Obturation in RCT

Obturation in RCT is the last step of the root canal therapy. It is done when the root canal is bio-mechanically prepared to receive the obturating material and free from infections.

link to 48 week course

 

Following are the eight steps of the Lateral Condensation technique of the obturation for a root canal prepared by step back technique:

  1. Make the canal dry with the help of sterile paper points.
  2. Determine the master cone size of Gutta Percha point and hermetic seal by tug back at the root apex. Note the exact length of master cone in relation to the reference point and mark the master cone.
  3. Tell your dental assistant to mix the root canal sealer up to proper consistency.
  4. Apply the sealer on the entire root canal wall with the help of a lentulo, reamer, file or the master cone itself. Do not use excess sealer.
  5. Insert the master cone up to already working length.
  6. Insert the additional Gutta Percha(GP) points by creating space using finger spreader of appropriate size and length till there remains no space for more G. P. point.
  7. Cut the Excess length of GP points using a scissors. You can cut every GP point immediately after insertion right from the master cone to increase the visibility and clean environment.
  8. Cut the remaining GPs by a red hot instrument (a plastic instrument) at the root canal opening in the cervical region with a clean sweep. Plug the root canal opening by heating and packing the remaining GPs using appropriate ball burnisher.

At this stage, your root canal treatment is complete.

Note: You need to do the needed modifications if you have prepared the canal using Protaper or rotary motor.

Now you need to know, Steps for filling the access cavity, which you can read by clicking here.

 

Article written by Dr. Ajai Singh

Local Anesthesia-Tips

 

Few tips about local anesthesia

Intraoral techniques  for Mandibular Nerve Block:

  1. Gow gates technique
  2. Akinosi technique

Extra oral technique for Mandibular nerve block:

The needle is inserted from below the zygomatic arch. Then it is directed posterior to the lateral pterygoid plate below the foramen ovale.

Extra oral technique for Maxillary nerve block:

The needle is directed anterior to the lateral pterygoid plate into the pterygopalatine fossa.

Except cocaine which is a naturally occurring local anaesthetic agent and vasoconstrictive, all other local anesthetics are synthetic compounds that are vasodilating in nature.

Walking time bomb:

The vasoconstrictive action of adrenaline is augmented when cocaine is used as a local anesthetic agent due to its vasoconstrictive property. So, if cocaine is given as LA agent with adrenaline, the risk of death increases in cocaine users. Therefore, they are known as walking time bombs.

The reaction that occurs in the submucosa at the normal tissue level ph is:

la-break

RN is lipophilic and is responsible for penetration into the nerve. If the tissue ph is decreased due to infection or pus, it results in abundance of H+ ions outside the nerve sheath. Therefore, the equilibrium of reaction in formation of lipophilic molecule (RN) shifts towards left. So, the RN+ fails to enter the nerve and can not block the nerve conduction.

 

Local anaesthetics as an example of the situation above

Local anaesthetics block action potential generated by blocking Na+ channels

Most local anaesthetics  are weak bases, with a pKa between 8 and 9, so that they are mainly but not completely ionised at physiological pH. The un-charged species (B) penetrates the nerve sheath and axonal membrane and is then converted to the BH+ active form, which then blocks the Na+ channels. Increasing the acidity of the external solution would favour ionisation and render local anaesthetics ineffective.

LOCAL ANAESTHETICS ARE INEFFECTIVE IN INFECTED TISSUE (ACIDIC).

Quaternary derivatives of local anaesthetics (Q+) do not work when applied outside but can block channels if introduced directly into cytoplasm.*

 

Nitrous Oxide Gas

  • 5-25%- causes moderate sedation, diminution of fear and anxiety, marked relaxation.
  • 25-45%- causes dissociation sedation and analgesia, floating sensation, reduced blink rate, euphoric state (laughing gas).
  • 45-65%- causes total anesthesia, complete analgesia, marked amnesia.
  • 45-65%- causes total anesthesia, complete analgesia, marked amnesia.

Advantages of addition of vaconstritive agent (Adrenaline) with local anesthetic agent:

  • Prevents rapid absorption of the local anesthetic agents and thus increases the concentration at the site of action.
  • Prolongs the duration of action
  • reduced absorption rate and increased efficiency in small doses of LA results in reduced toxicity of the LA agent.
  • Reduced bleeding in the area of surgery.

Types of local anesthetic block:

Nerve block- local anesthetic agent is deposited near main trunk of the nerve. e.g. Inferior nerve block, blocks sensation of all the teeth of the lower jaw including the labial buccal mucosa anterior to the mental nerve.

Field block-local anesthetic agent is deposited near the large branch of the peripheral nerve; e.g. mental nerve block.

Local infiltration- local anesthetic agent is deposited near the small nerve endings; e.g. Deposition of LA agent near the root apex of lower central incisor.

 

*Source: http://www.frca.co.uk/article.aspx?articleid=220

Diabetes Mellitus-Complications

Diabetes Mellitus-Complications

The association of sever periodontitis and diabetes mellitus is very strong and complex.

periodontitis
Improved condition of gingiva after one week period of scaling.

The periodontitis is a chronic inflammatory disease characterized by the destruction of supporting structures of the teeth, the periodontal fibers and alveolar bone. It is a highly prevalent disease. Severe periodontitis is prevalent in 10-15% of the population. It affects the quality of life adversely.

 

Epidemiological studies have shown that Diabetes is a major risk factor for periodontitis. Susceptibility to develop periodontitis increases approximately three folds if a person becomes diabetic.

It has been proved that there is a direct correlation between the severity of hyperglycemia and the severity of the periodontitis. The mechanism that plays role in this interaction has not been fully deciphered. It has been shown through few experiments that the defective neutrophil function, immunologic malfunctions and cytokines do play their roles. Emerging evidences show that the diabetes does have a role in the increase in the severity of periodontitis; and the inflammatory process of periodontitis makes the glycemic control difficult. Therefore, it is a two way relationship.

Not only the diabetes makes the periodontitis worst, but it becomes friend with the periodontitis when it comes to damage the other body organs. The incidence of end stage renal disease and macro albumin urea increases three times and two times respectively in diabetic individuals with severe periodontitis than those diabetic patients without severe periodontitis. Furthermore, the risk of having cardio-renal mortality (like ischemic heart disease and diabetic nephropathy combined) increases three folds in diabetics with sever periodontitis than diabetics without severe periodontitis.

Studies have shown that the treatment of periodontitis results in approximately 0.4% reduction in the level of HbA1C. The oral and periodontal health promotion should be made the integral part of the diabetes management.

Further Reading