Sunday, December 21, 2008

MOUTH ULCERS

Canker sores are a type of mouth ulcer.
Some of the medical terms used to refer to canker sores are "recurrent minor aphthous ulcers" and "recurrent minor aphthous stomatitis" (thus differentiating canker sores from other forms of aphthous ulcers or aphthous stomatitis).
Canker sores are the most commonly occurring type of mouth ulcer.

CAUSES


The precise mechanism by which canker sores form has not been definitively determined but it is likely that their development is related to a reaction of an individual's own immune system.

Canker sores are thought to form when, for unexplained reasons, a person's immune system identifies the presence of chemical molecules that it does not recognize.
The presence of these molecules activates an attack by the immune system's lymphocytes (a type of white blood cell), somewhat similar as when a person's immune system attacks a transplanted organ. The carnage created by the lymphocytes' attack on these unrecognized molecules results in the formation of mouth ulcers. We term these ulcers canker sores.

Risk factors are associated with aphthous ulcer breakouts

Several factors that seem to be triggers for outbreaks of canker sores have been identified. Any one or a combination of the following risk factors may play a role in the formation of canker sores for any one individual:

Toothpastes and mouthwashes that contain sodium lauryl sulfate (SLS).

Research has suggested that the use of products that contain sodium lauryl sulfate ("SLS"), a foaming agent found in most toothpaste and mouthwash formulations, can be associated with an increased risk for canker sore outbreaks. This may be due to a drying effect SLS has on the protective surface of oral tissues. Once this protective layer has been compromised the tissue underneath is more vulnerable to irritants such as acidic foods.
Several studies have reported that participants who brushed using SLS free toothpaste found that they experienced a reduction in the total number of canker sores that they had form. This reduction in mouth sores was found to be as high as 81% in one study. In this same study also reported that some of its participants stated that the canker sores that did form were less painful than those that developed during those time periods when they had been using a toothpaste that did contain SLS.

Mechanical trauma to oral tissues.

People state that they often recall some sort of physical trauma preceding the formation of their canker sores. This trauma might take the form of a self-inflicted bite, irritation from a sharp tooth edge, or possibly trauma from some type of food such as a crisp chip. 38% of the participants of one study felt that their canker sores were precipitated by trauma.

Emotional stress / Psychic stress.

Psychological stress has been shown to adversely affect the health of people in a number of ways. Many people who suffer from canker sores report that the appearances of their ulcers coincide with periods of stress.

Diet: Nutritional deficiencies.

Researchers have found that some people who suffer from canker sore outbreaks have poor diets and therefore an accompanying nutritional deficiency. Some of the nutritional deficiencies that have been correlated with the presence of canker sores are:

* Vitamin deficiencies: B1, B2, B6, B12, C
* Other nutrients: zinc, folic acid, iron, selenium, calcium

Diet: Allergies and sensitivities.


Allergies to foods and other substances have been postulated as being triggers for canker sore breakouts.
Any substance that comes into contact with the person's oral tissues must be considered to be a potential causative agent.
If an allergy is suspected the individual might choose to maintain a diary so to help them (and their dentist) identify the most likely candidates associated with the causation of their sores.
In some cases allergy testing might be considered.

Some of the dietary substances identified by researchers as being potential triggers for canker sore outbreaks are:

* Cereal grains: buckwheat, wheat, oats, rye, barley, the gluten protein found in grains
* Fruits and vegetables: lemons, oranges, pineapples, apples, figs, tomatoes, strawberries
* Dairy: milk, cheeses
* Other foods: nuts, chocolate, shellfish, soy, vinegar, French mustard
* Additives: cinnamonaldehyde (a flavoring agent), benzoic acid (a preservative)
* Other substances: toothpastes, mints, gums, dental materials, metals, medications

Hormonal changes.

Some women have reported that they find a relationship between the presence of canker sores and certain phases of their menstrual period.
It has also been reported that a woman may notice a remission of canker sores during pregnancy.
Neither of these observations has been adequately documented nor explained by research.

Genetics.

Some researchers have felt that they have identified a genetic predisposition for canker sores.
One study found that 35% of those persons who experience canker sores have at least one parent who suffers from these ulcers also. Another study found that 91% of identical twins both suffered from canker sores whereas only 57% of fraternal twins did.

Infectious agents (both bacterial and viral).


The fact that chemical compounds typically associated with bacterial and viral infections have been isolated from canker sores suggests that bacteria or viruses could be causative agents in the formation of these mouth ulcers.

Medical conditions.

Several different medical conditions can be associated with the presence of canker sores (and other forms of aphthous ulcers as well). For those patients who experience persistent difficulties with canker sores consideration must be given to the presence of an underlying undiagnosed systemic disease and the need for an evaluation and testing by a physician.
A few of the medical conditions that have been associated with the presence of mouth ulcers are: Behcet's disease, neutrophil dysfunction diseases, inflammatory bowel diseases (celiac and Crohn's), and HIV-AIDS.

Medications.


The use of nonsteroidal anti-inflammatory drugs (NSAIDs), beta blockers, chemotherapeutic agents, and nicorandil have each been suggested as possibly placing a person at greater risk for outbreaks of canker sores.


Source: http://www.animated-teeth.com

Bad Breath

For any individual, the exact status of their own breath can be difficult to ascertain. The reason for this lies in the fact that the oral cavity is connected to our nose by way of an opening which lies in the back of our mouth (in the region of our soft palate). Since noses tend to filter out and ignore background odors, it filters out and ignores the quality of our own breath. This means that it is quite possible for a person to have bad breath, yet not be aware of it.





How can a person can test the quality of their own breath?

There are ways you can objectively smell your own breath. However, you have to take a slightly indirect route.

Try this technique. Lick your wrist, wait about five seconds while the saliva dries somewhat, and then smell it. What do you think?

That's the way you smell. Or, more precisely, that's the way the end of your tongue smells (your tongue's "anterior" portion).



Simple tips that can help to minimize your potential for having halitosis.

1) Drink plenty of water.

Drinking plenty of water throughout the day can help to minimize a person's problems with bad breath (halitosis) This can be an especially important consideration for those people who suffer from xerostomia (chronically dry mouths).

If you allow yourself to become dehydrated, your body will attempt to conserve moisture by reducing its production of saliva. Saliva has a cleansing and diluting effect on the bacteria and bacterial waste products that cause bad breath. A reduction in the amount of saliva in your mouth will make it more likely that you will experience breath problems.

2) Rinse your mouth with water throughout the day.

Rinsing with water can mitigate bad breath problems for brief periods of time. Rinsing will both dilute and partially remove the bacterial waste products that are the cause of breath odors.

3) Stimulate your mouth's flow of saliva.

You can help to minimize breath malodor by stimulating your body's flow of saliva. This is because saliva has a cleansing and diluting effect on the bacteria and bacterial waste products that cause bad breath.

One way to stimulate salivary flow is to chew on something. Doing so will trick your body in to thinking that it is getting a meal. In preparation for digesting this meal, your body will increase its production of saliva. You might choose to chew on cloves, fennel seeds, or a piece of mint or parsley.

Chewing gum, breath mints, or lozenges can also be used to stimulate salivary flow. If you elect to use one of these products, make sure it is sugar-free since sweets will promote the growth of bacteria that cause tooth decay.

4) Clean your mouth well, especially after eating foods that are high in protein content.

The bacterial waste products that cause of bad breath are created when oral anaerobic bacteria digest proteins. After you eat a meal or snack, especially one that is high in protein content, make sure that you clean your mouth promptly and thoroughly. Doing so will minimize both the time duration and amount of food that is available for the offending bacteria.


Source:
http://www.animated-teeth.com/



The BANA test.

Some of the bacteria that cause periodontal disease (gum disease) produce waste products that are quite odiferous and as a result contribute to a person's breath problems. The presence of some of these types of bacteria can be tested for by way of performing a BANA test.

The bacteria in question have the characteristic of being able to produce an enzyme that degrades the compound benzoyl-D, L-arginine-naphthylamide (abbreviated BANA). When a sample of a patient's saliva that contains these bacteria is placed in with the BANA testing compound they cause it to break down, thus creating a color change in the testing medium.

Hi

Hi Friends,
My clinic started on 1st December, Started getting new OPDs, i was so startled to see cases of oral submucous fibrosis on a very regular basis.
The affected patients belonged to High class,Service class, Labour class.
Total of 6 patients, out of which 1 was female, rest of them were males.
So i thought of Putting up a post on this topic, I would highly appreciate if you would want to contribute to this post.

ORAL SUBMUCOUS FIBROSIS {OSMF}

















In 1952, Schwartz coined the term atrophica idiopathica mucosa oris to describe an oral fibrosing disease he discovered in 5 Indian women from Kenya.
Joshi subsequently termed the condition oral submucous fibrosis (OSMF) in 1953.

OSMF is a chronic, debilitating disease of the oral cavity characterized by inflammation and progressive fibrosis of the submucosal tissues (lamina propria and deeper connective tissues).
It results in marked rigidity and an eventual inability to open the mouth (Cox, 1996; Aziz, 1997).
The buccal mucosa is the most commonly involved site, but any part of the oral cavity can be involved, even the pharynx (Paissat, 1981).

The condition is well recognized for its malignant potential and is particularly associated with areca nut chewing, the main component of betel quid.
Betel quid chewing is a habit practiced predominately in Southeast Asia and India that dates back for thousands of years.
It is similar to tobacco chewing in westernized societies. The mixture of this quid, or chew, is a combination of the areca nut (fruit of the Areca catechu palm tree, erroneously termed betel nut) and betel leaf (from the Piper betel, a pepper shrub), tobacco, slaked lime (calcium hydroxide), and catechu (extract of the Acacia catechu tree) (Cox, 1996).
Lime acts to keep the active ingredient in its freebase or alkaline form, enabling it to enter the bloodstream via sublingual absorption.
Arecoline, an alkaloid found in the areca nut, promotes salivation, stains saliva red, and is a stimulant.

The ingredients and nomenclature of betel quid vary by region.
Freshly prepared betel quid (with or without tobacco) is simply known as pan.
Betel quid with tobacco, known as the manufactured version gutka (alternatively spelled gutkha, guttkha, or guthka), is primarily used in the Indian subcontinent (ie, India, Pakistan, Bangladesh).
Betel quid without tobacco is mostly used in Southeast Asian countries (eg, Taiwan, Myanmar, Thailand, China, Papua New Guinea, Guam).

Pan masala is a commercially manufactured powdered version without tobacco used in the Indian subcontinent.
Mawa is the combination of areca, tobacco, and lime.
Pan Parag is the brand name of a pan masala and gutka used in India. Manipuri tobacco, popular in parts of northern India, is a mixture of areca nut, tobacco, lime, and various condiments.
Depending on local preferences, sweeteners or spices (eg, cardamom, saffron, clove, anise seed, turmeric, mustard) are also added as flavorings (Centers for Disease Control and Prevention, 2006; Gupta, 1996).

In most patients with OSMF, areca nut was chewed alone more frequently than it was chewed in combination with pan (ie, betel leaf plus lime plus betel catechu, with or without tobacco) (Aziz, 1997) or had a higher areca nut content (Tilakaratne 2006).
Pathophysiology
The pathogenesis of the disease is not well established, but the cause of OSMF is believed to be multifactorial.
A number of factors trigger the disease process by causing a juxtaepithelial inflammatory reaction in the oral mucosa.
Factors include areca nut chewing, ingestion of chilies, genetic and immunologic processes, nutritional deficiencies, and other factors.


Areca nut (betel nut) chewing

The areca nut component of betel quid plays a major role in the pathogenesis of OSF (Liao, 2001). In a 2004 study, a clear dose-dependent relationship was observed for both frequency and duration of chewing areca nut (without tobacco) in the development of OSF (Jacob, 2004). Smoking and alcohol consumption alone, habits common to areca nut chewers, have been found to have no effect in the development of OSF (Ariyawardana, 2006; Ranganathan, 2004), but their addition to areca nut chewing can be a risk for OSF (Ranganathan, 2004). Commercially freeze-dried products such as pan masala, guthka, and mawa have higher concentrations of areca nut per chew and appear to cause OSF more rapidly than self-prepared conventional betel quid, which contains smaller amounts of areca nut (Tilakaratne, 2006).

Arecoline, an active alkaloid found in betel nuts, stimulates fibroblasts to increase production of collagen by 150% (Canniff, 1981). In one study, arecoline was found to elevate the mRNA and protein expression of cystatin C, a nonglycosylated basic protein consistently up-regulated in a variety of fibrotic diseases, in a dose-dependent manner in persons with OSF (Chung-Hung, 2006).

In 3 separate but similar studies, keratinocyte growth factor-1, insulinlike growth factor-1, and interleukin 6 expression, which have all been implicated in tissue fibrogenesis, were also significantly up-regulated in persons with OSF due to areca quid chewing and arecoline may be responsible for their enhanced expression (Tsai, Feb 2005; Tsai, Oct 2005; Tsai, 2004). Further studies have shown that arecoline is an inhibitor of metalloproteinases (particularly metalloproteinase-2) and a stimulator of tissue inhibitor of metalloproteinases, thus decreasing the overall breakdown of tissue collagen (Chang, 2001).

Insertion/deletion 5A polymorphism in the promoter region of the matrix metalloproteinase-3 gene, which results in alteration of transcriptional activities, has also been found in persons with OSF but not in those with oral squamous cell carcinoma (Tu, 2006). Conversely, insertion/deletion 2G polymorphism in the promoter of the matrix metalloproteinase-1 gene has been implicated in oral squamous cell carcinoma but not OSF (Lin, 2004).

Flavanoid, catechin, and tannin in betel nuts cause collagen fibers to cross-link, making them less susceptible to collagenase degradation (Harvey, 1986). This results in increased fibrosis by causing both increased collagen production and decreased collagen breakdown (Aziz, 1997). OSF remains active even after cessation of the chewing habit, suggesting that components of the areca nut initiate OSF and then affect gene expression in the fibroblasts, which then produce greater amounts of normal collagen (van Wyk, 1993; Meghji, 1987). Chewing areca quid may also activate NF-kappaB expression, thereby stimulating collagen fibroblasts and leading to further fibrosis in persons with OSF (Ni, 2006).

Areca nuts have also been shown to have a high copper content, and chewing areca nuts for 5-30 minutes significantly increases soluble copper levels in oral fluids. This increased level of soluble copper supports the hypothesis that copper acts as an initiating factor in persons with OSF by stimulating fibrogenesis through up-regulation of copper-dependent lysyl oxidase activity (Trivedy, 2000). Further, a significant gradual increase in serum copper levels from precancer to cancer patients has been documented (Khanna, 2006), which may have a role in oral fibrosis to cancer pathogenesis.

Ingestion of chilies

The role of chili ingestion in the pathogenesis of OSF is controversial. The incidence of OSF is lower in Mexico and South America than in India, despite the higher dietary intake of chilies (Pillai, 1992). A hypersensitivity reaction to chilies is believed to contribute to OSF (Aziz, 1997). One study demonstrated that the capsaicin in chilies stimulates widespread palatal fibrosis in rats (Sirsat, 1960), while another study failed to duplicate the results (Hamner, 1974).

Genetic and immunologic processes


A genetic component is assumed to be involved in OSF because of reported cases in people without a history of betel nut chewing (Liao, 2001; Seedat, Mar 1988) or chili ingestion (Seedat, Mar 1988). Patients with OSF have been found to have an increased frequency of HLA-A10, HLA-B7, and HLA-DR3 (Aziz, 1997).

An immunologic process is believed to play a role in the pathogenesis of OSF (Canniff, 1985). The increase in CD4 and cells with HLA-DR in OSF tissues suggests that most lymphocytes are activated and that the number of Langerhans cells is increased. The presence of these immunocompetent cells and the high ratio of CD4 to CD8 in OSF tissues suggest an ongoing cellular immune response that results in an imbalance of immunoregulation and an alteration in local tissue architecture (Haque, 1997). These reactions may be the result either of direct stimulation from exogenous antigens, such as areca alkaloids, or of changes in tissue antigenicity that leads to an autoimmune response (Haque, 1997).

Further, the major histocompatibility complex class I chain-related gene A (MICA) is expressed by keratinocytes and other epithelial cells and interacts with gamma/delta T-cells localized in the submucosa. MICA has a triplet repeat (GCT) polymorphism in the transmembrane domain, resulting in 5 distinct allelic patterns. In particular, the phenotype frequency of allele A6 of MICA in subjects with OSF was significantly higher and suggests a risk for OSF (Liu, 2004).

Some authors have demonstrated increased levels of proinflammatory cytokines and reduced antifibrotic interferon gamma (IFN-gamma) in patients with OSF, which may be central to the pathogenesis of OSF (Haque, 2000).

Nutritional deficiencies


Iron deficiency anemia, vitamin B complex deficiency, and malnutrition are promoting factors that derange the repair of the inflamed oral mucosa, leading to defective healing and resultant scarring (Aziz, 1997). The resulting atrophic oral mucosa is more susceptible to the effects of chilies and betel nuts.

Other significant factors

Some authors have found a high frequency of mutations in the APC gene and low expression of the wild-type TP53 tumor-suppressor gene product in patients with OSMF, providing some explanation for the increased risk of oral squamous cell carcinoma development in patients with OSMF (Liao, 2001). Other studies have suggested that altered expression of retinoic acid receptor-beta may be related to the disease pathogenesis (Kaur, 2004).
Frequency
United States

OSMF is rare in the United States and is found only in the immigrant members of the South Asian population who chew betel nuts.
International

Worldwide, estimates of OSF indicate that 2.5 million people are affected, with most cases concentrated on the Indian subcontinent, especially southern India (Cox, 1996).
The rate varies from 0.2-2.3% in males and 1.2-4.57% in females in Indian communities (Aziz, 1997). OSMF is widely prevalent in all age groups and across all socioeconomic strata in India.
A sharp increase in the incidence of OSMF was noted after pan parag came onto the market, and the incidence continues to increase.
OSMF also occurs in other parts of Asia and the Pacific Islands (Cox, 1996). Migration of endemic betel quid chewers has also made it a public health issue in many parts of the world, including the United Kingdom, South Africa, and many Southeast Asian countries (Paul, 2005).

Mortality/Morbidity


OSMF has a high rate of morbidity because is causes a progressive inability to open the mouth, resulting in difficulty eating and consequent nutritional deficiencies. OSMF also has a significant mortality rate because of it can transform into oral cancer, particularly squamous cell carcinoma, at a rate of 7.6% (Aziz, 1997).
Race

OSMF occurs on the Indian subcontinent, in Indian immigrants to other countries, and among Asians and Pacific Islanders as a result of the traditional use of betel quid endemic to these areas (Cox, 1997).
Sex

The male-to-female ratio of OSMF varies by region, but females tend to predominate. In a study from Durban, South Africa, a distinct female predominance was demonstrated, with a male-to-female ratio of 1:13 (Seedat, Dec 1988). This was later confirmed by others, with a male-to-female ratio of 1:7 (van Wyk, 1997). In addition, a female predominance in areca nut chewing was also noted in this region. Studies in Pakistan reported a male-to-female ratio of 1:2.3 (Aziz, 1997).

Conversely, a case-control study of 185 subjects in Chennai, South India revealed a male-to-female ratio 9.9:1.0 (Ranganathan, 2004). In Patna, Bihar (also in India), the male-to-female ratio was 2.7:1 (Ahmad, 2006). With the onset of new commercial betel quid preparations, trends in sex predominance and age of occurrence may shift.
Age

The age range of patients with OSMF is wide and regional; it is even prevalent among teenagers in India. In a study performed in Saipan, 8.8% of teenagers with a mean age 16.3 years (± 1.5 y) were found to have OSMF (Oakley, 2005). Generally, patient age ranges from 11-60 years (Ahmad, 2006; Aziz, 1997); most patients are aged 45-54 years and chew betel nuts 5 times per day (Aziz, 1997).


Clinical History


Symptoms of OSMF include the following (Murti, 1992; Cox, 1996):

* Progressive inability to open the mouth (trismus) due to oral fibrosis and scarring
* Oral pain and a burning sensation upon consumption of spicy foodstuffs
* Increased salivation
* Change of gustatory sensation
* Hearing loss due to stenosis of the eustachian tubes
* Dryness of the mouth
* Nasal tonality to the voice
* Dysphagia to solids (if the esophagus is involved)
* Impaired mouth movements (eg, eating, whistling, blowing, sucking)

Physical

OSF is clinically divided into 3 stages (Pindborg, 1989), and the physical findings vary accordingly, as follows (Murti, 1992; Cox, 1996; Aziz, 1997; Pindborg, 1989):

* Stage 1: Stomatitis includes erythematous mucosa, vesicles, mucosal ulcers, melanotic mucosal pigmentation, and mucosal petechia.

* Stage 2: Fibrosis occurs in ruptured vesicles and ulcers when they heal, which is the hallmark of this stage.
o Early lesions demonstrate blanching of the oral mucosa.
o Older lesions include vertical and circular palpable fibrous bands in the buccal mucosa and around the mouth opening or lips, resulting in a mottled, marblelike appearance of the mucosa because of the vertical, thick, fibrous bands running in a blanching mucosa. Specific findings include the following:
+ Reduction of the mouth opening (trismus)
+ Stiff and small tongue
+ Blanched and leathery floor of the mouth
+ Fibrotic and depigmented gingiva
+ Rubbery soft palate with decreased mobility
+ Blanched and atrophic tonsils
+ Shrunken budlike uvula
+ Sinking of the cheeks, not commensurate with age or nutritional status

* Stage 3: Sequelae of OSF are as follows:
o Leukoplakia is precancerous and is found in more than 25% of individuals with OSMF.
o Speech and hearing deficits may occur because of involvement of the tongue and the eustachian tubes.
* In addition to the above staging, in 1995 Khanna and Andrade developed a group classification system for the surgical management of trismus.
o Group I: This is the earliest stage and is not associated with mouth opening limitations. It refers to patients with an inter-incisal distance of greater than 35 mm.
o Group II: This refers to patients with an inter-incisal distance of 26-35 mm.
o Group III: These are moderately advanced cases. This stage refers to patients with an inter-incisal distance of 15-26 mm. Fibrotic bands are visible at the soft palate, and pterygomandibular raphe and anterior pillars of fauces are present.
o Group IVA: Trismus is severe, with an inter-incisal distance of less than 15 mm and extensive fibrosis of all the oral mucosa.
o Group IVB: Disease is most advanced, with premalignant and malignant changes throughout the mucosa.

Causes

The term oral submucosal fibrosis derives from oral (meaning mouth), submucosal (meaning below the mucosa of the mouth), and fibrosis (meaning hardening and scarring) (Aziz, 1997). Chewable agents, primarily betel nuts (Areca catechu), contain substances that irritate the oral mucosa, making it lose its elasticity. Nutritional deficiencies, ingestion of chilies, and immunologic processes may also have a role in the development of OSMF (Cox, 1996).


Treatment & Medical Care

The treatment of patients with OSMF depends on the degree of clinical involvement. If the disease is detected at a very early stage, cessation of the habit is sufficient.
Most patients with OSMF present with moderate-to-severe disease.
Moderate-to-severe OSMF is irreversible.
Medical treatment is symptomatic and aimed at improving mouth movements.


Treatment includes the following (Aziz, 1997):

* Steroids: In patients with moderate OSMF, weekly submucosal intralesional injections or topical application of steroids may help prevent further damage.

* Placental extracts: The rationale for using placental extract (PE) in patients with OSF derives from its proposed anti-inflammatory effect (Sur, 2003), hence, preventing or inhibiting mucosal damage. Cessation of areca nut chewing and submucosal administration of aqueous extract of healthy human PE (Placentrex) has shown marked improvement of the condition (Anil, 1993).

* Hyaluronidase: The use of topical hyaluronidase has been shown to improve symptoms more quickly than steroids alone. The combination of steroids and topical hyaluronidase shows better long-term results than either agent used alone (Kakar, 1985).

* IFN-gamma: This plays a role in the treatment of patients with OSF because of its immunoregulatory effect. IFN-gamma is a known antifibrotic cytokine. Patients treated with an intralesional injection of IFN-gamma experienced improvement of symptoms. IFN-gamma, through its effect of altering collagen synthesis, appears to be a key factor to the treatment of patients with OSF, and intralesional injections of the cytokine may have a significant therapeutic effect on OSF (Haque, 2001).
* The role of PEs, hyaluronidase, and interferon is still evolving. The US Food and Drug Administration has not yet approved these drugs for the treatment of OSF.

Surgical Care

Surgical treatment is indicated in patients with severe trismus and/or biopsy results revealing dysplastic or neoplastic changes. Surgical modalities that have been used include the following:

* Simple excision of the fibrous bands: Excision can result in contracture of the tissue and exacerbation of the condition.
* Split-thickness skin grafting following bilateral temporalis myotomy or coronoidectomy: Trismus associated with OSF may be due to changes in the temporalis tendon secondary to OSF; therefore, skin grafts may relieve symptoms (Canniff, 1986).
* Nasolabial flaps and lingual pedicle flaps: Surgery to create flaps is performed only in patients with OSF in whom the tongue is not involved (Kavarana, 1987; Hosein, 1994).

Consultations

* Consult an ear, nose, and throat specialist for evaluation of dysplasia and close follow-up monitoring for the development of oral cancer.
* Consult a plastic surgeon for patients with severe trismus, in whom reconstructive surgery may be possible.

Diet


Dietary focus should be on reducing exposure to the risk factors, especially the use of betel quid, and correcting any nutritional deficiencies, such as iron and vitamin B complex deficiencies (Cox, 1996).


Activity

Muscle stretching exercises for the mouth may be helpful to prevent further limitation of mouth movements.


Medication


The goals of pharmacotherapy are to reduce morbidity and to prevent complications. In addition to the medications listed below, PE has been used experimentally at a dose of 50 mcg/m2 SC 3 times per week if the patient's body surface area (BSA) is greater than 0.52 m2 or 1.5 mcg/kg/dose SC 3 times per week if the BSA is less than or equal to 0.5 m2.


Corticosteroids


Can be used in pharmacologic doses for their anti-inflammatory and immunosuppressant properties and their effects on blood and lymphatic systems in the palliative treatment of various diseases.

Dexamethasone (Decadron)

For various inflammatory diseases. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

4 mg IV/IM (suggested in studies)
Pediatric

Base dose on severity of disease and response rather than age, body weight, or BSA

* Dosing
* Interactions
* Contraindications
* Precautions

Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; decreases effect of salicylates and vaccines used for immunization

* Dosing
* Interactions
* Contraindications
* Precautions

Documented hypersensitivity; active bacterial or fungal infection

* Dosing
* Interactions
* Contraindications
* Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.
Precautions

Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications; caution with individuals exposed to viral illnesses, such as chickenpox or measles

Triamcinolone acetonide (Aristocort, Kenaject)

Suppresses immune system by reducing activity and volume of lymphatic system. Treats inflammatory mucosal lesions that are responsive to steroids. Decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and by reversing capillary permeability.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

Dental paste (for oral inflammatory or ulcerative lesions): Apply thin film bid/tid pc and hs IM: 40-80 mg (studies have used 10 mg/mL diluted in 1 mL of lidocaine 2% to avoid tissue irritation and facilitate proper distribution of drug)
Pediatric

Not established

* Dosing
* Interactions
* Contraindications
* Precautions

Coadministration with barbiturates, phenytoin, and rifampin decreases effects; effects of vaccine and toxoid may be reduced

* Dosing
* Interactions
* Contraindications
* Precautions

Documented hypersensitivity; fungal, viral, and mycobacterial mucosal infections

* Dosing
* Interactions
* Contraindications
* Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.
Precautions

Multiple complications (eg, severe infections, hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression) may occur; abrupt discontinuation may cause adrenal crisis

Betamethasone valerate (Diprosone)

For inflammatory reactions responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and by reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

Suggested dose: 0.05% topically q6h for 3 wk
Pediatric

Not established

* Dosing
* Interactions
* Contraindications
* Precautions

None reported

* Dosing
* Interactions
* Contraindications
* Precautions

Documented hypersensitivity; paronychia; cellulitis; impetigo; angular cheilitis; erythrasma; erysipelas; rosacea; perioral dermatitis; acne

* Dosing
* Interactions
* Contraindications
* Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.
Precautions

Do not use on skin with decreased circulation; can cause atrophy of groin, face, and axillae; may cause striae distensae and rosacealike eruption; may increase skin fragility; rarely may suppress HPA axis; if infection develops and is not responsive to antibiotic treatment, discontinue until infection is under control; do not use monotherapy to treat widespread plaque psoriasis
Extravasation antidotes

Can enhance diffusion of locally irritating or toxic drugs in the management of intravenous extravasation.

Hyaluronidase (Wydase Injection)

Stimulates hydrolysis of hyaluronic acid, one of the chief ingredients of tissue cement, which offers resistance to diffusion of liquids through tissues. Used to aid in absorption and dispersion of injected drugs.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

150 U added to vehicle solution and administered SC/ID
Pediatric

Administer as in adults

* Dosing
* Interactions
* Contraindications
* Precautions

Salicylates, cortisone, corticotropin, estrogens, and antihistamines may decrease effects

* Dosing
* Interactions
* Contraindications
* Precautions

Documented hypersensitivity

* Dosing
* Interactions
* Contraindications
* Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.
Precautions

Avoid injecting into inflamed or cancerous areas; perform intradermal skin test for sensitivity before initiating infusion; discontinue if sensitivity or extravasation occur
Interferons

Naturally produced proteins with antiviral, antitumor, and immunomodulatory actions. Alpha-, beta-, and gamma-interferons may be given topically, systemically, or intralesionally.

Interferon gamma (Actimmune)

Believed to act via ability to counteract cell surface expression of proinflammatory or proadhesion molecules on immune cells, among other effects. More studies needed to fully understand mechanisms of action.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

BSA >0.5 m2: 50 mcg/m2 SC 3 times/wk
BSA <0.5 m2: 1.5 mcg/kg/dose SC 3 times/wk
Pediatric

Not established



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SOURCE:

http://emedicine.medscape.com

Saturday, November 29, 2008

INVITATION

You are Cordially Invited to the opening of
BHAVATI DENTAL CLINIC
Time: 4 p.m. to 6p.m.
Date: 30/11/2008 .
Venue: Shop no.7, Sony House,
Chandavarkar road,
Borivli West
Mumbai 92

Saturday, October 18, 2008

ANTI-SMOKING PILL SHOWS PROMISE IN CURBING DRINKING

Tobacco cessation is the major concern now a days, as "Oral cancer" has created havoc worldwide especially in India.
Many products are available & coming up in the market as a substitute to tobacco.
The latest one is NRT-Nictine replacement therapy in the form of chewing gums, tobacco batches etc. but all of them have limited use & results are nott effective

Friday, October 17, 2008

HANDPIECE MAINTENANCE

For tips on maintaining your handpieces check out this link -

http://rapidshare.com/files/153692751/.pdf_hp_maintanance.pdf_1_.html

FREE MEDICAL BOOKS DOWNLOAD

From the following site:
http://rahulshetty87.googlepages.com/books

Thursday, October 16, 2008

HISTOLOGY OF TOOTH DEVELOPMENT






Bibliography: http://in.youtube.com/watch?v=LVC4_FIEeFs&feature=related

Wednesday, October 15, 2008

TOOTH ERUPTION






Bibliography: http://in.youtube.com/watch?v=0pzIRg8cW4A

CERVICAL CANCER VACCINE ENTERS INDIAN MARKET

Merck Sharp & Dohme (MSD), a wholly owned subsidiary of pharma major Merck & Co. Inc. launched a vaccine to prevent cervical cancer, the most common condition in India with more than 1,30,000 women diagnosed with it every year.
The vaccine is one of its kind & has been approved by the US Food & Drugs Authority.

The vaccine Gardasil was launched in 2006& is available in 108 countries.
Regulatory approvals & Immunogenity studies delayed its launch in India.
Currently, trials are being done by the Indian Council of Medical Research & "could take upto 3 years, but once they are done, the vaccine will be made available by the government as well," said Naveen A. Rao, mabaging director, MSD India.

Gardasil is priced at Rs2,800 ashot with three doses prescribed for efficacy.
According to a World Health Organisation Study, the risk of the cancer in India is 2.4% compared with an average of 1.3% for the world.

Tuesday, October 14, 2008

DENTAL FLUOROSIS

Dental fluorosis is a common disease in Punjab(India).

It is due to an unusually high dose of fluorides during odontogenesis causing a structural modification of hard dental tissues and thereby resulting in a hypomineralisation of these tissues.

Fuorotic enamel is a hypocalcified, porous,brittle and most unaesthetic tissue.



Bleaching has been suggested by several authors in order to treat the unaesthetic aspect of dental fluorosis, but many results are however unsatisfactory.

This is a novel method which is based on the structural characteristics of the fluorotic enamel & organic and exogenous nature of fluorotic enamel stains which includes four different stages:-

1) Cleansing the enamel surface with pumice
2) Enamel etching with hydrochloric acid
3) application of sodium hypochlorite.
4) application of dental adhesives.


INTRODUCTION

A frequent question asked by most of patients residing in the fluorotic belt of Punjab (India) is "will my tooth turn white?"
Usually the answer is a "yes" with the explanation that the modern dental treatment procedures are such as to esthetically synchronise the facial harmony of tooth structure.

The reason for this discoloration is a high fluoride concentration in water in certain areas of Punjab.

The normal colour of permanent teeth is greyish yellow, greyish white or yellowish white but the number of people with this colour are usually limited owing to over aggressive tooth brushing and abrasive cleansing materials, acidic food and drinks and last but not the least,ageing.

The elderly people thus, have more yellowish teeth as compared to younger persons.

These alterations in colour maybe physiologic or pathologic and endogenous or exogenous in nature.

The modern era is an era of esthetics.

People having teeth with normal colour also want to have whiter teeth to improve their smile.

So one cannot ignore the wishes of such patients and hence bleaching, as we know, has emerged as the simplest, most common, least invasive and least expensive means available to dentists to lighten discoloration.



HISTORY

Many agents have been used in the past and a number of new methods have continued to be introduced.

It was oxalic acid first by chappel in 1877 which was followed by various forms of chlorine, until hydrogen peroxide was first used by Harlan in 1884.

Many advances continued focussing basically on the ways to facilitate the absorption of bleaching agent.

The recent developments of hi-tech computer imaging have enhanced patient understanding, expectation and ultimately satisfaction.


MODE OF ACTION


Bleaching works by oxidation in which the bleaching agent enters the enamel &/or dentin of the discolored tooth and reduces the molecules containing discoloration. The bleaching depth depends on the cause of the stains and where and how deep the stain has permeated the tooth structure plus how deep the bleaching agent can permeate to the source of discoloration and remain there long enough to release deep stains.



ETIOLOGY OF TOOTH DISCOLORATION

Extrinsic discolorations are found on outer surface of teeth and are usually Of local origin e.g. Tobacco, paan, tea, coffee,turmeric, silver nitrate stains, oral intake of iron suspensions, continuous use of mouth washes and gum paint.

Intrinsic stains are found within the enamel and dentin and are caused by the deposition of the substances within these structures e.g. Tetracycline, Fluorosis stains, amelogenesis imperfecta, dentinogenesis imperfecta, pulp necrosis etc.



HISTOPATHOLOGY


Fluorosed teeth are also called mottled teeth .

Such teeth appear when child ingests excessive fluoride during enamel formation or calcification in areas where drinking water contains more than 1ppm of Fluoride.

The higher concentration of fluoride is believed to cause a metabolic alteration in the ameloblasts which results in defective matrix & improper calcification.

1 ppm of fluoride has no biological side effects on the vital organs of human body i.e. Kidney, heart & lungs.

Fluoride up to 4ppm in drinking water occasionally produces skeletal fluorosis but above 8ppm coupled with malnutrition positively causes not only skeletal fluorosis but irreversible bone changes & deformity as well.



HISTLOGY


Histological examination shows hypomineralised, porous sub-surface enamel below a well mineralised surface layer.

The most affected teeth (in decreasing order) are premolars, 2ndmolars, followed by maxillary incisors, canines & 1st molars.
Mandibular incisors are affected least.



STAGES OF FLUOROSIS


The appearance of teeth depends upon the severity of the lesion which in turn depends upon the fluoride contents consumed by a particular individual through the water supply.

1) the constant use of water having fluoride to the extent of 1ppm causes mildest grade of mottling in 10% of the population.

2) as concentration of fluoride increases, the effect worsens, so much so that when the concentration reaches 6ppm,incidence of mottling is 100%.

3) very mild :- in this type there are very small white areas occasionally seen on the tooth surfaces, but do not involve more than 25% of tooth surfaces.

(4) mild :- in this type there is more extensive tooth involvement and involves 50% of tooth surfaces.

(5) moderate :- more surfaces are involved here and are subjected to attrition. They show marked wear with yellow or brown pigmentation.

(6) severe :- all enamel surfaces are involved, so much so that the tooth morphology is affected.there is discrete or confluent pitting of enamel surfaces.
Brown stains are widespread & the tooth often presents a corroded surface.



OPTIMUM FLUORIDE LEVELS:

In cold climate, recommended fluoride levels may be as high as 1.2 ppm whereas in extremely hot climate, a level of 0.7 ppm is recommended.
In moderate climate, the optimum fluoride level is 1 ppm.

High temperature causes increase in mottling because there is increased consumption of water containing fluoride.

Distribution of mottling in various areas of teeth has no relation with periods of mineralisation of crown.

Teeth are only affected provided the child lives in the area of fluorosis during the time of enamel mineralisation.

Brown tooth stains respond to treatment but white stains are not effectively resolved.

It has been observed that teeth in process of eruption receive maximum benefit from optimum amount of fluoride plus teeth exposed to fluoride shortly after eruption were also protected although to a lesser degree.



DIFFERENT FLUORIDE LEVELS IN PUNJAB & OTHER STATES OF INDIA


I) Punjab
1) bhatinda - 4.5 ppm
2) mansa - 4.2 ppm
3) mukatsar - 3.3 ppm
4) faridkot - 3 ppm
5) ferozepur - 2.6 ppm
6) moga - 2 ppm
7) sangrur - 1.35 ppm
8) jalandhar - 0.55 ppm
9) amritsar - 0.45 ppm 10) hoshiarpur - 0.44 ppm
11) nawanshahar - 0.4 ppm
12) fatehgarh sahib - 0.37 ppm
13) patiala - 0.35 ppm
14) ropar - 0.3 ppm
15) kapurthala - 0.25 ppm
16) ludhiana - 0.22 ppm
17) gurdaspur - 0.15 ppm

II) Andhra Pradesh
1) nalgonda - 20.6ppm
2)prakasan - 12.0ppm
3)vishakhapatnam - 11.0ppm
4) anantpur - 10.1ppm
5)guntar - 10 ppm
6)medak - 9.8ppm
7)kunoor - 9.6ppm
8)nellore - 8 ppm
9)mehboobnagar - 6.4 ppm 10)warrangal - 5.8 ppm
11) kareemnagar - 4.9 ppm
12) hyderabad - 4.8ppm
13) cuddapah - 4.6ppm
14) nizamabad - 3.0ppm
15) chittoor - 2.9 ppm
16) adkabab - 2.8 ppm
17) srikakalam - 2.8 ppm
18) Godavari - 1.6 ppm

III) Gujarat
1) kutch - 1.2 -- 11 ppm
2) bhavnagar - 1.5 - 4ppm
3) jamnagar - 1.5 - 4ppm
4) rajkot - 2.5ppm
5) saurashtra - 1.5 - 2.5 ppm
6) rajpur - 0 - 2.5 ppm 7) banakanta - 1.5 - 2ppm
8) godar - 1.6 - 1.7ppm
9) godhra - 0 - 1.6 ppm
10) surinderanagar - 0 - 1.5 ppm
11) surat - 0 - 1.3 ppm

IV) Tamil Nadu
1) Coimbatore 2) Dharampur 3) Madurai 4) Narkot 5) Salem 6) Trichi
all 1.5 --- 5ppm

V) Kerala
1) Allepey 2) Eranakulam 3) Quillon 4) Trichur
all 0 -- 1.5 ppm

V) Rajasthan
1) Bharatpur - 28ppm
2) Tonk - 21ppm
3) Alwar - 20.6ppm
4) Sikar - 19.1ppm
5) Ajmer - 18.4ppm
6) Bhilwara - 16.5ppm
7) Swaimadhopur - 16.1ppm
8) Jhalawar - 16ppm
9) Churu - 16ppm
10) Jodhpur -16ppm
11) Sirohi - 15.8ppm
12) Jaipur - 15ppm
13) Nalpur - 14.2ppm
14) kota - 14.2ppm
15) dungarpur - 12ppm
16) bikaner - 10.2ppm
17) barmer - 10ppm
18) pali -- 9.1ppm
19) ganganagar - 9ppm
20) jalour -- 8ppm
21) wagpur - 7.1ppm
22) chittorgarh - 6ppm
23) bundi - 5.8ppm
24) banswara - 4.3ppm
25) jhunjhunu - 2.2ppm

VI) Uttar Pradesh
1) Gorakhpur - 0.6-6.8ppm
2) Shahjahanpur - 4ppm
3) Lakhpur -0.1-4ppm
4) Rai bareilly - 0.6-3ppm
5) Banda - 0.6-3ppm
6) Agra - 0.2-3ppm
7) Kanpur - 0.2-3ppm
8) Varanasi - 0.2-3ppm
9) Unna - 0.1-3ppm
10) Aligarh - 0.4-2ppm
11) Allahabad - 0.2-2ppm
12) Itah -0.8-1.6ppm
13) Hamirpur - 0.6-1.6ppm
14) Azamgarh - 0.1-1.6ppm
15) Muradpur - 1.0-1.4ppm
16) Jamalpur - 1.0-1.2ppm
17) Lucknow - 0.8-1.2ppm
18) Meerut - 0.4-1.2ppm
19) Bulandshahar - 0.4-1.2ppm
20) Dijnor - 0.2-1.2ppm
21) Jhansi - 0.2-1.2ppm
22) Bareilly 0.1-0.9ppm
23) Balliya - 0.4-0.8ppm
24) Barabanki - 0.4-0.8ppm 25) fatehgarh - 0.4-0.8ppm
26) mirzapur - 0.4-0.8ppm
27) gadhepur - 0.3-0.8ppm
28) gonda - 0.2-0.8ppm
29) basti - 0.2-0.8ppm
30) jalpum - 0.1-0.8ppm
31) dehradun - 0.1-0.8ppm
32) pratapgarh - 0.4-0.6ppm
33) manipuri - 0.4-0.6ppm
34) lahtpur - 0.1-0.6ppm
35) muzaffarnagar - 0.2-0.5ppm
36) rampur - 0.2-0.4ppm
37) pilibhit - 0.2-0.4ppm
38) bijnor - 0.1-0.4ppm
39) fatehabad - 0.1-0.4ppm
40) badari - 0.1-0.4 ppm
41) sitapur - 0.1-0.4ppm
42) saharanpur - 0.1-0.4ppm
43) mathura - 0.1-0.4ppm
44) faizabad - 0.2ppm
45) etawah - 0.1-0.2ppm
46) nainital - 0.1-0.2ppm
47) dahrich - 0.1-0.2ppm
48) sultanpur - 0.1ppm



TREATMENT OPTIONS

Basically for all these stains or in particular fluorotic stains the treatment options available to us include :-

1) Veneering / laminates or placement of porcelain crowns
2) Micro / macroabrasion
3) Bleaching -
a) vital tooth inoffice bleaching
b) nightguard home bleaching
c) our novel method of inoffice bleaching



1) VENEERING OR LAMINATES OR CRAMIC CROWNS

Advantages:

1) esthetically more acceptable
2) Long lasting
3) Durable
4) Simple
5) Can be given over endodontically treated tooth
6) more strength and resistance to forces

Disadvantages:

1) brittle
2) less shear strengh
3) causes loss of tooth structure
4) patient may not be willing
5) susceptible to fracture
6) due to tooth reduction, pulp & other tissues may face trauma
7) overcontouring may make it appear & feel unnatural
8) vitality tests cannot be done once crowns are properly fit
9) post cementation caries difficult to detect
10) lab.procedure needs precision for proper marginal seal
11) gingival irritation- may cause hyperaemia & bleeding



2) MICRO / MACRO ABRASION:-

This technique involves applying of 18% hcl to soften the enamel And then abrading it with a controlled abrasive technique With pumice to remove superficial stains / defects. Instead of pumice, even silicon carbide may be used with 11%hcl.

Advantages:

1) improved method for superficial stains
2) safer method
3) involves physical removal of tooth structure

Disadvantages:

1) can cause sensitivity
2) causes wearing of tooth structure
3) patients might not allow cutting of tooth structure
4) defect may persist after finishing of technique for which a restorative alternative is needed



3) BLEACHING:-

This procedure has many methods and techniques involving various solutions in each technique.

Advantages:


1) easy
2) time saving
3) cheaper
4) patient acceptance better
5) can be carried out both in office & at home

Disadvantages:


1) requires patient cooperation(especially for home bleaching)
2) cannot be used where teeth have large pulps
3) cannot be used where teeth are too dark
4) cannot be used where the patient expectations are too high
5) cannot be used in impatient patients
6) causes cervical resorption
7) cannot be used in attritioned teeth which might cause sensitivity
8) cannot be used where teeth are bonded, laminated or have extensive restorations
9) not a perfect technique & merely changes colour to variable depths
10) lasts for only 1 - 3 years (short period)



A) Vital tooth inoffice power bleaching

This technique uses a combination of 37% phosphoric acid & 35%hydrogen peroxide.the oxidation reaction is generally promoted by a heated instument or with intensive light.in this method, one application is carried out weekly for 2 - 6 appointments with each treatment lasting 30 minutes. Use of phosphoric acid by this technique is optional.

Advantages:

1) caustic chemicals are totally under dentist's control.
2) soft tissue protection is better achieved by dentist.
3) bleaching of tooth is achieved more rapidly

Disadvantages:

1) slightly costly procedure.
2) unpredictable results.
3) uncertain duration of treatment
4) soft tissue damage possible for both dentist & patient.
5) rubber dam causes discomfort.
6) can cause post operative sensitivity.


B) Night guard home bleaching

This procedure involves making an impression of the teeth & pouring a cast of the same, trimming of the cast, application of a blockout resin & fabrication of a night guard tray by a vaccum former machine.
After cooling, the tray is trimmed & a 10 - 15% gel of carbamide peroxide is recommended for the same.
In this procedure the total treatment time is 2 - 6 weeks.

Advantages:

1) use of lower concentration.
2) ease of application.
3) minimal side effects.
4) lower cost (as compared to veneers)
5) lesser chair time.
6) much lesser labour intensive.

Disadvantages:

1) have to rely a lot on patient compliance for results.
2) longer treatment time.
3) unknown potential for soft tissue changes with excessive use.
4) treatment results are time & dose dependent.
5) peroxide solution may cause irritation of gingival papilla.
6) teeth become sensitive to temperature changes.


Another method using macken's solution has been described
1 part anaesthetic ether 0.2 ml - removes surface debris 5 parts hcl 38% 1ml --- etches 5 parts hydrogen peroxide 30% 1 ml --- bleaches


Our Approach For Inoffice Bleaching

Indications:

1) Fluorosis stains / systemic fluorosis
2) Tetracycline stains

Contra indications:

1) Hyperaemic gingiva
2) Persistant periodontal problem cases
3) Fractured incisors / anteriors



CLINICAL APPLICATION


The various steps are
1) Cleansing
2) Isolating
3) Etching
4) Rinsing
5) Dehydration
6) Application of solution
7) Scrapping
8) Rinsing
9) Filling


The Steps in detail:
1) cleansing the tooth surface with a nylon tooth brush & a mixture of pumice and water to remove surface debris.

2) isolation is done by application of rubber dam.

3) then dry the tooth surface & do enamel etching with 35% hcl for 20 - 25 seconds.

4) copious rinsing is done to eliminate acid residues & the tooth is subjected to thorogh drying.

5) application of 95% ethyl alcohol to dehydrate the enamel surface.

6) now,the application of 30% hydrogen peroxide(h2o2) is done first for 1 minute followed by alternative application of 5.25% sodium hypochlorite (naohcl) is done for 5 minutes during which it can be re-applied to the tooth surface to keep it wet.

7) the removal of staining molecules can be accelerated by gently scrapping the tooth surface.

8) this is followed by thorough rinsing of tooth surface.

9) this procedure is repeated at the interval of three days for successive sittings till the results are satisfactory.

10) in the end, fill the microcavities caused in the tooth by this solution with a light cure dental adhesive.


Advantages:

1) HCl etches enamel,but does not penetrate.
2) Tooth structure is not damaged.
3) Very very few chances of post - operative sensitivity of tooth.
4) No heat / application is required.
5) Very economical as all the three solutions in quantity of 50 ml. Each cost rs. 250 - 300 (total ).
6) Very low quantity of solutions required at each sitting.


Disadvantages :

1) Fluorosed teeth require larger & repeated sessions to decolorise Them.
2) Some blanching of gingiva can occur which is reversible within Half an hour.
3) Transitory decrease in bond strengh occurs when composite is applied to bleached / etched enamel.however,after a week,no decrease is seen.
4) Unknown duration of treatment.



DISCUSSION

The different hypothesis concerning the fluorotic stains removal are:

1) if a fluorotic tooth is put into a NaOHCl solution,it removes all the stains within a few hours.this confirms the organic & exogenous nature of fluorotic tooth stains which are due to elementary impregnation of a hypocalcified & porous tissue. said by :- Triller m. Alterations des tissues by marie curie in 1984.

2) scanning electron microscope study (sem) study shows that Posteruptive calcified layer covers the fluorotic enamel surface ; hence the mineral layer removal is essential.



CONCLUSION

In the end, i would like to conclude that this system of stains removal seems to be clinically applicable & satisfactory with minimal abrasion of enamel surface to make this technique Universally acceptable , lot of cases have to be treated with this technique.

TWO MINUTE BRUSHING HELPS ACHIEVE CLEANER TEETH: STUDY

NEW YORK (Reuters Health) - Although hard work tends to pay off in other areas of life, forceful toothbrushing appears to be no better at ridding the mouth of plaque than a medium effort.

A group of European researchers discovered that the most efficient means of reducing plaque appears to be brushing for about two minutes at a medium force.

More vigorous teeth cleaning may actually do more harm than good, said Dr. Peter A. Heasman of the University of Newcastle upon Tyne, UK. Research suggests that heavy brushing can damage gums and wear down teeth, both potentially serious oral health problems, he said.

"Although we found that you have to brush your teeth reasonably long and hard to get rid of the harmful plaque which causes dental diseases, our research shows that once you go beyond a certain point you aren't being any more effective," Heasman said in a statement.

"You could actually be harming your gums and possibly your teeth," he added.

Heasman and his colleagues designed the study, published in the Journal of Clinical Periodontology, to determine the most efficient way to brush away plaque. Plaque is a sticky substance that can contain more than 300 species of bacteria, which adhere to tooth surfaces and produce cavity-causing acid. Plaque is a leading cause of gum disease.

During the study, Heasman and his colleagues measured plaque levels in the mouths of 12 people after they brushed their teeth using four different forces and for four periods of time -- 30 seconds, 60 seconds, 120 seconds, and 180 seconds.

The study participants brushed using a power toothbrush, which exerted set forces of between 75 grams and 300 grams. All spent 24 hours without cleaning their teeth before testing how well each technique stripped their mouths of plaque.

Heasman said that a force of 75 grams feels much lighter than one of 300 grams. However, he recommended that people visit their dentist to determine how different brushing forces feel.

"It is very difficult for a lay person to differentiate between brushing forces," Heasman told Reuters Health.

Longer brushing generally appeared better, but the researchers found that 120 seconds of brushing was roughly just as effective at removing plaque as longer brushing. And during those longer sessions, people removed about the same amount of plaque using a force of 150 grams as when they employed forces of 225 and 300 grams.

Although different people may require more or less time to get at all the plaque-ridden nooks and crannies in their mouth, spending around two minutes brushing your teeth seems "about right", Heasman said.

And applying a force beyond 150 grams -- somewhere in between light and forceful brushing -- "offered little benefit to plaque removal," Heasman added.

Furthermore, in toothbrushing, it is possible to have too much of a good thing, the researcher said.

"In the short term, gum changes may become apparent, but in the longer term, tooth wear or toothbrush abrasion is likely with too abrasive a technique, toothpaste, brush or force," Heasman said.

SOURCE: Journal of Clinical Periodontology 2003;30:409-413.

BRUSHING RIGHT AFTER DRINKING SODA (CARBONATED DRINKS) MAY HARM THE TEETH

BERLIN (Reuters Health) - If you rush to brush your teeth right after drinking soda (aerated cold drinks), think again.
Doing so may actually do more harm than good, and it's better to wait 30 or 60 minutes before brushing, according to new research.


Because carbonated drinks are highly acidic and have the potential to damage a tooth's enamel, dentists at Goettingen University, Germany, conducted a study to determine the best time to brush after drinking such beverages.
They found that later -- rather than immediate -- brushing is between three and five times more effective at protecting enamel from the erosive effects of carbonated drinks.


In the study, 11 volunteers wore a sterilized piece of tooth-like material in a removable prosthesis for three weeks.
This was removed in the mornings and evenings and soaked for 90 seconds in a liquid similar in acidity to soda.


Afterwards, the prosthesis was brushed using an electric toothbrush at different times after the 'drink.'
Three weeks later, the researchers measured the thickness of the enamel to see how much damage had been inflicted on the 'tooth.'


Professor Thomas Attin, director of the university's department for tooth protection, preventative dentistry and periodontology, said, "The loss of material was less when the participants waited with cleaning for between 30 and 60 minutes."


Professor Attin presented the research at the annual meeting of the German Association for Tooth Protection, where it was awarded a prize from chewing gum firm Wrigley.


He said tooth enamel appears to suffer less damage when brushing occurs after the tooth has had time to mount its own defence against acidic erosion.


Acidic substances attack tooth enamel, he said, and upper layers of the tooth can even be dissolved in some acidic drinks. However, protective agents in saliva may help repair and rebuild damaged tooth enamel.

Waiting for a while seems to give the teeth a chance to rebuild, the researchers said, while immediate cleaning of such teeth can increase the damage by literally brushing off the affected layers.

CHLORHEXIDINE MOUTHWASH

Chlorhexidine has been proven to be the most effective chemical agent for the reduction of plaque and gingivitis.

1. Reduces pellicle formation.

2. Alters bacterial cell wall causing lysis.

3. has High degree of substantivity i.e., it adheres to tissues and remain for a long time, increasing its effectiveness in fighting bacteria.

5. Non specific antimicrobial activity of chlorhexidine has not been associated with development of resistance of pathological oral bacteria.

6. Due to its fungicidal action, chlorhexidine may benefit HIV infected people because of their propensity to contract oral candidiasis.



As a mouth rinse to control plaque and gingivitis, it is recommended to be used twice daily.
It should not be used within 30 to 60 minutes of a tooth paste since most tooth pastes contain sodium laural sulphate, which can deactivate chlorhexidine.
Also, stannous fluoride products should always be used after chlorhexidine since stannous ion and chlorhexidine both compete for and occupy the same site on the tooth.

Some side effects of chlorhexidine include staining of teeth reversible desquamation in young children, alteration of taste.

Sunday, October 12, 2008

DRY SOCKET

Dry socket is a condition which affects millions of patients around the world specially those who undergo tooth extraction.
This painful event can be avoided in majority of cases by proper understanding. It will then save unnecessary agony to patients and loss of countless hours of dentist's practice in dealing with it.


This condition occurs after tooth extraction, particularly after traumatic extraction, resulting in a dry appearance of the exposed bone in the socket, due to disintegration or loss of the blood clot.
It is basically a focal osteomyelitis without suppuration and is accompanied by severe pain (alveolalgia) and foul odor.
It is also called alveolar osteitis and alveolitis sicca dolorosa. (Dorland, 27th Ed)


The most common, most dreaded and most painful complication of tooth extraction. Clinicians call it a "dry socket" a misnomer that fails to stress the importance of infection in its etiology.
Affected person complains of unbearable pain and sensitivity of intake of food or drinks.


Dry socket usually develops after 3 to 5 post surgical days.
The pathogenesis of dry socket (also called fibrinolytic alveolitis) is a subject of debate with two main opinions.
The first one is based on the presumption that there is a absolute absence of blood clot.
According to the second opinion there is initial blood clot formation, which subsequently gets lysed leaving behind an empty socket.
Streptococci have been implicated as causative organisms, but lysis might occur without bacterial presence also

The following factors are considered important in causation of dry socket:

1. Insufficient blood supply to the alveolus.

2. Preexisting infection. (Granuloma, periodontal or pericoronal infection)

3. Use of large amounts of local Anesthetic, leading to vasoconstriction.

4. Post operative bleeding.

5. Trauma to alveolus during extraction.

6. Infection during or after extraction.

7. Root/bone fragments or foreign bodies left in the socket.

8. Excessive irrigation and curettage.

9. Fibrolytic or proteolytic activity in the clot.

10. Loss of clot due to patient's negligence

11. Predisposing factors in patient, eg smoking, poor general health

12. Dry socket is more often seen in the mandibular molars particularly the third molars. This condition is associated with excruciating pain, foul breath, unpleasant taste, empty socket and gingival inflammation and Lymphadinopathy.


By avoiding all possible averse factors, risk of dry socket becomes less.

Prophylactic packing of alveolus with medicated dressing and advising patient to use 0.2% chlorhexidine mouth rinse may be helpful to avoid dry socket in suspect cases.


Treatment of dry socket is mainly done to control pain by analgesics, advice warm saline rinse to remove food debris, dressing the cavity to protect & heal the socket.
In early stages just initiating fresh bleeding in the socket and giving a pack will resolve this condition.


Zinc oxide dressing also have been advised.


With these precautions and treatment the pain should reduce and granulation of the socket should be observed.
Antibiotic therapy may be used if desired.
Most sockets resolve in 4-5 days.


USEFUL Tips:

1. Always compress the socket after extraction so that chances of clot retention are better.

2. Give all instructions to patient so that he does not disturb the extraction site wound.

3. Ask smoker to stop until extraction wound has healed.

Body has great healing capacity, avoid unnecessary routine irrigation of socket with antiseptic solutions.

If dry socket develops do a simple trick it works for 99.99% cases, take a sharp sickle scaler and scrap the gums surrounding socket, let fresh blood fill the socket, give a pack (wet squeezed gauze)
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Saturday, October 4, 2008

TONGUE SCRAPING





Tongue scraping is a daily health-maintenance procedure that very few people bother with, probably because they don't yet realize they need to keep their tongues clean.
However, maintaining fresh breath & healthy gum tissue means you have to remove plaque on a regular basis to keep both your breath & tongue fresh & healthy; food debris, odorous dead bacteria & skin cells, as well as stagnant oral fluids have health & social consequences that are largely avoidable.
Nobody wants bad breath or gum disease, & this section will show you how to take better control of both problems through the use of a tongue scraper.

Why should we bother to scrape our tongues?
First, it is important to realize that the tongue doesn't have a smooth surface, as most people assume.
Rather, it is covered by wormlike projections called filiform papillae that can be long or short, & generally number in the thousands.
One way to visualize these filiform papillae is to compare them to a shag rug.
The wet, not-very-clean shag is what the upper surface of the tongue is like in the majority of people.
The larger surface area of the tongue may harbor many more micro-organisms; there can be literally trillions of living, dying, rotting, stinking micro=organisms on top of the tongue.
Dead skin cells, food debris, & oral fluids are literally saturating the area around the papillae, intermingling with the innumerable micro-organisms -- & they are most definitely not harmless or unnoticed by others (for e.g. bad breath)
Whether the stew is on the tongue or trapped in the sulci, it still stinks, still causes soft tissue breakdown, & still creates inflammation, sometimes dramatically.
Sometimes patients' tongues will be quite tender, & will bleed on tongue scraping efforts-not surprising considering that the same tissue-destroying enzymes & odors that are under the gums in the sulci are in the stew on the top of the tongue.
The tenderness & bleeding usually abate quickly once the tongue gets cleaned daily.

Most scrapers come either as a plastic strip with serrated edges, or as a single-handled metal or plastic device.
Tongue can be cleaned with the toothbrush also.

When scraping the tongue, it is very important to scrape as far back as possible, since getting rid of micro-organisms & odorous debris depends on how effectively this step is performed.
The gag reflex can be a problem for some just starting this important habit, but it is usually overcome quickly & generally ceases to be a problem.
Having a healthy mouth & fresh breath can be a powerful motivator.

How do you know when your tongue is clean?
You'll know when you are scraping & no longer getting any odorous residue, & when your tongue is totally pink



fig. 1. surface of tongue with VSCs & gram negative bacteria
fig. 2. toothbrushing just breaks apart bacteria
fig. 3. scraper sweeps away gram negative bacteria
fig. 4. Rinse clean the deep fissures

Friday, October 3, 2008

DOWN'S SYNDROME / MONGOLIANISM / MONGOLISM / TRISOMY 21






Down syndrome (DS), also called Trisomy 21, is a condition in which extra genetic material causes delays in the way a child develops, both mentally and physically.
It affects about 1 in every 800 babies.

The physical features and medical problems associated with Down syndrome can vary widely from child to child.
While some kids with DS need a lot of medical attention, others lead healthy lives.

Though Down syndrome can't be prevented, it can be detected before a child is born. The health problems that can go along with DS can be treated, and there are many resources within communities to help kids and their families who are living with the condition.



Normally, at the time of conception a baby inherits genetic information from its parents in the form of 46 chromosomes: 23 from the mother and 23 from the father.
In most cases of Down syndrome, a child gets an extra chromosome 21 — for a total of 47 chromosomes instead of 46.
It's this extra genetic material that causes the physical features and developmental delays associated with DS.

Although no one knows for sure why DS occurs and there's no way to prevent the chromosomal error that causes it, scientists do know that women age 35 and older have a significantly higher risk of having a child with the condition.
At age 30, for example, a woman has about a 1 in 900 chance of conceiving a child with DS.
Those odds increase to about 1 in 350 by age 35.
By 40 the risk rises to about 1 in 100.




Kids with Down syndrome tend to share certain physical features such as a flat facial profile, an upward slant to the eyes, small ears, and a large or protruding tongue.



Low muscle tone (called hypotonia) is also characteristic of children with DS, and babies in particular may seem especially "floppy." Though this can and often does improve over time, most children with DS typically reach developmental milestones — like sitting up, crawling, and walking — later than other kids.


At birth, kids with DS are usually of average size, but they tend to grow at a slower rate and remain smaller than their peers.
For infants, low muscle tone may contribute to sucking and feeding problems, as well as constipation and other digestive issues.
Toddlers and older kids may have delays in speech and self-care skills like feeding, dressing, and toilet teaching.


Down syndrome affects kids' ability to learn in different ways, but most have mild to moderate intellectual impairment.
Kids with DS can and do learn, and are capable of developing skills throughout their lives.
They simply reach goals at a different pace — which is why it's important not to compare a child with DS against typically developing siblings or even other children with the condition.

Kids with DS have a wide range of abilities, and there's no way to tell at birth what they will be capable of as they grow up.


Dental association with DS
Introduction:
The orofacial and skeletal development associated with Down's Syndrome contribute to dental problems. It is important to be aware of the type of anatomical soft tissue and dental anomalies which are part of the typical developmental pattern of people with Down's Syndrome, which have influence on dental problems.

Anatomical development changes the cranial base, the mid third of the face and the proportion between the maxilla and mandible. This alteration of the skeleton leads to people with Down's Syndrome having a recognisable facial appearance. The soft tissue feature most affected is the tongue, which is fissured and protrusive. The tongue appears large because it has to rest in a narrow dental arch. The tonsils and adenoids are also enlarged.

Dental anomalies are related to the tooth morphology in that there is:

* Decreased root to crown ratio
* Decreased tooth size
* Hypodontia or partial anodontia
* Delayed eruption


DENTAL PROBLEMS:


The normal development of oral structure and function is altered leading to compromised development of suckling, swallowing, mastication and speech; and to drooling unless there is effective intervention.

The degree of difficulty varies from person to person:




Preventive measures and therapy are needed to ameliorate the problems found in swallowing and mastication. Here an integrated approach can be adopted with the Speech and Language Therapist.




DENTAL DISEASE


People with Down's Syndrome are prone to the same degree of dental disease as the general population.

Periodontal disease
: People with Down's Syndrome develop more severe forms of periodontal disease than the general population.
This may be related to immunological deficiency factors.
This disease is most rampant in young people between 16 and 20 years old.
The progression of the disease gives rise to periods of acute infection and pain, which may result in changes in behavior, refusal to eat or swallowing food whole.

Caries: Various studies have shown a reduced incidence of caries in children and young adults with Down's Syndrome.
This may be due to the fact that many of these children are under supervision in regard to their diet in order to prevent their tendency to obesity.
This is where the dentist and the dietician can work together to make sure the food being consumed is working towards oral and general health improvement.

Risk associated with infection is raised in people with Down's Syndrome as the incidence of congenital cardiac disease is increased in this group (3% to 40%), resulting in a serious risk of endocarditis.

The gag reflex can occur even in the anterior portion of the oral cavity. Any further back than the premolars a gag reflex may be accompanied by a gastro-oesophegal reflux. Children find this most uncomfortable.

Bruxism occurs in people with Down's Syndrome and may be triggered by a state of chronic anxiety, dental malocclusion, temporo mandibular joint dysfunction due to laxity of the supporting ligaments, and/or underdeveloped nervous control.

Dental trauma is frequently experienced due to lack of motor development.
Fracture or luxation of the anterior teeth is frequent and often involves loss of tooth vitality.

TREATMENT & PREVENTION

* Good oral hygiene and supervised tooth brushing programmes
* Education, e.g. via videotapes
* Diet, communication and use of oral muscles. This requires an integrated approach to care, as it involves a team of professionals and carers.
* Management of any malocclusion requires a multi-disciplinary team to carry out diagnosis and treatment planning (e.g. Orthodontist, Restorative and Oral Maxillo-Facial Surgeons)