Dilaceration is a developmental disturbance in shape of teeth. It refers to an angulation, or a sharp bend or curve, in the root or crown of a formed tooth.

Presence of curvature may pose difficulty in root canal instrumentation. The final result of instrumentation of curved canals may be influenced by several factors such as flexibility and diameter of the endodontic instruments, instrumentation techniques, location of the foraminal opening and the hardness of dentin.

The recession on tooth #24 is into the mucogingival junction without loss of surround interdental area.

Limitations
Miller’s classification used the criteria of diagnosis and prognosis for classification.  Although Miller’s classification has been used extensively, there are limitations that need to be considered:

The reference point for classification is MGJ. The difficulty in identifying the MGJ creates difficulties in the classification between Class I and II.  There is no mention of presence of keratinized tissue. A certain amount of keratinized gingiva (in the form of free gingiva) will be evident in any tooth with the gingival recession; the marginal tissue recession cannot extend to or beyond the MGJ. In such a case, Class II cannot be a distinct class and Classes I and II would represent a single group.

In Miller’s Class III and IV recession, the interdental bone or soft-tissue loss is an important criterion to categorize the recessions. The amount and type of bone loss has not been specified. Mentioning Miller’s Class III and IV doesn’t exactly specify the level of interdental papilla and amount of loss. A clear picture of severity of recession is hard to project.

Class III and IV categories of Miller’s classification stated that marginal tissue recession extends to or beyond the MGJ with the loss of interdental bone or soft-tissue is apical to the CEJ. The cases, which have inter-proximal bone loss and the marginal recession that does not extend to MGJ cannot be classified either in Class I because of inter-proximal bone or in Class III because the gingival margin does not extend to MGJ. Two such cases have been presented in Figure  and Miller’s classification doesn’t specify facial (F) or lingual (L) involvement of the marginal tissue.

Recession of interdental papilla alone cannot be classified according to the Miller’s classification. It requires the use of an additional classification system.

Classification of recession on palatal aspect is another area of concern. The difficulty of the applicability of Miller’s criteria on the palatal aspect of the maxillary arch can be reasoned out to the fact that there is no MGJ on palatal aspect. Therefore, a classification is required, which specifies the type of recession and can also quantify the amount of loss. The classification should be able to convey the status of the gingival recession and the severity of the condition on palatal aspect. Recession on palatal aspects changes the overall diagnosis and prognosis of a case. Mucogingival treatment of the recession may be required for reasons other than esthetics.

Miller’s classification estimates the prognosis of root coverage following grafting procedure. Miller stated that 100% coverage can be anticipated in Class I and II recessions, partial root coverage in Class III and no root coverage in Class IV.  Pini-Prato stated that anticipation of 100% root coverage does not mean that it will occur. Root coverage percentage ranging from 9% to 90% have been reported by different authors in Class I and II recessions using different techniques. Outcome of treatment may depend on other prognostic factors and categorization to predict the outcomes of root coverage in Classes I and II are not correct.

Another classification had been proposed based on the assessment of clinical attachment level at both buccal and interproximal sites.

Considering the above limitations, a new classification system is being proposed which is more detailed, informative and lucid. This classification system is based on an amalgamation of certain criteria of Miller’s classification with the certain features of Nordland and Tarnow’s classification. A distinct classification for gingival recession on palatal aspect is also being proposed.

Red dots are placed above the probing depth number to indicate that there was bleeding upon probing in the pocket.

O’Leary Plaque Index

Your patient has 21 teeth x 4 surfaces=84 surfaces, with 32 plaque surfaces.  32/84=38%

Your patient has 21 teeth x 4 surfaces=84, with 52 plaque free surfaces.  52/84=62%

There are several causes of tooth discoloration, including:
Foods/drinks. Coffee, tea, colas, wines, and certain fruits and vegetables (for example, apples and potatoes) can stain your teeth.

Tobacco use. Smoking or chewing tobacco can stain teeth.

Poor dental hygiene. Inadequate brushing, flossing, and rinsing with an antiseptic mouthwash to remove
plaque and stain-producing substances like coffee and tobacco can cause tooth discoloration.

Disease. Several diseases that affect enamel (the hard surface of the teeth) and dentin (the underlying material under enamel) can lead to tooth discoloration. Treatments for certain conditions can also affect tooth color. For example, head and neck radiation and chemotherapy can cause teeth discoloration. In
addition, certain infections in pregnant mothers can cause tooth discoloration in the infant by affecting enamel development.

Medications. The antibioticstetracycline and doxycycline are known to discolor teeth when given to children whose teeth are still developing (before age 8). Mouth rinses and washes containing chlorhexidine and cetylpyridinium chloride can also stain teeth. Antihistamines (like Benadryl), antipsychotic drugs, and drugs for high blood pressure also cause teeth discoloration.

Dental materials. Some of the materials used in dentistry, such as amalgam restorations, especially silver sulfide-containing materials, can cast a gray-black color to teeth.

Advancing age. As you age, the outer layer of enamel on your teeth gets worn away, revealing the natural yellow color of dentin.

Genetics. Some people have naturally brighter or thicker enamel than others.

Environment. Excessive fluoride either from environmental sources (naturally high fluoride levels in water) or from excessive use (fluoride applications, rinses, toothpaste, and fluoride supplements taken by mouth) can cause teeth discoloration.

Trauma. For example, damage from a fall can disturb enamel formation in young children whose teeth are still developing. Trauma can also cause discoloration to adult teeth.

Intrinsic tooth stains are those that originate from within the tooth structure and are typically attributed to internal factors such as developmental defects, systemic diseases, or exposure to excessive fluoride during tooth development. These stains give teeth a yellow or gray hue and are often more challenging to remove compared to extrinsic stains. Unlike extrinsic stains, which are primarily caused by external factors such as dietary habits and tobacco use, intrinsic stains affect the deeper layers of the tooth and may require professional intervention, such as tooth whitening or cosmetic bonding, for effective management. Understanding the characteristics and etiology of intrinsic tooth stains is essential for dental hygiene students, as it influences treatment planning and patient education regarding tooth discoloration and aesthetic concerns.

What Are Extrinsic Stains?
Extrinsic stains are stains on the outside of your teeth, or the enamel, and are the most familiar type of tooth discoloration. Ways that your tooth enamel may stain can range from everyday eating and drinking to smoking and lack of good dental hygiene. From that morning cup of coffee to whatever adorns your dinner plate; all have the potential to cause extrinsic staining.

What Is Intrinsic Discoloration?
Intrinsic discoloration is when the inner layer of the teeth, or dentin, becomes discolored. This is usually caused by internal problems, or even from taking certain medications. This is harder to treat than extrinsic staining because this deals with the dentin on the inside of your tooth.  When the dentin becomes discolored, giving your teeth a yellow or gray hue. There could be something occurring that is more serious than just discoloration, like potential tooth decay, or other oral health issues.

The periodontal relevance of anterior and posterior crowding concerns 3 main aspects:
1. oral hygiene/plaque retention,
2. altered topography of gingiva, septum and orofacial alveolar bone and
3. periodontal therapy (scaling, root planing, regenerative approaches).

Nicotine stomatitis is a diffuse white patch on the hard palate, usually caused by tobacco smoking, usually pipe or cigar smoking. It is painless, and it is caused by a response of the palatal oral mucosa to chronic heat. A more pronounced appearance can occur with reverse smoking, sometimes distinguished from stomatitis nicotina by the term reverse smoker’s keratosis.

A gumma is a soft, non-cancerous growth resulting from the tertiary stage of syphilis. It is a form of granuloma. Gummas are most commonly found in the liver (gumma hepatitis), but can also be found in brain, heart, skin, bone, testis, and other tissues, leading to a variety of potential problems including neurological disorders or heart valve disease.

*Mad cow disease facts medically edited by Charles Patrick Davis, MD, PhD
• Mad cow disease (bovine spongiform encephalopathy or BSE) is a progressive neurological disorder.
• Mad cow disease is caused by an infectious transmissible agent termed a prion.
• Mad cow disease was first noted in the 1970s and is thought to be related to another prion-caused disease termed scrapie that occurs in sheep; the first major outbreak of mad cow disease was in the United Kingdom, where more than 184,500 cases have been noted in cattle (2010 U.K. data found only 11 infected cattle).
• There is a relationship between mad cow disease and a human prion disease called variant Creutzfeldt-Jakob disease.
• In the United States, four cattle have been identified as having been infected with mad cow disease prions, while in Canada, 20 cases have been identified.

*Mad cow disease facts medically edited by Charles Patrick Davis, MD, PhD
• Mad cow disease (bovine spongiform encephalopathy or BSE) is a progressive neurological disorder.
• Mad cow disease is caused by an infectious transmissible agent termed a prion.
• Mad cow disease was first noted in the 1970s and is thought to be related to another prion-caused disease termed scrapie that occurs in sheep; the first major outbreak of mad cow disease was in the United Kingdom, where more than 184,500 cases have been noted in cattle (2010 U.K. data found only 11 infected cattle).
• There is a relationship between mad cow disease and a human prion disease called variant Creutzfeldt-Jakob disease.
• In the United States, four cattle have been identified as having been infected with mad cow disease prions, while in Canada, 20 cases have been identified.

Focal sclerosing osteomyelitis
-mandibular molar usually involves, most often 1st molar
-sclerotic bone or bony scar

Cementoblastoma
-Benign
-cementum-like tissue
-younger adults
-lesions may be painful & tooth remains vital
-lesion is attached to tooth root and appears as an opaque calcified mass

Complex odontoma
-collection of hard tissue and pulp all together in a mass-like calcified

Compound odontoma
-resembles small teeth
-found in anterior maxilla

Odontoma
-mixed odontogenic tumors of both epithelial & mesenchymal tissue
-tissue is mixture of enamel, dentin, cementum, and pulp
-most common type of odontogenic tumor
-under age 20

Cementoblastoma
-Benign
-cementum-like tissue
-younger adults
-lesions may be painful & tooth remains vital
-lesion is attached to tooth root and appears as an opaque calcified mass

Intraoral dental sinus (also termed a parulis and commonly, a gumboil) is an oral lesion characterized by a soft erythematous papule (red spot) that develops on the alveolar process in association with a non-vital tooth and accompanying dental abscess.  A parulis is made up of inflamed granulation tissue.

Chemical Composition of Calculus
Plaque in situ is composed of almost 80% water and bulk of the solid phase is comprised of protein (glycoproteins). Immunoglobulins such as IgA, IgG and IgM have been detected in the dental plaque. The protein composition of dental plaque appears to be little influenced by the composition of the diet.
Plaque contains carbohydrates and there is little doubt that the amount of carbohydrate in plaque is influenced by the composition of the diet. The type of carbohydrates formed is also determined by the diet. The bulk of the polysaccharide in plaque is also determined by the diet. Most of the polysaccharide in plaque is extracellular. The two common and important extra-cellular polysaccharides are glucan and fructan. The synthesis of polysaccharide probably represents an attempt by microorganisms to store sources of energy as fructans can be readily metabolized by plaque bacteria. The glucans help in colonization of bacteria on tooth surfaces.

Plaque contains inorganic materials of which Ca, P04and F are of great importance. The level of Ca and P04in plaque play a crucial role in the pathogenesis of dental caries and formation of dental calculus. Significantly higher levels of Ca and P04 are found in the plaque from areas where calculus forms most frequently. Whereas lower levels of Ca and P04 are generally associated with carious areas in the oral cavity.

Fluoride is cariostatic. Therefore, the level of fluoride in plaque can significantly influence the cariogenic activity of the micro-organisms and the stability of the tooth enamel. The fluoride in plaque is not derived from tooth enamel and is concentrated from saliva, gingival fluid and drinking water.

Saliva plays a crucial role in maintaining oral health, and understanding the anatomy of salivary glands and their ducts is essential for dental hygienists. Saliva from the parotid gland flows over the facial surfaces of upper molars via Stensen’s duct, while Wharton’s duct and Bartholin’s duct deliver saliva to the lingual surfaces of lower incisors from the submandibular and sublingual glands, respectively. This distribution of saliva helps lubricate oral tissues, facilitate chewing and swallowing, and provide protection against dental caries and oral infections. Recognizing the pathways of saliva delivery from major salivary glands to specific tooth surfaces is crucial for dental hygiene students, as it informs patient education and oral hygiene recommendations aimed at optimizing salivary flow and oral health.

• Option A) Incorrectly suggests that oral mucoceles are consistently large and always transparent with a blue tinge, which is not accurate. They can vary in size and appearance.
• Option B) Misrepresents the characteristics of oral mucoceles by stating that they consistently appear fluctuant and firm on palpation, without any recurrent swelling or rupturing of contents, which may occur in some cases.
• Option C) Accurately describes the various characteristics of oral mucoceles, including their size variability, slightly transparent appearance with a blue tinge, variable consistency on palpation, duration ranging from days to years, and potential for recurrent swelling and rupturing of contents.
• Option D) Incorrectly describes oral mucoceles as always small and firm, without any fluctuation, recurrent swelling, or rupturing of contents, which is not consistent with their presentation.
• Option E) Misrepresents the typical characteristics of oral mucoceles by suggesting they are usually large, solid, and cystic, without any transparency or potential for rupture or recurrence, which is not accurate.
Therefore, C) provides an accurate description of the characteristics of oral mucoceles, covering their variability in size, appearance, palpation findings, duration, and potential for recurrence.

The bacterial equilibrium position varies at different stages of formation. Below is a summary of the bacteria that may be present during the phases of plaque maturation.
• Early biofilm: primarily gram-positive cocci
• Older biofilm (3–4 days): increased numbers of filaments and fusiforms
• 4–9 days undisturbed: more complex flora with rods, filamentous forms
• 7–14 days: vibrios, spirochetes, more gram-negative organisms

The area that the yellow arrow is pointing to is clearly not a restoration, so the most likely response is a carious lesion. It could also be a defective filling, but that is not among the choices listed.

One should be able to eliminate answer choices C and D as gingivitis and periodontitis affects where teeth are present. In this case, there are no teeth where the arrows are pointing to so one can eliminate answer choices C and D. There are no crowns present where the arrows are pointing and the root tips are visible. Therefore, answer choice B is correct.
Correct Answer is: B

In utilizing picture C, radiograph A and the bitewings available, it is clear that there are root tips remaining.

How do you take aspirin?

Your doctor will recommend a dose of aspirin and how often to take it. Most people take aspirin every day to help prevent a heart attack or a stroke, but others might take aspirin every other day. Be sure you know what dose of aspirin to take and how often to take it.

Low-dose aspirin (81.25 mg) is the most common dose used to prevent a heart attack or a stroke. But the dose for daily aspirin can range from 81.25 mg to 325 mg. One low-dose aspirin contains 81.25 mg. One regular-strength aspirin contains about 325 mg.

For aspirin therapy, do not take medicines that combine aspirin with other ingredients such as caffeine and sodium.

Low-dose aspirin seems to be as effective in preventing heart attacks and strokes as higher doses.
Take aspirin with food if it bothers your stomach.

Alcoholic patients frequently consume more than 50% of their daily caloric intake in the form of ethyl alcohol, with much of the remaining caloric intake coming from sweet drinks high in simple sugars. Alcohol is also the most common cause of sialadenosis of the parotid gland, a peripheral autonomic neuropathy occurring in 30%–80% of patients with cirrhosis. This condition manifests with noninflammatory swelling of the parotid gland and decreased secretion of saliva, which in turn reduces the ability to neutralize cariogenic acid.

Prolonged exposure to ultraviolet (UV) radiation from sunlight is recognized as a significant risk factor for the development of oral cancer, particularly in individuals with outdoor occupations or recreational habits. UV radiation can induce DNA damage and mutations in the cells of the oral mucosa, increasing the risk of malignant transformation and the development of oral cancer. Other established risk factors for oral cancer include tobacco use (smoking and smokeless tobacco), heavy alcohol consumption, human papillomavirus (HPV) infection, and a history of prior oral cancer or precancerous lesions. Dental hygienists play a crucial role in educating patients about these risk factors and performing routine oral cancer screenings to facilitate early detection and referral for further evaluation and treatment. Understanding the risk factors associated with oral cancer is essential for dental hygiene students preparing for board examinations, as it underscores the importance of comprehensive oral health assessment and patient education in preventing and managing oral cancer.

Amlodipine (Norvasc) is in a group of drugs called calcium channel blockers. Amlodipine relaxes (widens) blood vessels and improves blood flow.

Amlodipine is used to treat high blood pressure (hypertension) or chest pain (angina) and other conditions caused by coronary artery disease. This medication is for use in adults and children who are at least 6 years old.

Hyperdontia is the condition of having supernumerary teeth, or teeth that appear in addition to the regular number of teeth. They can appear in any area of the dental arch and can affect any dental organ.

Hyperdontia is the condition of having supernumerary teeth, or teeth that appear in addition to the regular number of teeth. They can appear in any area of the dental arch and can affect any dental organ.

The purpose of informed consent is to assure that the patient has a full understanding of proposed treatment and can make a relevant health-care decision based on the information provided by the health-care professional. Many health-care professionals see the process as burdensome and time-consuming. However, according to the CNA HealthPro Risk Management Program, “The informed consent discussion represents the first step in managing the patient’s expectations for treatment outcomes and reducing the possibility of a misunderstanding.” Patients are less likely to file a lawsuit if they are fully informed about risks and possible outcomes.

There are several components of the informed consent discussion. They are:

1. The nature of the proposed treatment, including necessity, prognosis, time element, and cost.
2. Viable alternatives to the proposed treatment, including what a specialist might offer or the choice of no treatment.
3. What are the foreseeable risks, including things likely to occur and risks of no treatment.

When obtaining informed consent, the dental professional should:

1       Use language that is easily understandable.
2       Provide opportunities for patient questions, such as “What more would you like to know?” or “What are your concerns?”
3       Assess patient understanding by stating, “If I have not explained the proposed dentistry clearly or if you have difficulty understanding, please tell me so we can discuss anything you do not understand.”

The palatal rugae are the wrinkles/folds on the hard palate the are found behind the lingual surfaces of the maxillary anterior teeth.

Merriam Webster defines palatal rugae as: One of the folds of the mucous membrane of the roof of the mouth.

Supraeruption (supereruption, hypereruption) is the process of the continued axial migration of a tooth without an opposing tooth to prevent the migration.

The eruption of the permanent first molars, also known as the “six-year molars,” typically occurs around 6-7 years of age. These molars are the first permanent teeth to erupt in the oral cavity and are located distal to the primary second molars, often emerging behind them. Understanding the approximate timing of tooth eruption is crucial for dental hygienists in assessing dental development and providing appropriate guidance to parents and caregivers regarding oral hygiene practices and preventive dental care for pediatric patients. Dental hygienists should be familiar with the typical sequence and timing of tooth eruption to effectively monitor dental development and address any concerns or deviations from the norm during routine dental examinations.

Cardiac patients on anti-platelet therapy may require extractions for their diseased teeth. It is a common practice among physicians and treating surgeons to stop aspirin prior to tooth extraction because of fear of bleeding complications. This practice often predisposes the patient to adverse thromboembolic events. This practice is based on theoretical risk of bleeding and on isolated case reports of excessive bleeding with aspirin therapy. The current consensus and recommendations are in favor of continuing aspirin therapy during simple tooth extraction as the bleeding complication incidence is very less and if it occurs can be controlled efficiently with local hemostasis measures.

Dental attrition is a type of tooth wear caused by tooth-to-tooth contact, resulting in loss of tooth tissue, usually starting at the incisal or occlusal surfaces.

Abfraction is a theoretical concept explaining a loss of tooth structure not caused by tooth decay (non-carious cervical lesions). It is suggested that these lesions are caused by forces placed on the teeth during biting, eating, chewing and grinding; the enamel, especially at the cementoenamel junction (CEJ), undergoes large amounts of stress, causing micro fractures and tooth tissue loss.

Acid erosion, also known as dental erosion or dental corrosion, is a type of tooth wear. It is defined as the irreversible loss of tooth structure due to chemical dissolution by acids not of bacterial origin.

Alveolar ridge deficiency
In 1983, Seibert classified alveolar crestal defects:

Class I: buccolingual loss of tissue with normal apicocoronal ridge height
Class II: apicocoronal loss of tissue with normal buccolingual ridge width
Class III: combination-type defects (loss of both height and width)

Usually dark brown to black in color (color is from blood).

What bacteria are associated with the carious process?
streptococcus mutans

associative role:
lactobacillus
bifidobacteria

Bacteria associated with periodontal disease: 

class I
pit, fissures, grooves

class II
proximal surface of posteriors

class III
proximal surface of anteriors

class IV
proximal surface of anteriors with incisal edge or angle involvement

class V
smooth surface in F/L on gingival third of clinical crown

class VI
incisal edge of anterior or cusp tip of posterior