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.
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.
|Permlastic is a polysulfide, condensation-cured, elastomeric impression material in three viscosities|
Anaesthesia has been described as a series of four Stages.
The period between administration of an anaesthetic and loss of consciousness.
The period after loss of consciousness, which may include actions such as uncontrolled movement, delirium, vocalization.
The level at which surgery can be performed. Stage 3 anaesthesia is divided into four planes.
|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 |
Pulpitis is the inflammation of the pulp. It is the most common cause of pain in young persons.
It is of two types.
Irreversible pulpitis has been divided into further two types
|Anatomical and physiological forament of the root|
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).
|Fig1: Caries free beautiful teeth with proper maintenance #|
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, 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.
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:
As a clinician, you will see them in the same way.
You can not understand changes in dentine during caries progression and caries arrest without considering the spread of the enamel lesion.
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.
The lesion, in both enamel and dentine, entirely reflects the activity of the bacterial biofilm.
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.
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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.
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.
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.
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 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.
In this first part of the article, we shall discuss the following aspects of hepatitis:
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.
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 factors that determine the risk category of a person are as follows:
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.