Dentin wreb hygienists sample

DENTIN™ | WREB-HYGIENISTS

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TABLE OF CONTENTS CHAPTER 1 PERIODONTICS Periodontium & Fibers .......................................................................................................................... 7 Flaps, Grafts, & Surgery ..................................................................................................................... 13 Osseous Defects ................................................................................................................................ 18 Gingivitis & Periodontitis .................................................................................................................... 22 Pocket Depth, CAL, & Periodontal Prognosis .................................................................................... 34 Gingival Recession & Toothbrush Abrasion ....................................................................................... 36 Plaque & Calculus .............................................................................................................................. 38 LANAP, SRP, & Gingival Currettage .................................................................................................. 44 Occlusal Trauma & Mobility ............................................................................................................... 48 Abscesses of the Periodontium ......................................................................................................... 51 LAA to Treat Periodontal Disease ...................................................................................................... 54 Periodontal Treatment Planning ......................................................................................................... 55 Plaque Induced Gingival Diseases ..................................................................................................... 55 Non-Plaque Induced Gingival Lesions ............................................................................................... 58 Oral Hygiene Instruction & Irrigants ................................................................................................... 60 Staining & Dental Index ...................................................................................................................... 63 Hygiene Instrumentation .................................................................................................................... 66 Instrument Sharpening ....................................................................................................................... 75 Implants .............................................................................................................................................. 78

CHAPTER 2 ORAL PATHOLOGY Metabolic & Genetic Diseases ........................................................................................................... 81 Inflammatory Jaw Lesions.................................................................................................................. 87 Connective Tissue Lesions ................................................................................................................ 89 Benign Epithelial Tumors ................................................................................................................... 93 Verrucal Papillary Lesions .................................................................................................................. 95 Neoplasms ......................................................................................................................................... 96 Odontogenic Abnormalities .............................................................................................................. 105 White Lesions ................................................................................................................................... 111 Red-Blue Lesions ............................................................................................................................. 118 2

Pigmented Lesions ........................................................................................................................... 121 Blood Diseases ................................................................................................................................ 124 Neurologic & Muscle Disorders ........................................................................................................ 130 Non-Odontogenic & Developmental (Fissural) Cysts ....................................................................... 131 Odontogenic Cysts .......................................................................................................................... 134 Non-Odontogenic Tumors ............................................................................................................... 137 Odontogenic Tumors ....................................................................................................................... 143 Pseudocysts ..................................................................................................................................... 148 Salivary Gland Tumors ..................................................................................................................... 149 Malignant Salivary Gland Tumor ...................................................................................................... 152 Ulcerative Conditions ....................................................................................................................... 156 Major & Minor Aphthous Ulcers ....................................................................................................... 158 Vesiculo-Bullous Diseases & Herpes ............................................................................................... 161 Oral Pathology Test Pearls ............................................................................................................... 169

CHAPTER 3

RADIOLOGY Osteonecrosis .................................................................................................................................. 175 Digital Radiography .......................................................................................................................... 176 Radiation, Collimnation, Filtration .................................................................................................... 177 Panoramic and Cone Beam ............................................................................................................. 180 Cephalometrics & BWXs .................................................................................................................. 181 Submental-Vertical ........................................................................................................................... 182 Water’s View .................................................................................................................................... 183 Towne’s View ................................................................................................................................... 184 Chemicals, Solution, & Developing Errors ....................................................................................... 185 Radiographic Techniques & Erros .................................................................................................... 186

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CHAPTER 4 DENTAL EMERGENCY PROTOCOL & MEDICALLY COMPROMISED Dental Emergency Protocol ............................................................................................................. 194 Medically Compromised Patients .................................................................................................... 198

CHAPTER 5 DENTAL PHARMACOLOGY Pre-Medication & Guidelines............................................................................................................ 202 DEA Drug Schedule.......................................................................................................................... 204 NSAIDs ............................................................................................................................................. 205 Salicylates ........................................................................................................................................ 206 Heparin & Warfarin ........................................................................................................................... 207 Prothrombin Time (PT) .................................................................................................................... 208 Acetaminophen ................................................................................................................................ 209 Opioids ............................................................................................................................................. 210 Drugs & Xerostomia & Oral Hypoglycemics ..................................................................................... 211 Bronchodilators & Beta/Alpha Blockers ........................................................................................... 212 Diuretics ........................................................................................................................................... 213 Corticosteroids ................................................................................................................................. 215 Local Anesthetics, EPI, & Nitrous Oxide .......................................................................................... 215

CHAPTER 6 NUTRITION Amino Acids ..................................................................................................................................... 220 Diet ................................................................................................................................................... 222 Hyperglycemia & Hypoglycemia ...................................................................................................... 223 Triglycerides ..................................................................................................................................... 225 Caffeine & Sugars............................................................................................................................. 226 BMR ................................................................................................................................................. 228 Vitamins Deficiencies & Diseases .................................................................................................... 230 Digestive Disorders .......................................................................................................................... 236

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CHAPTER 7 BEHAVIORAL SCIENCE, INFECTION CONTROL, OSHA

Behavioral Science ........................................................................................................................... 243 Behavioral Modification .................................................................................................................... 244 Effective Patient Communication ..................................................................................................... 246 Anxiety, Fear, & Stress ..................................................................................................................... 247 Universal Precautions ...................................................................................................................... 249 OSHA Blood Borne Pathogens ........................................................................................................ 250 Hepatitis B & C ................................................................................................................................. 251 Occupational Exposure & Protocol .................................................................................................. 252 Sharps .............................................................................................................................................. 253 MSDS ............................................................................................................................................... 254 Infection Control (Sterilization & Disinfection) .................................................................................. 255 Public Health Assessment (Sensitivity & Specificity) ....................................................................... 261

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DENTINâ„¢ | WREB-HYGIENISTS

DENTIN™ | WREB-HYGIENISTS

THE PERIODONTIUM & FIBERS Periodontium-tissues that surround and support the teeth consisting of the gingiva, PDL, cementum, alveolar & supporting bone. The main functions are to support, protect, and nourish the teeth. ! Attachment apparatus-consists of the alveolar bone proper, PDL fibers, and cementum that attaches the root to alveolar bone. ! Gingival apparatus-describes the gingival fibers and epithelial attachment. ! Gingival ligament-consists of dentogingival, alveologingival, and circular fibers. ! Indifferent Fiber Plexus-small collagen fibers located in the PDL that run in all directions, and are associated with the larger principal collagen fibers.

Alveolar Process-the part of the maxilla and mandible that HOUSES TEETH and consists of two main parts.

1. Alveolar bone proper-the only essential part o the bone socket (alveolar process) that is always present. It is a thin inner layer of compact lamellar bone that immediately surrounds the root where PDL fibers attach. It is a perforated cribiform plate through which vessels and nerves pass between the PDL and bone marrow. It consists of two layers of bone (compact lamellar bone & layer of bundle bone (the layer that PDL fibers insert into). Alveolar bone proper helps form the attachment apparatus.

2. Supporting alveolar bone-is not always present, but surrounds the alveolar bone proper to provide SUPPORT to the socket (alveolar process) and consists of: ! Cortical plate (compact lamellar bone)-forms outer & inner plates of alveolar processes, and is thicker in the mandible than in the maxilla. !

Spongy bone (cancellated bone)-fills in the area between the cortical plates of bone.

Spongy bone is NOT present in the anterior region of the mouth (here the cortical plate is fused to the cribiform plate). This is also true over the radicular buccal bone of maxillary posterior teeth.

GINGIVA COMPONENTS: FREE GINGIVA (unattached or marginal gingiva)-the collar of tissue not attached to the tooth or alveolar bone composed of: 1. Gingival margin-most coronal part of the free gingiva.

2. Free gingival groove-separates free gingiva from attached gingiva; only present in 33% of adults.

3. Gingival sulcus-the shallow groove between the marginal gingiva & tooth surface, bound by sulcular epithelium laterally, and by JE apically.

4. Interdental (interproximal) gingiva-occupies the interdental spaces coronal to the alveolar crest.

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DENTIN™ | WREB-HYGIENISTS GINGIVAL FIBERS (Supracrestal C.T. Fibers)-Type I collagen fibers that support and attach the gingiva to tooth and alveolar bone. Gingival fibers are found ONLY within the FREE GINGIVA (not in attached gingiva or mucogingival junction). Gingival fibers are continuous with the PDL (which is also C.T that surrounds the root and connects the root to alveolar bone by its principal fibers). Gingival fibers are designated by their orientation: 1. Alveologingival fibers-insert in the crest of the alveolar process and spread out through the lamina propria into the free gingiva. Also helps form the gingival ligament.

2. Circular fibers (Circumferential fibers)-resists ROTATIONAL FORCES applied to a tooth, and help form the gingival ligament. These fibers encircle the tooth around the most cervical part of the root, and insert into cementum and lamina propria of the free gingiva and alveolar crest.

3. Dentogingival fibers-extend from cementum apical to the epithelial attachment (JE) and travel laterally and coronally into the lamina propria of the gingiva. Also help form the gingival ligament.

4. Dentoperiosteal fibers-extend from cervical cementum over the alveolar crest, to the periosteum of the cortical plates of bone.

5. Transseptal fibers: connect two adjacent teeth (tooth-to-tooth) and are sometimes classified within the PDL principal fibers, although they are actually tooth-to-tooth fibers, not tooth-tobone fibers. These fibers extend from tooth-to-tooth, coronal to the alveolar crest, and are embedded in cementum of adjacent teeth. They are not found on the facial aspect, and have no attachment to the alveolar crestal bone. They maintain integrity of the dental arches.

2. ATTACHED GINGIVA-the gingiva attached to underlying periosteum of alveolar bone and to cementum by C.T. fibers and epithelial attachment. Present between the free gingiva and more movable alveolar mucosa. Attached gingiva contains KERATINIZED EPITHELIUM & LAMINA PROPRIA of dense, well-organized fiber bundles with few elastic fibers. It is firmly joined to underlying tooth structure, periosteum, & bone, and structured to withstand frictional stresses of mastication and brushing. " NARROWEST BAND of attached gingiva is found on FACIAL SURFACES of the mandibular canine & first premolar, and lingual surfaces adjacent to mandibular incisors & canines. Narrow attached gingival zones may also occur at the MB root of maxillary first molars (associated with prominent roots and sometimes with bony dehiscences), and at mandibular third molars. "

Width of FACIAL attached gingiva ranges from 1-9mm. It is WIDEST on the facial surface of the maxillary lateral incisor, & narrowest on facial surfaces of mandibular canine & first premolar.

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“functionally adequate” zone of gingiva-a zone that is keratinized, firmly bound to tooth and underlying bone, ~2mm or more wide, and is resistant to probing and gaping when the lip is distended.

BOUNDARIES that define the ATTACHED GINGIVA extend from the mucogingival junction (MGJ) to the free gingival groove (base of the sulcus). ! Mucogingival Junction-separates attached gingiva from alveolar mucosa. However, the free gingival groove separates the free gingiva from attached gingiva. !

Free gingiva-extends from the free gingival groove (sulcus base) to the gingival margin.

ATTACHED GINGIVA is normally CORAL PINK in color and firmly bound down to underlying tooth structure, periosteum, and bone. Its color varies depending on the degree of keratinization, thickness of epithelium, presence of melanin, and number of blood vessels.

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DENTIN™ | WREB-HYGIENISTS STIPPLING-the irregular surface texture of the attached gingiva that resembles an orange peel’s surface. Stippling occurs at the intersection of epithelial ridges that cause the depression, and the interspersing of C.T. papillae between these intersections that form the small orange peel bumps. ! In the absence of stippling, edema of underlying C.T., inflammatory degradation of gingival collagen fibers, and normal variation in gingival topography may result in areas of the attached gingiva.

ALL ORAL MUCOSA is STRATIFIED SQUAMOUS EPITHELIUM regardless if it is keratinized or nonkeratinized. ! Non-Keratinized Oral Mucosa: buccal & alveolar mucosa, tongue’s inferior (ventral) surface, soft palate, floor of mouth, specialized mucosa, and lining mucosa, gingival col, and crevicular epithelium, o Alveolar Mucosa-functions as a LINING TISSUE, located APICAL to the attached gingiva on the facial & lingual surfaces. Consists of a thin, NON-KERATINIZED epithelium, loosely textured, contains elastic fibers in the mucosa and submucosa, and is loosely bound to periosteum of alveolar bone. Alveolar mucosa is well-adapted to permit movement, but cannot withstand frictional stresses. !

Keratinized Oral Mucosa: hard palate & attached gingiva.

Functional Oral Mucosa: 1. Masticatory mucosa-composed of free & attached gingiva, and mucosa of the hard palate.

The epithelium of these tissues is KERATINIZED, and the lamina propria is a dense, thick, firm C.T. of collagenous fibers. Important: the surface epithelium of the gingiva is highly impermeable, which makes it resistant to bacterial invasion.

2. Lining Mucosa (Reflective Mucosa)-mucosa that lines most of the oral cavity EXCEPT the gingiva, anterior palate, and dorsum of the tongue. Lining mucosa is a thin, movable tissue with a thin, non-keratinized epithelium, and a thin lamina propria. ! Mucogingival junction-the junction of the lining mucosa with the masticatory mucosa.

3. Specialized Mucosa-consists of non-keratinized epithelium that covers the tongue dorsum and taste buds PERIODONTAL LIGAMENT (PDL)-a complex, specialized, soft, fibrous C.T. containing numerous cells, blood vessels, nerves, & extracellular substances consisting of fibers (gingival & prinicipal), & ground substance. PDL is a HIGHLY VASCULAR & CELLULAR C.T. that surrounds the roots of teeth and bridges root cementum with alveolar bone. Most PDL fibers are collagen, while ground substance consists of various proteins and polysaccharides. When the tooth loses its function, the PDL becomes very thin and loses its regular arrangement of fibers. " PDL is hour-glass shaped with the narrowest part at the middle of the root. "

PDL occupies the space between cementum and the periodontal surface of alveolar bone.

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Cementum and alveolar bone are the tissues immediately adjacent to the PDL.

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MOST ABUNDANT CELLS in the PDL are FIBROBLASTS. Fibroblasts are ovoid or elongated cells oriented along the PDL principal fibers and exhibit pseudopodial-like processes.

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Epithelial Rests of Malassez-remnants of Hertwig’s epithelial root sheath, found as groups of epithelial cells in the PDL. Some epithelial rests degenerate, while others become calcified (cementicles).

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DENTIN™ | WREB-HYGIENISTS

2. Offset blade: the blade’s blade is offset at a 70° angle relative to the instrument’s lower shank.

3. Only one cutting edge is used: the LONGER, OUTER CUTTING EDGE. 4. The blade curves in two planes: toe curves up and to the side, making it more adaptable to the tooth surfaces convexities and concavities of the tooth surface. 1 Only the lower one third of the blade is in contact with the tooth during instrument. Only the lower 1/3 of the blade contacts the tooth during instrumentation using a PULL STROKE.

AIR SYRINGE-can be used to detect supragingival & subgingival calculus. Supragingival calculus is often seen easily when it is dry, as saliva often conceals it, and deflecting the gingival tissue slightly makes subgingival calculus easier to detect. WEARING EYE LOOPS IMPROVES YOUR ABILITY TO DELIVER HIGH QUALITY HYGIENE (AND DETECT CALCULUS), SO INVEST IN A PAIR IF YOU HAVEN’T ALREADY. When using the EXPLORER to detect calculus, a LIGHT instrument grasp should be used to increase tactile sensitivity. The lateral side of the instrument’s tip should be placed in contact with the tooth surface when exploring for calculus.

• Note: The sequence and control of strokes is important. If heavy lateral pressure is continued with long, even strokes, it will produce a smooth but “ditched” root surface. To avoid this, deliberate transition from short, powerful scaling strokes to longer, lighter root planing strokes must be made as soon as the calculus and initial roughness have been removed.

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When root planing, vertical strokes should be used first, followed by oblique and then horizontal strokes. Light pressure should be utilized with root planing strokes to maximize tactile sensitivity.

Transillumination-is using the mirror to reflect light from the lingual surfaces through the tooth while it is being examined on the buccal surface to help detect calculus and dental caries. It is effective only with anterior teeth because they are thin enough to allow light to pass through. Ex: A dental hygienist is using a dental mirror to reflect light from the lingual surface through the tooth while it is being examined on the buccal surface.

• Illumination is the lighting of an area by reflection of light from the mirror.

• The dental unit light is used with the mirror to provide both illumination and transillumination.

• The mirror is used to see things intra-orally indirectly when direct vision is not possible (i.e. when observing teeth lingual surfaces), and is used to retract the cheeks, lips, and tongue.

A FIRM instrument grasp is to be used during an instrument stroke WHEN REMOVING CALCULUS to help facilitate calculus removal because you have more control over the instrument. The heavier the deposit you are attempting to remove the more rigid the shank of the instrument should be. A LIGHTER grasp is needed for increased tactile sensitivity during assessment strokes when checking to see whether you have successfully removed all calculus.

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DENTIN™ | WREB-HYGIENISTS PALM GRASP- is an instrument grasp that is NOT USED with scaling, root planing, and gingival curettage instruments except when using a chisel scaler in a push stroke to remove gross calculus. USED FOR BULKY INSTRUMENTS. • With the palm grasp, the instrument’s handle is held in the palm of the hand and is surrounded by the index finger, middle, ring, and little fingers. The thumb acts as a fulcrum when needed.

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Palm Grasp Limitations: Less tactile sensitivity and flexibility of movement. Not used with scaling, root planing, and gingival curettage instruments except when using a chisel scaler in a push stroke to remove gross calculus.

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The palm grasp is used for bulky instruments such as air/water syringe, rubber dam clamp forceps straight chisels, and surgical forceps.

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When using the palm grasp, the index, middle, ring, and little finger hold the instrument so it rests in the palm of your hand. Your thumb remains free to stabilize your hand in the patient's mouth, or it may be used to support an instrument when sharpening This grasp is rarely used in the mouth and only when exceptional force is needed.

PALM-THUMB GRASP- used by the assistant for holding the oral evacuator (high speed suction).

MODIFIED PEN GRASP-the most useful for the hygienist to maneuver the instrument around a tooth while applying the correct direct pressure application for calculus removal without damaging the tissue.

• The modified pen grasp is similar to the pen grasp except the operator uses the pad of the middle finger on the handle of the instrument. The tips of the thumb, finger, and middle finger are all in contact with the instrument. The ring finger is the finger rest (fulcrum) which improves control of the instrument and application of forces by the working-end against the tooth. THE MODIFIED PEN GRASP IS USED WITH SCALING, ROOT PLANING, & GINGIVAL CURETTAGE INSTRUMENTS.

PEN GRASP-resembles the position commonly used to hold a pen or widely used for most operative instruments.

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Working Stroke Firm Grasp Moderate/Heavy Stroke Pressure Pull Stroke (away from tissue) Vertical/oblique/horizontal strokes Used for calculus removal and root planing

Strokes are short, even, and overlapping to ensure complete coverage Longer strokes are then used for finishing and smoothing

Exploratory Stroke Light, but secure grasp Light Stroke pressure Push Stroke (apically toward tissue) Vertical/oblique strokes Used during curet insertion to guide instrument apically to base of calculus deposit or bottom of sulcus (also called the preliminary stroke) When performing this push stroke, be careful not to damage the epithelial attachment.

When performing this push stroke, be careful not to damage the epithelial attachment.

Stroke-the action of an instrument in the performance of the task for which it was designed. Strokes can be directed vertically, horizontally, or obliquely/diagonally. There are several types of strokes: • Probing Stroke (Walking Stroke)-upward and downward movement within a periodontal pocket (a pocket that extends beyond the realm of the gingival, reaching into deeper and at least partially destroyed periodontal tissues). Also called the walking stroke.

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Exploratory Stroke (Assessment Stroke)-used to assess the smoothness or roughness of the tooth surface and the effectiveness of instrumentation. The instrument handle is grasped lightly to increase tactile sensitivity.

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Placement Stroke-used when an instrument is being positioned to be used for its specific purpose.

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Scaling Stroke-a short, powerful PULL STROKE used to remove calculus (more pressure).

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Root Planing Stroke- long, overlapping strokes for final smoothing of the root surface usually in a pull motion which exerts less pressure. Pulling strokes are safer than pushing strokes push strokes, as push strokes can cause calculus to become embedded in the soft tissue.

*The amount of pressure applied during a stroke becomes lighter as surface becomes smoother *Exploratory, scaling, and root planing strokes differ in length, pressure, direction, and angulation.

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METABOLIC & GENETIC DISEASES HYPERTHYROIDISM-caused by excessive production of thyroid hormone (THYROXIN). Thyroxin’s stimulates cellular metabolism, growth, and differentiation of all tissues. In excess, it leads to high basal metabolism, fatigue, weight loss, excitability, elevated temperature (heat intolerance, sweating), generalized osteoporosis, fine hair, diarrhea, tremor (shakiness), tachycardia (rapid heart rate).

Oral manifestations are not uncommon, but if the disturbance starts early in life, premature tooth eruption and loss of deciduous dentition are common. GRAVES DISEASE & EXOPTHALMOS (bulging eyes). Two types of Hyperthyroidism: 1. Graves Disease (Toxic Diffuse Goiter)-most common form that occurs mostly in WOMEN ages 20-40. Usually arises after an infection or physical or emotional stress. Typical signs of hyperthyroidism are present plus GOITER & EXOPHTHALMOS (bulging eyes).

2. Plummer’s Disease (Toxic Multinodular Goiter)-caused by the presence of many toxic thyroid nodules (adenomas) within the thyroid gland. Plummer’s is uncommon in adolescents and young adults, and increases with age. Exophthalmos (bulging eyes) is rare.

HYPOTHYROIDISM-a clinical feature is WEIGHT GAIN, cold intolerance, lowered pitch of voice, mental and physical slowness, constipation, dry skin, coarse hair, and puffiness of face, eyelids, and hands.

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Myxedema-very severe hypothyroidism in adults, much more common in WOMEN than men.

Characterized by puffiness of face and eyelids, swelling of tongue and larynx. The skin becomes dry and rough, and hair sparse. The individual has a low basal-metabolic rate and low body temperature, poor muscle tone, low strength, tires easily, and are mentally sluggish. Myxedema is alleviated by administering thyroid hormones

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Cretinism-severe hypothyroidism in a child, due to lack of thyroid hormone causing retardation of growth and abnormal bone development. Severe mental retardation is caused by improper CNS development. If recognized early, Cretinism can be improved with thyroid hormones. !

Dental findings in a child with hypothyroidism are a LARGE TONGUE, underdeveloped mandible, over-developed maxilla, delayed teeth eruption, and deciduous teeth are retained longer.

HYPERPARATHYROIDISM-a common complication is KIDNEY STONES (renal calculi). Kidney stones form due to an increase in urinary excretion of calcium and phosphate. Osteoporosis, GIANT CELL GRANULOMAS, and metastatic calcifications are manifestations of hyperparathyroidism.

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The main cause is an ADENOMA (benign tumor of the gallbladder epithelium). Laboratory findings include hypercalcemia, decreased serum phosphorus, and increased serum alkaline 81

DENTIN™ | WREB-HYGIENISTS phosphatase and serum PTH. Clinical characteristics: cystic bone lesions (osteitis fibrosa cystica or von Recklinghausen’s Disease of bone), nephrocalcinosis, kidney stones (renal calculi), and peptic duodenal ulcers. May find well-defined cystic radiolucencies on a panorex or peri-apical radiograph.

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EXCESS LOSS OF CALCIUM in urine stimulates the parathyroid glands to undergo hyperplasia because the feedback mechanism that detects low serum calcium elicits growth of the gland. The resulting metabolic effects are identical to primary hyperparathyroidism effects.

HYPOPARATHYROIDISM-in rare instances, associated with congenital thymic hypoplasia (DiGeorge’s syndrome). Hypoparathyroidism is most commonly caused by accidental surgery excision during thyroidectomy.

ACROMEGALY –a hormonal disorder that occurs when the PITUITARY GLAND produces EXCESS GROWTH HORMONE (HYPERPITUITARISM) due to a BENIGN TUMOR after adolescence (fusion of long bone epiphyses). Most commonly affects MIDDLE-AGED ADULTS and can cause serious illness and premature death.

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In > 90% of acromegaly patients, GH overproduction is caused by a BENIGN TUMOR of the pituitary gland (ADENOMA). Whether or not the epiphyses of the long bones have fused with the shaft is the main determinant of whether gigantism or acromegaly will occur when there is oversecretion of GH by the pituitary gland.

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Clinical Signs: soft tissue swelling of the hands & feet (an early feature), with patients noticing a change in ring or shoe size. Gradually, bony changes alter the patient’s facial features (i.e. brow & lower jaw protrude, nasal bone enlarges, and teeth spacing increases).

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Oral Manifestations of Acromegaly & Gigantism: enlarged tongue, mandibular prognathism, teeth are tipped to buccally or lingually due to an enlarged tongue, and roots may be longer than normal.

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GIGANTISM-caused by a benign tumor BEFORE adolescence (non-fusion of epiphyses).

DWARFISM (Pituitary Dwarfs) – characterized by arrested growth caused by undersecretion of GROWTH HORMONE. Dwarfs often have limbs and features not properly proportioned or formed.

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Oral Manifestations: delayed eruption rate & shedding of teeth, clinical crowns & roots appear smaller, dental arch is smaller causing malocclusion, and an under-developed mandible.

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The MOST COMMON type of Dwarfism is ACHONDROPLASIA. Child is very short (~50 inches), fingers are stubby, bowed legs, bulging forehead, bossing of frontal bones, saddle-like nose, and mandibular prognathism.

OSTEOGENESIS IMPERFECTA (“BRITTLE BONES”) –a rare genetic defect/disorder that affects the COLLAGEN PRODUCTION (major protein of the body’s C.T.). Person either has less collagen than normal, or poorer quality of collagen than normal causing WEAK BONES THAT FRACTURE/BREAK EASILY often from little or no cause.

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While the characteristics vary greatly, and not all are evident in each case, the main clinical characteristic is EXTREME FRAGILITY & POROUS BONES with a proneness to fracture due to the effects of inadequate osteoid production.

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Additional Clinical Features: BLUE SCLERA, deafness due to osteosclerosis, loose joints, low muscle tone, triangular face, and a tendency toward spinal curvature.

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DENTIN™ | WREB-HYGIENISTS •

Teeth have bulbous crowns with a cervical constriction, partially or completely obliterated pulps, and narrower & shorter roots. Deciduous (primary) teeth are more severely affected than permanent teeth. Teeth are poor and abnormal due to dentin malformation (Type 1 Dentinogenesis Imperfecta); may be linked to DENTINOGENESIS IMPERFECTA.

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Treatment: NO KNOWN CURE; treatment is directed toward preventing/controlling the symptoms.

HYPOPHOSPHATASIA –resembles OSTEOGENESIS IMPERFECTA. It’s an inherited metabolic (chemical) BONE DISEASE that results from LOW LEVELS of ALKALINE PHOSPHATASE (enzyme essential the calcification of bone tissue). Loosening, hypocalcification, and premature loss of deciduous teeth are characteristic. Radiographically, large pulp chambers and alveolar bone loss are present.

Hypophosphatasia’s severity greatly varies from patient to patient. Some have blue sclera that resembles osteogenesis imperfecta. Others have deformity of the arms, legs, and chest and/or frequent bouts of pneumonia and recurrent fractures. Patients are classified as having either: PAGET’S DISEASE OF BONE (OSTEITIS DEFORMANS) – a common, chronic, non-metabolic bone disorder characterized by an INCREASE in serum ALKALINE PHOSPHATASE levels. Bones become enlarged & deformed, dense, but fragile due to excessive breakdown and formation of bone. Has potential to undergo “spontaneous” malignant transformation. There is excessive bone destruction and unorganized bone repair.

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Radiographic Features: “COTTON-WOOL” APPEARANCE ON PANOREX (skull and jaws).

Hypercementosis of roots and loss of lamina dura around roots.

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Effects males & females, but rarely people under 40yrs (affects middle-aged & elderly people).

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Cause is hereditary. Patients are predisposed to developing OSTEOSARCOMAS.

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Signs & Symptoms: PAIN in affected area, bone deformity & susceptibility to fractures in the affected area, headache, and hearing loss if the affected area is the skull. Symptoms develop SLOWLY.

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Clinical Features: Patients may give a history of progressively INCREASE IN HAT SIZE OR NEED FOR NEW DENTURES being made more frequently due to bony changes.

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Bones are warm to touch due to increased vascularity.

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Lab tests show highly increased serum alkaline phosphatase, urinary calcium, & hydroxyproline; with normal levels of SERUM PHOSPHATE & CALCIUM.

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Treatment: Administer anti-metabolites or CALCITONIN to decrease bone resorption, or treat with a high-protein & high calcium diet.

PAGET’S DISEASE (Enlarged Alveolar Ridges)

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OSTEOMALACIA (Adult Rickets) – SOFTENING of bones in adults because osteoid tissue in bones failed to calcify due to LACK OF VITAMIN D. More common in women, and may be asymptomatic until a bone fracture occurs.

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Steatorrhea-one of the most common causes of Osteomalacia due to FAT MALABSORPTION where the body cannot absorb fats, so fats are passed directly out of the body in stool causing poor absorption of vitamin D (fat soluble) and calcium. Osteomalacia affects ALL BONES, specifically at their epiphyseal growth plates.

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Signs & Symptoms: pain in bones of the arms, legs, spine, and pelvis.

RICKETS (Child Osteomalacia) –causing skeletal deformities, and usually accompanied by irritability and generalized muscle weakness. Bowlegs, pigeon breast, and protruding stomach are signs. Teeth are affected by delayed eruption, malocclusion, and developmental abnormalities of dentin and enamel, with a higher caries rate.

CEREBRAL PALSY – a group of disorders affecting body movement and muscle coordination due to an insult or anomaly of the brain’s motor control centers. This damage interferes with messages from brain to the rest of the body. The effects vary greatly among people.

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CP is mainly characterized by SPASTIC PARALYSIS or impairment of control or coordination over voluntary muscles. Often accompanied by mental retardation, seizures, & disorders of vision/communication.

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NO ORAL PATHOLOGIC MANIFESTATIONS are present in people with cerebral palsy, but several conditions are more common, or more severe than in the normal population: & Higher incidence of periodontal disease, caries, bruxism, and malocclusion. & Prone to gingival hyperplasia if Dilantin is used to control seizures. & More susceptible to trauma, especially maxillary anterior teeth.

DOWN SYNDROME – a congenital defect caused by a chromosomal abnormality (TRISOMY 21), marked by various degrees of mental retardation and characteristic physical features (short, flattened skull, slanting eyes, thickened tongue/fissured, broad hands/feet, etc.)

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Oral Manifestations: mandibular prognathism, increased periodontal disease, thickened or fissured tongue, delayed teeth eruption, higher incidence of congenitally missing teeth, malocclusion, & enamel dysplasia.

MUSCULAR DYSTROPHY –group of genetic diseases marked by progressive weakness & degeneration of skeletal or voluntary muscles that control movement.

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DENTIN™ | WREB-HYGIENISTS

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Oral Manifestations: increase in dental disease if oral hygiene is neglected, weakness in muscles of mastication causing decreased maxillary biting force, higher incidence of mouth breathing, and open bite.

ECTODERMAL DYSPLASIA – hereditary condition characterized by abnormal development of the skin and associated structures (hairs, nails, teeth, & sweat glands). ED involves all structures derived from ECTODERM, affecting MALES more than females. Manifests orally as reduced/missing teeth.

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Clinical Signs: hypothrichosis (decrease in hair (fine sparse hair), anhidrosis (no sweat or sebaceous glands, causing heat intolerance), Anodontia (complete absence of teeth), Oligodontia (partial absence of teeth), no tooth buds of the primary or permanent dentition (edentulous), depressed nose bridge, lack of salivary glands, and child appears much older than their true age.

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Affects tooth bud development causing congenitally missing teeth (lack of permanent teeth) and/or peg-shaped or pointed teeth. Enamel may also be defective.

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Treatment: Dentures can be fabricated for young children, but they will need to be replaced periodically to accommodate the patient’s jaw growth. Implants can be placed once the jaw if fully developed, or orthodontics to close spaces. Use a multi-disciplinary treatment approach as treatment is often complex.

ECTODERMAL DYSPLASIA

CLEIDOCRANIAL DYSPLASIA (DYSOSTOSIS)-genetic disorder of bone development characterized by absent or incomplete formed COLLAR BONES, heavy protruding jaw, wide nasal bridge, and dental abnormalities (malaligned teeth, multiple supernumerary teeth, and unerupted teeth). Observing a panorex or FMX alone often suggests the diagnosis.

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DENTIN™ | WREB-HYGIENISTS CLEIDOCRANIAL DYSPLASIA (DYSOSTOSIS)

PIERRE-ROBIN SYNDROME – an inherited disorder with the following findings in the NEONATE: o Micrognathia-smallness of the jaws. o Glossoptosis-downward displacement or retracted tongue. o Breathing problems & cleft palate.

LATERAL CLEFTING OF THE LIP – results from failure of the MAXILLARY & FRONTAL NASAL PROCESSES TO MERGE. Cleft lip occurs during the 5th-6th week of embryonic life. It can be bilateral or unilateral, more common in males, and involves the LEFT SIDE more than the right side.

CLEFT PALATE – occurs in 6th-8th week of embryonic life. Isolated cleft palates are more common in females, characterized by a fissure in the midline of the palate due to failure of the two sides to fuse during embryonic development. The most severe handicap caused by cleft palate is an impaired mechanism PREVENTING NORMAL SPEECH & SWALLOWING. Important: Speech problems associated with Cleft Lip & Cleft Palate are usually due to the inability of the soft palate to close airflow into the nasal area.

CHERUBISM – a BENIGN genetic autosomal dominant disease of the maxilla & mandible, typically in children by age 5 (affects males 2:1). Most cases occur in the MANDIBLE. The jaws are firm and hard to palpation, and regional lymphadenopathy may be present. BILATERAL expansion of the jaws gives the child a very round face, reminding one of cherubs (cupids) in paintings. The tumors stop growing shortly after puberty. As the patient’s age and size increases, the deformity is less noticeable.

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Histologically, cherubism lesions closely resemble Central Giant Cell Granulomas. Histology shows a giant cell lesion with some reactive bone formation. However, perivascular collagen cuffing is pathognomonic for cherubism.

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Radiographically: lesions appear as multiple, well-defined, multi-locular radiolucencies of the jaw.

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No associated systemic manifestations. However, the deciduous dentition may spontaneously shed prematurely, starting as early as age 3. There is often delayed eruption of the permanent dentition, which is often defective with the absence of numerous teeth and displacement of those teeth present.

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Treatment: cautious waiting as Cherubism tends to regress in early adulthood. Do not treat with radiation therapy.

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DENTIN™ | WREB-HYGIENISTS DENTAL PUBLIC HEALTH-science and art of preventing and controlling dental disease, and promoting dental health through organized community efforts. A form of dental practice that serves the community as a patient rather than serving the individual. Dental public health involves providing dental education to the public, research, and applying research findings with the administration of dental care programs for groups, and the prevention and control of dental disease through a community approach.

Fundamental principles of public health are prevention, cost-efficiency, and teamwork. Prevention is the major objective of public health programs because it entails ethics, teamwork, and cost-efficiency.

It is more ethical to prevent disease than to cure it. Teamwork is necessary to handle large groups efficiently. Cost-efficiency plays a major role because prevention is cheaper than a cure.

• Education plays an important role in public health because it decreases the need for government intervention. When people learn why regulations are of value, they will comply. Ex: when people learn how many lives are saved annually by seatbelts, they are more inclined to wear them.

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Any school-based program to promote oral health should have these 3 components: 1. Oral health services: involves preventive procedures, health screening and treatment, referral, and follow-up.

2. Health instruction: includes personal and community health topics.

3. Healthy environment: attention to all aspects of the school environment that could affect the health of students or school personnel. The more successful school-based programs use a high degree of active involvement of the participants.

RANDOMIZED STUDY-a study where ALL subjects have an equal chance of being assigned to either the study or control group. Statistical probability is such that the assumption can then be made that the groups differ ONLY in terms of the agent under study. Any uncontrolled variables influencing the outcome are likely to affects subject in both groups equally. Thus, researchers prefer the “random assignment method” for placing subjects into either the study or control group.

BLIND STUDY-a study where subjects are unaware of if they are in a test or control group. One way of achieving a blinded study is using placebos. Double Blind Study-neither participants (subjects) nor examiners know the group allocations (test or control groups).

Two Variables Used in Research Studies: 1. Dependent variable-the variable whose value depends on those of others (i.e. in the formula x = 3y + z) x is the dependent variable.

2. Independent variable-the variable whose value determines the other variable values (i.e. x = 3y + z) y & z are the independent variables.

The ethical rules and principles of professional conduct for the practice of dentistry are set forth in the ADA’s publication “Principles of Ethics and Code of Professional Conduct”. The ethical principles found in this code are justice, autonomy, and beneficence.

• Justice-the quality of being impartial and fair.

• Autonomy-to inform patients about treatment, to be truthful, and protect their confidentiality.

• Beneficence-to be kind and give the highest quality of care one is capable of providing.

Good Samaritan Law-a law enacted in all states that provides immunity from suit for specified health practitioners who render emergency aid to victims of accidents, provided there is no evidence of gross negligence. Not all states include dentists in the Good Samaritan Law.

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DENTIN™ | WREB-HYGIENISTS

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