Author: Anisha Valli

SPLINTS 4m ***** 2m***

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  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

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  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

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  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?

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  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?

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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?

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  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).

Osseointegration

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  1. direct structural and functional connection between the implants and the bone. 
  2. [ hemidesmosomes like structures, no CT insertion, no Sharpey’s fibers ] – the first cell to contact the implant is osteoblast 
  3. It’s normal to have up to 2 mm of bone resorption around the neck of the implant in the first year. 
  4. Implants only have a periosteal blood supply
  5. No innervation & no proprioception 
  6. Since implants do not have CT [ no shock absorption ] – if there is any traumatic occlusion or excessive force it will lead to bone resorption [ cervically] or the implant might mechanically fail. 

garden gatekeeper

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I have a little garden of affection, where I feel affection for anyone who steps into that garden. I will be loyal to them, help them if they need it, devote time and attention to them. This garden is (mostly) unconditional; it does not decide who within it gets its fruits, or if they’re worthy enough to eat; the only requirement is to be in the garden.

But my garden has the gatekeeper, who decides who to let into the garden. I might see someone who doesn’t have their shit together, who needs a lot of emotional labor, who might cause me a lot of pain, who I will struggle to understand, and know that I could love and care for them.

The question is not if I have a garden that would accept them, but rather if I want to let them into my garden. My gatekeeper is cold and brutal. It checks how many resources my garden has, how many people are in there already, how sustainable it is. It evaluates potential entries on concrete facts – how emotionally mature are they, how intelligent? How much power do they have? Are they socially strategic to be associated with? Will they increase your garden capacity to hold others in the future?

And so, right now my choices around who new to allow into my garden is associated mainly with an unflattering calculating strategy. My life is a chess game, and these players are the potential pieces.

This is particularly true with my life right now; I’m looking at potential mates as strategic moves. Really I suspect this is what I was doing all along, and likely what many other people are doing, it was just much more subconscious before.

But the gatekeeper itself is not allowed in the garden; once in the garden, the newcomers are free from evaluation. If they drop in power, if they stop helping me, if they start absorbing way more emotional energy, then in my garden they remain; doused in affection and unconditionally accepted.

My garden carries many powerless people from earlier places in my life, or from high-proximity adventures, or people who came in attached to someone else who my gatekeeper wanted more. I am not evaluating them, my love for them is not dependent on what they can offer me; they simply reside in my heart. I have no regrets about this and it’s not an issue for me that my gatekeeper might continue to reject people similar to them.

(also to be clear, the garden analogy isn’t perfect and I’m oversimplifying; people don’t always stay in my garden forever, it’s not exactly binary if you’re in/out of the garden, there are different garden levels, and I don’t think literally everybody would be automatically and unconditionally drowned in affection once they got past the gatekeeper)

Histopathology of Dentinal caries

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  1. As the carious lesion invades dentin, dentinal tubules become involved.
  2. As dentin is part of the dentin pulp complex, it leads to reparative dentine formation.

FIVE PATHOLOGICAL ZONES

  1. Zone 1: Zone of fatty degeneration of Tomes fibers.
    1. Starts at pulp
    2. No fat degeneration (misnomer name)
    3. Alteration by dentin by fat deposition leads to impermeability of tubules which leads to sclerosis 
    4. Sclerosis is reaction between vital pulp and vital dentin
    5. It is the calcification of tubules against further penetration of microorganisms.
  2. Zone 2: Zone of dentinal sclerosis characterized by deposition of calcium salts in dentinal tubules.
    1. Sclerotic zone is minimum in rapidly advancing caries and prominent in slow/chronic caries.
    2. This is a translucent zone due to the vital reaction of odontoblasts
    3. High mineral content
    4. Reflected Light: Appears Dark
    5. Transparent Light: Appears White
  3. Zone 3: Zone of Decalcification of dentin
    1. Tubules are made of pure microorganisms such as pioneer bacteria (Cocci and Bacilli etc)
    2. Intertubular matrix is mainly affected by waves of acid produced by bacteria in the zone of bacterial invasion
    3. Initial decalcification occurs in the wall of tubules. 
    4. Softened infected dentin cannot be differentiated with sterile soft dentine, clinically.
    5. Appears yellow-brown
  4. Zone 4: Zone of bacterial invasion of decalcified but intact dentin.
    1. Bacteria multiply within dentinal tubules.
    2. Acidogenic microorganisms: Seen in early caries
    3. Proteolytic organisms—predominate in deeper layers
    4. It supports the hypothesis that initiation and progression are two distinct processes and must be differentiated
  5. Zone 5: Zone of decomposed dentin.
    1. Bacteria invade both peritubular and intertubular dentin. Hence, Little architecture of dentin remains
    2. Liquefaction foci of miller enlarge and increase in number.
    3. Transverse Clefts: Perpendicular to tubules
    4. Acute Caries: necrotic dentin is very soft and yellowish-white
    5. Chronic Cases: Dentin is leathery and brownish-black

SUGAR SUBSTITUTES

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  1. Xylitol
    1. its 5 carbon sugar
    2. comes from birch trees. 
    3. preferential binding to Mutans strep but it cant ferment xylitol to acid
    4. Hence, no decrease in pH
  2. Sorbitol = caloric sweetness
  3. Aspartans = non caloric sweetener = 4Kcal/g = 200 times sweeter than sugar