and other defects are considerations (Rivera & Walton 2008), as is whether an abscess or radiographic rarefaction is present prior to treatment.
  5. These two factors would lower the prognosis of the tooth in question (Berman & Kuttler 2010).
  6. One study found that cracked teeth had a two-year survival rate of 85.5% (Tan et al. 2006).
  7. Another study found that after five years, the survival rate of root-filled cracked teeth was 92%, with the odds of extraction increasing if the cracks were in the root (Sim et al. 2016).
  8. Finally, a recent study from Korea showed a 90%, two-year survival rate for a cracked tooth, probing depths greater than 6 mm being a signifi- cant factor in the prognosis (Kang et al. 2016).

What are the types of cracks one may see in a suspected tooth fracture?

According to the American Association of Endodontics (Rivera & Walton 2008), there are five categories of crack:

  • Craze lines: Only involving the enamel;
  • Split tooth: Complete fracture through the tooth, usually centered mesial to distal;
  • Fractured cusp: Usually non-centered and affect- ing one cusp;
  • Cracked tooth: An incomplete fracture that extends from the crown to the subgingival area of the tooth; and
  • Vertical Root Fracture (VRF):This may be sympto- matic or non- symptomatic.The majority of the VRFs are associated with root-filled teeth. It may be a complete or an incomplete fracture.

How is a fractured tooth diagnosed?

  1. There are multiple ways to determine whether or not a tooth is fractured. It is important to start with a good dental history of the tooth.
  2. A clinical exam should include a bite stick, ice for vitality testing, and a periodontal probing to check for deep narrow pockets.
  3. A radiographic exam is important to check for periapical rarefactions or possibly to reveal a fracture itself if it is large enough.
  4. Finally, a stain (methylene blue), or trans-illumination may be used to visualize the fracture.
  5. Sometimes the tooth may be mobile or a sinus tract may have developed due to fracture necrosis.
  6. If a tooth is non-vital with minimal or no restorations, suspect a crack or fracture (Berman & Kuttler 2010).
  7. The older the tooth, the more susceptible it is to fracture (Berman & Kuttler 2010).
  8. Cracked teeth are more commonly found in lower molars, followed by maxillary pre- molars (Cameron 1976).
  9. Another study found that lower 2nd molars were more likely to have cracks after root canal treatment (Kang, Kim & Kim 2016).