Oral Leukoplakia

Oral leukoplakia

Oral leukoplakia (OL) is a clinical term for a nonremovable white lesion that is not easily recognisable as any particular condition and therefore requires further investigation.

Oral leukoplakia manifests as patches that are bright white and sharply defined. The surfaces of the patches are slightly raised above the surrounding mucosa.

Oral leukoplakia may be homogenous (uniform lesion often with a fissured surface), or nonhomogeneous (with surface irregularity and textural or colour variation for example speckled-see below given photograph.

Oral Lichen Planus

Oral Lichen Planus on left mucosa [1]


Question: What is oral lichen planus?

Answer: It is a chronic inflammatory condition that affects the skin, nails, hair, and mucous membranes, characterised by purplish, itchy, flat eruptions.


Question: How common is the condition?

Answer: It is a common condition in India. Its cases are reported more than 10 lakh per year in India. 


Question: How much time does it need for recovery?

Answer: It can last several years or remains lifelong.



Question: Is the condition treatable? 

Answer: Treatments can help manage conditions. There is no known cure present. 

 

Question: Does diagnosis require lab tests or imaging? 

Answer: Its diagnosis rarely requires lab tests or imaging. 

 

 

 

Condition Highlights 

  1. It commonly occurs for ages 35-50. 
  2. It is more common in females. 
  3. Family history may increase likelihood to occur. 

 

Polysulfide Impression Materials

Permlastic is a polysulfide, condensation-cured, elastomeric impression material in three viscosities


Polysulfide impression materials are flexible but do not have the major changes in dimensions during storage like agar and alginate. Furthermore, the polysulfide impression is much stronger and more resistant to tearing than agar or alginate. It can be electroformed and therefore metal dies or models, in addition to gypsum models, can be prepared. 

Stages and Phases of Anaesthesia

Assessment of the depth of anaesthesia 

Anaesthesia has been described as a series of four Stages. 

Stage 1

The period between administration of an anaesthetic and loss of consciousness. 

Stage 2

The period after loss of consciousness, which may include actions such as uncontrolled movement, delirium, vocalization.

Stage 3 

The level at which surgery can be performed. Stage 3 anaesthesia is divided into four planes

  1. Plane 1: "light" anaesthesia - the animal still has blink and swallowing reflexes, and regular respiration.
  2. Plane 2: "surgical" anaesthesia - the animal has lost blink reflexes, pupils become fixed and respiration is regular.
  3. Plane 3: "deep" anaesthesia - the animal starts losing the ability to use the respiratory muscles and breathing becomes shallow; may require assisted ventilation. The surgeries are performed in this plane.
  4. Plane 4: the animal loses all respiratory effort, and breathing may stop entirely. 

Stage 4

Anaesthetic crisis! Respiratory arrest and death from circulatory collapse imminent.

Pulpitis

Photograph showing Pulpal hyperaemia. While bacteria are still some distance from the pulp, acid permeating along the dentinal tubules gives rise to dilation of the blood vessels, oedema and a light cellular inflammatory infiltrate in the pulp [1]

What is Pulpitis?

Pulpitis is the inflammation of the pulp. It is the most common cause of pain in young persons.


Types

It is of two types.

  1. Reversible

  2. Irreversible

Irreversible pulpitis has been divided into further two types

  1. Acute pulpitis

  2. Chronic pulpitis

Causes of Pulpitis

Root Apex-Anatomical And Physiological Foramen

Anatomical and physiological root apex
Anatomical and physiological forament of the root 

Apical constriction (Physiological foramen)

  • is conside­­red narrowest diameter of the root canal

  • located at the cement-dentinal junction.

  • it is the apical limit of root canal preparation preparation.

  • it is also known as the histological foramen, because it is located at the junction between the

  • pulpal connective and interstitial loose connective tissues of the periodontal ligament.

  • not visible on x-ray (we may find it only using WL determination methods).

Dental Caries-Part 6: Prevention

Fig1: Caries free beautiful teeth with proper maintenance #

The carious process can be termed as metabolic activity in the plaque. The result of the metabolic activity may not be anything to see or there may be demineralisation resulting in a visible carious lesion. As we have discussed earlier, plaque is the cause of caries and a tooth completely free of plaque will not have caries. However, it is not always possible to show a strong association between the presence of dental plaque and caries. Mostly because people are unable to completely remove plaque themselves, even when guided properly. In addition, although the bacterial biofilm is the cause of caries, there are other factors involved. This is the reason that caries is described as a multifactorial disease. These factors, when combined, may increase or decrease the rate of demineralization. 

Dental Caries-Part 5: Clinical Aspect of Caries Pathology

Arrested caries and remineralization  

  

Pre-Cavitation, or “white spot” caries lesions, can stop when the balance between demineralization and remineralization is changed in favor of remineralization. This could follow the restriction of sucrose, the application of fluoride, or the loss of an adjacent tooth to a proximal caries. This loss of tooth uncovers the area of stagnation and allows proper oral hygiene procedures. The source of the calcium and phosphate for remineralization of the lesion is saliva and plaque. The caries progresses slowly, and even under natural conditions, about 50% of proximal enamel lesions may show no radiographic evidence of progression for 3 years, showing that a small change may be needed to encourage reversal of the process. Although remineralization can bring the mineral content of an enamel lesion closer to that of the original enamel, the deposition is irregular and disorganized at the single crystal level, and the structure of the original enamel cannot be recovered. Despite this, remineralized lesions that have incorporated fluoride may be less prone to caries attack than intact enamel. Arrested enamel cavities can remain dull and white or more often discolored due to the incorporation of an extrinsic dye. This is known as inactive lesion or brown spot.   

Dental Caries-Part 4: Dentine Caries

Normal Structure of Dentin


Dentine is the part of the tooth that is covered by enamel and covers the pulp tissues. It comprises of inorganic hydroxyapatite 45-50%, organic matrix 30% and water 25%.
It is a vital tissue as opposed to enamel. It is elastic and permeable. Therefore, it is never possible for a restorative material to create a totally hermetic seal between itself and the cavity wall.
Dentine consists of dentinal tubules, peritubular dentine and inter tubular dentine. Dentinal tubules contain extensions of the odontoblast cells that line along the inner surface of the dentine and remain in the pulp. The peritubular dentine makes the walls of the dentinal tubules, are devoid of collagen matrix and are highly mineralised. The inter tubular dentine is the main structural component; present between the dentinal tubules; consists of hydroxyapatite crystals lying in the collagen matrix. 

Dental Caries-Part 3: Enamel Caries

 

Clinical and Histological Features of Dental Caries

Now we shall describes the clinical features of carious lesions on smooth,

occlusal, and root surfaces.  We shall relate the clinical features to their histological

features. We shall consider Enamel and Dentine together, the reasons being:

  1. As a clinician, you will see them in the same way.

  2. You can not understand changes in dentine during caries progression and caries arrest without considering the spread of the enamel lesion.

  3. Changes in Dentine occur before the enamel lesion cavitates. Removal of the biofilm will arrest the lesion in dentine as well as the lesion in enamel.

  4. The lesion, in both enamel and dentine, entirely reflects the activity of the bacterial biofilm.


Before I start talking about the clinical and histological features of dental caries, You must know the 

Basic Structure of Enamel


Sound enamel consists of crystals of hydroxyapatite packed tightly together in an orderly arrangement which is known as enamel prisms. The amount of hydroxyapatite ranges between 86 to 95%; the organic component between 1% to 2 % and water between 4% to 12% by volume. The total inorganic content of enamel ranges between 95% to 98% by mass, thats why it looks like crystals.


The crystals are so tightly packed that the enamel gets a glass-like appearance and appears translucent. This is the reason that it allows the varying degrees of yellow colour of the dentine to shine through it. Here, you should know that even though the crystal packing is very tight, each crystal is actually separated from its neighbours by tiny intercrystalline spaces or pores. These spaces are filled with water and organic material. When enamel is exposed to acids produced in the microbial biofilm, mineral is removed from the surface of the crystal which shrinks in size. Thus, the intercrystalline spaces enlarge and the tissue becomes more porous. This increase in porosity can be seen clinically as a white spot.

Dental Caries-Part 3: Video series



Lecture Series on Dental Caries

To watch video lectures, click at the following links

1. Introduction

2. Etiology of dental caries

3. Bacterial plaque in dental caries

4. Microbiology of dental caries

5. Sucrose and dental caries

6. Acid production in dental plaque

7. Saliva and dental caries

8. Early enamel caries


Dental Caries-Part 2: Treatment Planning

In this chapter, you will know about the treatment planning of dental caries. In previous chapter you studies the etio-pathogenesis and clinical characteristics of dental caries. If you have not gone through it, it is advised that you study the previous chapter before proceeding further.

Mechanism of Remineralisation of Enamel

When the oral environment of a person is favourable where the pH is above 5.5 and saliva contains enough calcium and phosphate ions, the remineralisation process of enamel occurs. The supersaturated saliva acts as driving force for remineralisation. In a non cavitated enamel caries lesion, the original crystalline structure of rods remains intact. When it is etched, it acts as nucleating agent for remineralisation. When trace amount of fluoride ions is added to the environment, it enhances the remineralisation process by enhancing the precipitation of calcium and phosphate. The inclusion of fluoride ions results in the formation of fluorapatite crystals in enamel rods which is more resistant to acid attack compared to calcium apatite of the natural enamel rods. Thus, the new enamel becomes resistant to caries process. 

Dental Caries-Part 1: Etio-pathogenesis and Clinical Features

This lesson presents basic definitions, terminologies, etiologies, demineralisation-remineralisation of enamel and clinical characteristics of the caries lesion in the context of clinical operative dentistry. 

Definitions of Dental Caries and Dental Plaque 

Dental caries is defined as a multifactorial, transmissible, infectious oral disease caused primarily by the complex interaction of cariogenic oral flora (biofilm) with fermentable dietary carbohydrates on the tooth surface over time.

Dental plaque is a gelatinous mass of bacteria adhering to the tooth surface. Carious lesions occur only under the plaque. The plaque bacteria metabolises the refined carbohydrate (sucrose mainly) for energy production and produces organic acids as a by product. These acids cause dissolution of crystalline structures of enamel that result in caries lesions of the tooth.  

Hepatitis B-Part 1: Epidemiology and Clinical Features

Overview 

Hepatitis is an inflammation of the liver that's caused by a variety of contagious viruses and non-infectious agents leading to a range of health problems, some of which can be fatal. There are five main strains of the hepatitis virus, known as types A, B, C, D and E. While their infection results in liver disease, they differ in important ways including modes of transmission, severity of the illness, geographical distribution and prevention methods. 

Particularly types B and C lead to chronic disease in hundreds of millions of people and together are the most common cause of liver cirrhosis, liver cancer and viral hepatitis related deaths. 

An estimated 354 million people worldwide having no access to testing and treatment live with hepatitis B or C. 

Some types of hepatitis are preventable through vaccination. A WHO study found that an estimated 4.5 million premature deaths could be averted in low-and middle- income countries by 2030 through vaccination, individual tests, drugs and education campaigns. WHO’s global hepatitis strategy, championed by all WHO Member States, aims to reduce new hepatitis infections by 90 and deaths by 65 between 2016 and 2030.


Hepatitis B is a potentially life-threatening liver infection caused by the hepatitis B virus (HBV). It can cause chronic infection and puts people at high risk of death from cirrhosis and liver cancer.

In this first part of the article, we shall discuss the following aspects of hepatitis:

  1. Epidemiology, 
  2. Mode of transmission
  3. Sign and symptoms 
  4. Groups at risk
  5. Relationship of HBV and HIV infection H
  6. How to confirm the diagnosis
  7. Sample MCQs

Hepatitis B-Part 2: Treatment and Prevention

Hepatitis B is a potentially life-threatening liver infection caused by the hepatitis B virus (HBV). It can cause chronic infection and puts people at high risk of death from cirrhosis and liver cancer.

In the first part of the article, you have read the epidemiology, mode of transmission of Hepatitis B virus, its sign and symptoms, groups at risk, the relationship of HBV and HIV infection, and how the diagnosis is confirmed. In this part of the article, we shall discuss about its treatment and prevention.

If you want to read a short note on Hepatitis B in Indian context, read it HERE.

You can also take a free mock test on Hepatitis B.

Seven Ways to Prevent Dental Caries in Your Child

Dental caries is an endemic disease in children. It is caused by a bacterial infection. The causative bacteria are known as Streptococcus Mutans and Lactobacilli.


Although the dental caries is caused by bacteria, the initiation and progression of dental caries depend on several factors. The less the risk factors present, the less are the chances of dental caries development in your child’s tooth.


I shall discuss those factors for you so that you can understand the developmental process of dental caries and take appropriate measures to prevent developing it in your son’s or daughter’s mouth. Broadly, we can categorize a child belonging to either high risk or low risk category. The children of high-risk category have higher chances of developing dental caries compared to those of lower category.


The rampant caries develops rapidly in young children and involves all anterior teeth within a very short period. Early intervention may prevent its development. So, my advice to you, visit a dentist when you see his/her first tooth. 



Sign of rampant caries: Note caries in all teeth
 


The factors that determine the risk category of a person are as follows: 

  1. Social factors 
  2. General Health Factors 
  3. Dietary factors 
  4. Preventive Factors 
  5. Plaque factors 
  6. Salivary factors 
  7. Clinical factors 

  

  1. 1. Social Factors 

    A socially deprived or isolated child with frequent snacking habit, irregular dental visits, siblings having dental caries, with parents having little knowledge of dental disease, will be at higher risk of developing dental caries compared to the child who is not having the above-mentioned factors. You should always try to remove and maintain these factors at low level to keep your child in low category. 

  1. 2. General Health Factors 

    If your child is medically compromised, disabled, having xerostomia or on long term cariogenic medicine, s/he is at higher risk of developing caries. The lesser number of factors present with your child, the risk of developing dental caries is less. If your child is having any of these factors, help him/her to remain in the low-risk category by visiting a dentist. 

  1. 3. Dietary Factors 

    The most important factor is frequent intake of sugars. As the frequency of sugar increases, the risk goes up. So, encourage your child to reduce the frequency of sugar intake. For example, you can give him/her two chocolates/candy instead of one and encourage him/her to eat them all together. Afterwards, you can clean his/her teeth off of sticky chocolates/candy. 

  1. 4. Preventive Factors- Uses of Fluoride/CPP-ACP 

    If your child is living in a non-fluoridated area, with no fluoride supplementation and using non-fluoridated toothpaste, s/he is at high risk. Living in an area supplied by fluoridated water, or using fluoride supplement or using a toothpaste containing fluoride decreases the risk of caries development. 
    The newly developed protective material Casein phosphopeptide-amorphous calcium phosphate (CPP-ACP), a milk derivative helps in remineralization of the carious lesion by replenishing lost minerals like calcium, phosphate ions into the tooth structure. Using a toothpaste containing CCP-ACP will remineralize the enamel of your child and make it more resistant to caries development. 

  1. 5. Plaque Control Factors 

    If your child does infrequent or ineffective tooth brushing s/he is at higher risk. Teaching him or her regular and effective tooth brushing to remove plaque. This habit decreases the risk of developing tooth decay. If s/he cannot perform effective tooth brushing, help him/her. 

  1. 6. Salivary Factors 

    Low flow of saliva, low buffering capacity of saliva and higher Streptococcus Mutans and Lactobacilli count in saliva put your child in a high-risk category. Removing these factors with the help of a dentist will shift your son/daughter into the low-risk category. 

  1. 7. Clinical Factors 

    New carious lesions, premature extractions, caries or restorations (fillings) in anterior teeth, multiple restorations, history of repeated restorations, no fissure sealants, multi-band orthodontics and presence of partial dentures increase the risk of caries development and put the child in high risk. As these factors decrease, the child moves from high to low-risk category.


Conclusion 


So, now you know the causes that may put your child at high risk for developing dental caries. I advise you to understand these factors and take appropriate action. The first step you must take is to start using a toothpaste that contains either fluoride or CCA-ACP. Also, plan for and have your child get checked by a dentist.