Diseases of Gastrointestinal Tract, Hepatobiliary Renal diseases.pdf
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ORAL DIAGNOSIS AND DENTAL RADIOLOGY-II Diseases of Gastrointestinal Tract, Hepatobiliary, and Renal Diseases Assoc. Prof. Büşra YILMAZ School of Dental Medicine Department of Oral and Maxillofacial Radiology [email protected] Gastrointestinal Tract Diseases Gastroesophageal Reflux Disease...
ORAL DIAGNOSIS AND DENTAL RADIOLOGY-II Diseases of Gastrointestinal Tract, Hepatobiliary, and Renal Diseases Assoc. Prof. Büşra YILMAZ School of Dental Medicine Department of Oral and Maxillofacial Radiology [email protected] Gastrointestinal Tract Diseases Gastroesophageal Reflux Disease (GERD) is a condition that develops when there is a retrograde flow of stomach contents back into the esophagus. “Heartburn” is the cardinal symptom of GERD and is defined as a sensation of burning or heat that spreads upward from the epigastrium to the neck GERD Patients who experience GERD may complain of extraesophageal symptoms including; dental erosion, dysgeusia (foul taste), halitosis, tongue sensitivity, burning sensations, chest pain GERD Oral mucosal changes are minimal; however, erythema and mucosal atrophy may be present as a result of chronic exposure of tissues to acid. In particular, patients with erosion on the palatal and lingual surfaces should be questioned for a history of GERD Dental Management Dental management include early dietary and preventive advice Topical fluoride applications to ensure optimal dental mineralization and reduction of thermal sensitivity. Peptic and Duodenal Ulcers It is a common benign ulceration of the epithelial lining of the stomach (gastric ulcer) or duodenum (duodenal ulcer) Dental Management Dentist should avoid administering drugs that exacerbate ulceration and cause gastrointestinal distress, such asaspirin and other NSAIDs As many antiacids contain calcium, magnesium, and aluminum salts that bind antibiotics, for instance erythromycin and tetracycline, patients should be advised to take their antibiotics 1 hour before or 2 hours after their antacids to avoid a significant (75%–85%) reduction in antibiotic absorption. Inflammatory Bowel Disease Inflammatory bowel disease (IBD) is a term for two conditions (Crohn's disease and ulcerative colitis) that are characterized by chronic inflammation of the gastrointestinal (GI) tract. Ulcerative colitis is characterized by irritable bowel symptoms consisting of watery diarrhea with intervening episodes of constipation. Abdominal cramping is also a feature. Inflammatory Bowel Disease Crohn’ s Disease is an inflammatory disease that can affect any part of the small or large intestine, from the mouth to the rectum. Discontinuous segments of disease ("skip lesions"), ileal involvement, and granulomatous inflammation are suggestive of Crohn’sDisease IBD is frequently associated with extraintestinal manifestations, including a wide range of oral lesions. Dental Management The orofacial presentation includes cervical lymphadenopathy, lip swelling, angular cheilitis, oral ulceration, mucosal tags, cobblestone appearance of the oral mucosa, full-thickness gingivitis, submandibular duct “staghorning” Dental Management The oral manifestations of IBD may precede the onset of intestinal radiographic lesions by as much as 1 year or more. The oral lesions may be the first indication of this intestinal disease. Some patients with ulcerative colitis develop diffuse serpentine oral erosions that are exudative and erythematous Gluten Enteropathy (Celiac) It is the result of a hypersensitivity reaction to the wheat gluten allergen. Oral ulcers are oval and small, being less than 5 mm in diameter, and are multiple. Unlike aphthae they are persistant and chronic. Any patient with a history of chronic oral ulcerations and intestinal cramping should be evaluated for gluten enteropathy. Peutz-Jeghers Syndrome Peutz–Jeghers syndrome (PJS) is an autosomal dominant condition characterized by characteristic hamartomatous polyps and distinctive mucocutaneous pigmentation. A clinical diagnosis of PJS requires any two of (1) two or more Peutz–Jeghers-type hamartomatous polyps of the gastrointestinal tract; (2) typical hyperpigmentation of the mouth, lips, nose, eyes, genitalia, or fingers; or (3) family history of PJS Peutz-Jeghers Syndrome Almost all patients present with mucocutaneous pigmentation, in the form of macules. These are often the first clinical sign and may affect the perioral tissues, lips, gingiva, hard palate, and buccal mucosa. The perioral pigmentation is distinctive in crossing the vermillion border While most of the cutaneous macules fade with age, the buccal mucosal pigmentation often persists. Gardner Syndrome Gardner syndrome (GS), a rare autosomal dominant inherited disease and is characterized by the presence of multiple polyps in the intestine as well as bony, cutaneous, dental, and ocular abnormalities. The extraintestinal manifestations include multiple osteomas, multiple impacted supernumerary teeth, connective tissue tumors, thyroid carcinomas, hypertrophy of the pigmented epithelium of the retina Gardner Syndrome As craniofacial bony and dental signs of GS often precede gastrointestinal symptoms. Dentists may play an important role in the diagnosis of this syndrome. In a patient with a family history of GS, dental radiography (such as a panoramic radiograph) can provide the earliest indication of the presence of this condition. Dental abnormalities are present in 30%–75% and osteomas in 68%–82% of GS patients Gardner Syndrome Osteomas are slow growing and predominantly affect the mandible and maxilla, but can additionally affect the skull and long bones. Bony exostoses, also called peripheral osteomas, can be palpable and be detected by routine radiography. In the mandible, the osteomas may be central (characteristically near the roots of the teeth) or lobulated arising from the cortex, most commonly at the angle of the mandible. Dental anomalies include impacted teeth, supernumerary teeth, odontoma, congenitally missing teeth, and hypercementosis. The simultaneous presence of osteoma(s) with dental anomalies is highly suggestive of underlying GS Hepatobiliary Diseases Jaundice (tr:sarılık) Hemolytic Jaundice Obstructive Jaundice Hereditary Disorders of Conjugation Direct Hyperbilirubinemia Indirect Hyperbilirubinemia Alcoholic Liver Disease and Alcoholic Hepatitis Drug Induced Hepatotoxicity Liver Cirrhosis (Tr: siroz) Viral Hepatitis Hepatobilliary System 1. The Liver 2. Biliary Tract 3. Pancreas, which have interrelated functions in relation to the digestive system. Of these the liver is both the largest structure and has the highest number of roles, and therefore has a greater focus. The liver serves as the major locus of synthetic, catabolic, and detoxifying activities in the body and is the site of all intermediary metabolism of foodstuffs. The liver is essential in the excretion of heme pigments, and also participates in the immune response. Synthesize and store glycogen, a major source of glucose. Lipids are metabolized in the liver to form cholesterol and triglycerides. Bile salts are essential in the absorption of fat in the small intestine. Proteins, albumin, and clotting factors I, II, IV, VII, IX, and X are synthesized and stored in the liver. Since some of the clotting factors (II, VII, IX, and X) are also dependent on vitamin K, coagulopathy can occur from hepatocyte dysfunction and/or vitamin K malabsorption due to biliary problems. • Local anesthetics, analgesics, sedatives, antibacterials, and antifungals are all metabolized in the liver. • Consequently, cautious use of these drugs in a person with liver dysfunction is essential. • Lastly, the liver inactivates or metabolizes hormones such as insulin, aldosterone, antidiuretic hormone,estrogens, and androgens. Liver dysfunction can manifest through multiple symptoms, most commonly as jaundice, and the disease process can lead to liver failure and cirrhosis. Etiology of Liver disease; Trauma, Viral or chemically induced hepatitis, Alcohol intake, Nonalcoholic fatty liver disease, Autoimmune liver diseases, and Hereditary diseases such as hemochromatosis, α1-antitrypsin deficiency, and Wilson’s disease. The Fate of Bilirubin Hemoglobin from old red blood cells becomes bilirubin The liver converts bilirubin into conjugated bilirubin Bilirubin passes on to the intestine Bacteria convert it to urobilinogen º Some is lost in feces º Most is reabsorbed into the blood via portal circulation Jaundice (or icterus) is a yellow discoloration most often seen in the Skin Mucous membranes Sclera of the eyes which results from excess bilirubin in the circulation and its resultant accumulation in the tissues. This excess bile pigment may be caused by (1) increased production of unconjugated bilirubin as a result of hemolysis of red blood cells (hemolytic jaundice) (2) disturbances of bile flow caused by diseases either in the hepatocytes, intrahepatic bile ducts, or extrahepatic biliary system, preventing the excretion of bilirubin (obstructive jaundice) (3) liver parenchymal disease (hepatocellular jaundice). Alcoholic Liver Disease (ALD) and Alcoholic Hepatitis (AH) • Regular alcohol use leads to fatty changes in the liver that can develop into inflammation, fibrosis, and eventually cirrhosis. • Alcoholic hepatitis (AH) is acute inflammation of the liver, which can occur in patients with ALD, and accounts for 44% of all deaths associated with liver disease. • AH generally occurs with excessive alcohol intake over a period of at least 20 years and so usually presents in the fourth or fifth decade of life. Alcoholic Liver Disease (ALD) and Alcoholic Hepatitis (AH) Fatty changes Enlarged liver No symptoms Reversible Inflammation Fever, fatigue Jaundice Painful, enlarged liver Scar Tissue (fibrosis) Hepatitis to end-stage Liver shrinks irreversible Alcoholic Liver Disease (ALD) and Alcoholic Hepatitis (AH) • AH has a strong association with malnutrition, while nutrient deficiencies are implicated in ALD. Associated liver diseases, particularly hepatitis C, may also accelerate progression. • The ongoing presence of these factors triggers ineffective anti-inflammatory pathways, resulting in activation of stellate cells and myofibroblasts in the liver, which lead to fibrosis and alcoholic cirrhosis. Alcoholic Liver Disease (ALD) and Alcoholic Hepatitis (AH) The earliest indication of ALD is an enlarged liver. The patient may also exhibit signs of both AH (jaundice, fever, anorexia, and malaise) and more chronic liver disease, which may include spider angiomas, gynecomastia, jaundice, ascites, changes in mental status, and ethanol intoxication. The clinical problems associated with AH reflect the disordered metabolism and circulation in the liver. Jaundice reflects the inability of the hepatocyte to conjugate and excrete bilirubin, bleeding the decreased synthesis of clotting factors, and mental confusion the failure of the liver cells to metabolize and excrete toxins such as ammonia. Alcoholic Liver Disease (ALD) and Alcoholic Hepatitis (AH) Oral Health Considerations There may be extraoral and/or intraoral petechiae, ecchymosis, or gingival crevicular hemorrhage due to clotting factor deficiency. Alcoholic Liver Disease (ALD) and Alcoholic Hepatitis (AH) Oral Health Considerations Yellow pigmentation of the mucosa may also be observed, accompanied by cutaneous and scleral jaundice. Additional oral findings such as pallor, angular cheilitis, and glossitis may be present as a result of associated malnutrition, vitamin deficiencies, and anemia. spider angiomas Alcoholic Liver Disease (ALD) and Alcoholic Hepatitis (AH) Oral Health Considerations The presence of sweet ketone breath, indicative of liver gluconeogenesis, should raise the suspicion of hepatotoxicity. Alcoholic Liver Disease (ALD) and Alcoholic Hepatitis (AH) Oral Health Considerations Patients with parenchymal liver disease have impaired hemostasis and a clotting screen including prothrombin, together with any necessary medical preparation, is indicated prior to surgical intervention. The type and severity of the liver disease, as well as induction or inhibition of hepatic drug-metabolizing enzymes, by previous or current medications, mean that the effects of drugs are not entirely predictable. The drug effects may also be enhanced by depressed protein binding due to hypoalbuminemia. Alcoholic Liver Disease (ALD) and Alcoholic Hepatitis (AH) Oral Health Considerations Adverse interactions between alcohol or resultant ALD and medications used in dentistry include but are not limited to acetaminophen, aspirin, ibuprofen, some cephalosporins, erythromycin, metronidazole, tetracycline, ketoconazole, pentobarbital, secobarbital, diazepam, lorazepam, chloral hydrate, and opioid analgesics. Routine dental treatment for a patient with a history of ALD is not contraindicated unless there is significant cirrhosis and resultant impaired hepatic function. Consultation, the patient’s liver function status with the appropriate physician prior to commencing treatment. Drug-Induced Hepatotoxicity Drug-induced hepatotoxicity is an acute or chronic liver injury secondary to drugs or herbal compounds. Drug-induced liver disease is an uncommon but challenging clinical problem that can mimic any acute or chronic liver disease. Drug-Induced Hepatotoxicity Medical Aspects Ingested drugs are absorbed into the portal circulation and pass through the liver en route to distant sites of action. Drug-induced hepatotoxicity can result in hepatocellular injury, cholestatic drug reactions, abnormal lipid storage, cirrhosis, and vascular injury. Drug-Induced Hepatotoxicity Oral Health Considerations As reactions often have an immuno-allergic basis, the patient may present with fever, dermatitis, arthralgias, and eosinophilia in addition to features associated with the hepatic damage such as jaundice. Amoxicillin-clavulanate is the most frequent cause of idiosyncratic prescription drug-related hepatotoxicity Other common oral healthcare medications with an occurrence rate >1% include azithromycin, ciprofloxacin, diclofenac, phenytoin, and azathioprine. Liver cirrhosis Cirrhosis results from different mechanisms of liver injury that lead to necroinflammation and fibrogenesis. Histologically it is characterized by diffuse nodular regeneration surrounded by dense fibrotic septa and pronounced distortion of hepatic vascular architecture. This distortion results in increased resistance to portal blood flow, leading to portal hypertension and hepatic synthetic dysfunction. Ascites results from high pressure in the blood vessels of the liver (portal hypertension) and low levels of a protein called albumin. Liver Cirrchosis Medical Aspects Most chronic liver disease is asymptomatic until clinical decompensation occurs, when the presenting features include ascites, sepsis, variceal bleeding, encephalopathy, and nonobstructive jaundice. Imaging by ultrasonography, CT, or MRI of an irregular and nodular liver together with impaired liver synthetic function is sufficient for the diagnosis of cirrhosis. Liver Cirrchosis Medical Aspects Less frequently seen are nonspecific findings of clubbing, cyanosis, and spider angiomas. A liver biopsy is seldom needed, but study of a sample can provide a definitive diagnosis and confirm the etiology in cases of uncertainty. Conventional imaging can lead to false-negative diagnosis in early cirrhosis and non-invasive markers of fibrosis are increasingly used. Liver cirrhosis Oral Health Considerations The oral cavity may show evidence of cirrhosis, with the presence of hemorrhagic changes, petechiae, hematoma, jaundiced mucosal tissues, gingival bleeding, or icteric mucosal changes. Patients with cirrhosis are frequently malnourished and may have nutritional deficiencies or anemia, resulting in mucosal pallor, glossitis, and angular cheilitis, which may be complicated by candidal infection. Liver cirrhosis Oral Health Considerations Salivary gland dysfunction secondary to Sjögren’s syndrome may be associated with primary biliary cirrhosis. Patients with chronic hepatitis C (HCV)–related cirrhosis may report oral and ocular dryness. The virus has not been shown to directly infect salivary gland tissue, (a host immune-mediated mechanism, rather than a direct viral effect) Liver cirrhosis Oral Health Considerations Sialosis, a bilateral, painless hypertrophy of the parotid glands, may be associated with cirrhosis. The enlarged glands are soft, nontender, and are not fixed. The dental patient who presents with a history of liver cirrhosis can usually undergo routine dental treatment provided any necessary precautions are undertaken in consultation with the patient’s physician. Liver cirrhosis Hemostatic defects, because of an inability to synthesize clotting factors and the presence of a secondary thrombocytopenia. The current status and need for any preoperative measures (e.g., fresh frozen plasma or platelets) should therefore be established prior to any surgical procedure. Reduced ability to detoxify substances so that drugs and toxins may accumulate. Encephalopathy due to an ammonia buildup from the incomplete detoxification of nitrogenous wastes. Liver cirrhosis Ascites, which may make it difficult for them to fully recline in the dental chair because of increased pressure on abdominal vessels. Immunosuppression associated with liver transplantation patients and hence an increased risk of opportunistic and postoperative infections as well as acute graft-versus-host disease (mucositis) or chronic graft- versus-host disease, which resembles oral lichen planus. Viral Hepatitis Hepatitis viruses cause inflammation of the liver known as hepatitis. There are five main clinical types: 1. hepatitis A (HAV), 2. hepatitis B (HBV), 3. hepatitis C (HCV), 4. hepatitis D (HDV), 5. hepatitis E (HEV), with different modes of transmission, severity, and geographic distribution. Out of the five, types B and C lead to chronic disease, causing liver cirrhosis, cancer (hepatocellular carcinoma), and deaths. Viral Hepatitis HAV infection can lead into mild to severe illness and is transmitted through contaminated food and water or from an infected individual (fecal–oral route). The majority of infected individuals recover completely after a short illness, with immunity lasting lifelong. HAV is prevalent in countries where there is a lack of clean water, sanitation, among MSM, and in persons who inject drugs. Prevention is through the HAV vaccine. Viral Hepatitis HBV infection presents as either an acute or a chronic disease, transmitted through contact with blood or other body fluids and vertical transmission from an infected mother to a child. Those who are chronically infected are prone to complications such as liver cirrhosis and hepatocellular carcinoma. HBV is highly contagious. It is generally diagnosed via serologic testing. The best mode of prevention is through an effective vaccination against HBV. Viral Hepatitis HCV generally presents as a chronic disease with varying degrees of disease severity, including cirrhosis and liver cancer. HCV is highly infectious and can be transmitted through a very small quantity of infected blood, such as in case of the bore of a needle. The main mode of HCV transmission is through • Injecting drug use, • Accidental exposure, • And unsafe conditions in healthcare practices, and transfusion of infected blood. • Sexual activities are thought to play a minor role in HCV transmission. Viral Hepatitis Diagnosis is by testing for anti-HCV antibodies. Viral Hepatitis However, many patients spontaneously clear HCV infections, so HCV ribonucleic acid (RNA) is required to confirm an active chronic infection. In chronic HCV infection, the two main concerns are liver damage, leading to cirrhosis, and hepatocellular carcinoma. A liver ultrasound is generally the screening test of choice for both. Patients with active HCV should be managed by antiviral medications, which are curative. Unfortunately, there are no effective HCV vaccines available yet. Viral Hepatitis HDV requires HBV for its replication, hence it occurs as a super-infection or simultaneously with HBV and can be chronic. The main mode of transmission is through infected blood, body fluids, and, though rare, vertical transmission from mother to child, among Persons Who Inject Drugs (PWIDs), and through hemodialysis. HDV can be treated with interferon-based regimens. There is no vaccine for HDV, so the best prevention is vaccination for HBV. Viral Hepatitis • HEV is also a highly infectious virus and can lead to serious illness and death. • The main mode of transmission is through the fecal–oral route via contaminated water. • Pregnant women are at particularly high risk of complications from HEV. Viral Hepatitis Orofacial Manifestations and Considerations Hepatitis viruses cause serious liver damage and its consequences, especially susceptibility to bleeding and contraindications of certain drugs that depends upon the severity. There are several physical signs of end-stage liver disease, such as icterus or yellowing of the mucous membrane due to jaundice, petechial hemorrhages and ecchymosis, palmar erythema, urticaria, gynecomastia, and spider nevi. However, these features are nonspecific and may be present from other conditions, including alcoholrelated liver disease. Viral Hepatitis Orofacial Manifestations and Considerations With regard to orofacial structures, sialosis affecting the parotid glands and a close relationship with oral lichen planus, Sjögren syndrome, and sialadenitis has been documented. Halitosis, cheilitis, atrophic tongue, xerostomia, bruxism, and crusted perioral rash have also been reported. Viral Hepatitis Considering modern oral health practices, there is no cause for concern in treating hepatitis patients as long as all infection control measures are in place. If a healthcare professional is infected, they must avoid patient care during the infectious stages with active signs and symptoms of the disease. Potential exposure to hepatitis virus in an oral health practice may include needle stick or other sharps injury, contact with potentially infectious body fluids, and exposure to mucus membranes. Dental health care personnel should report any bloodborne exposures. Depending on the nature of the exposure, baseline serologic data may be obtained from both the patient and the dental healthcare worker. Exposed healthcare workers should be monitored closely after exposure and, depending on the nature of the exposure, postexposure prophylaxis (PEP) may be ordered. RENAL DISEASES Acute Kidney Injury (AKI) It is defined by a rapid increase in serum creatinine, a decrease in urine output, or both. AKI is not a single disease, but rather a loose collection of diverse syndromes such as sepsis, cardiorenal syndrome, and urinary tract obstruction. Sepsis, shock, medications, surgery, pregnancy-related complications, and trauma are the most common causesof AKI. RENAL DISEASES Prerenal Acute Kidney Injury (AKI) It is caused by inadequate blood flow to the kidneys without significant structural damage. Intrinsic Acute Kidney Injury It is characterized by the presence of structural damage to the kidneys Postrenal Failure It refers to conditions that obstruct the flow of urine from the kidneys at any level of the urinary tract, and that subsequently decrease the glomerule filtration rate RENAL DISEASES Chronic Kidney Disease (CKD) Chronickidneydiseaseisanongoingdeteriorationofrenalfunctionthatoftenprogresses toend-stagerenaldisease. CKD is classified according to the Glomerular filtration rate (GFR) RENAL DISEASES Chronic Kidney Disease (CKD) Diabetes and hypertension are major disease processes that lead to CKD and End Stage Renal Disease (ESRD.) High sodium intake may exacerbate CKD progression. In CKD, need for dialysis is frequently based on advanced uremic symptoms such as nausea, vomiting, metallic taste, loss of appetite or failure to thrive, intractable volume overload or metabolic acidosis, and life-threatening electrolyte abnormalities such as hyperkalemia. Oral Manifestations In end-stage renal disease, the urea nitrogen levels are extremely high, resulting in secretion of ammonia into the saliva AMMONIA ODOR Uremic stomatitis occurs only in severe uremia. It is the most common presentation, characterized by extremely painful ulcerations on the tongue, cheeks, lips, and palate with indefinite margins, often covered by a thick, adherent, yellowish covering on the tongue. The oral lesions consist of buccal mucosa erythema with a gray pseudomembrane or ulcerations of the gingival and buccal mucosa Oral Manifestations Oral Manifestations Uremic patients also complain of metallic or sour taste. Increased salivation is usually observed. Dysesthesia of the lips and tongue may also evolve, probably as a consequence of neuritis secondary to metabolic acidosis. The clinical manifestations of end-stage uremic stomatitis resemble those of (ANUG) Oral and cutaneous purpura are accompaniments to end-stage kidney disease. Oral Manifestations Renal osteodystrophy may ocur in late-stage kidney disease secondary to either glomerulonephritis or pyelonephritis. Impaired tubular hyperparathyroidism function leads to secondary Deminarelization of bone Ground glass appearances Brown tumor Oral Manifestations Dialysis-Related Amyloidosis This is a rare and late complication of long-term KD. It is characterized by multiple soft, painful, whitish-to-yellow nodules of various sizes >1 mm and with a cobblestone appearance on the dorsum and lateral borders of the tongue, causing macroglossia. Whitish-yellow firm nodules in the tongue which appeared in various sizes greater than 5 mm in diameter Dental Management The major concerns for dentistry are related to the; patients’ blood pressure status, drug metabolism, bleeding tendencies, anemia. In the transplant patients, sepsis is a complication, since these patients are maintained on immunosuppressive medications. Dental Management The renal disease patient on hemodialysis requires specific attention. Most patients are dialyzed from two to three times weekly. During the process of hemodialysis, the patient is heparinized, to avoid coagulation at the needle insertion site. Dental Management The effects of heparin are no longer extant the following day. For this reason, dental procedures that cause bleeding should be performed the day after, not the day of hemodialysis. Dental Management There is also a tendency for bleeding in patients with advanced kidney disease. Clinical laboratory indicators of hemostasis should be evaluated when oral surgery is to be undertaken; International normalized ratio [INR], Prothrombin time, partial thromboplastin time, platelet function Dental Management The administration of local anesthetics is usually not problematic, although both amide and ester anesthetics are cleared through the kidney. It is prudent to consult a patient's physician regarding any medication or medication beingconsidered for dental care. Dental Management In addition to local anesthetics, concern would include potential drug interactions and medications metabolized by the kidney. Additionally, some of the diuretics used to control hypervolemia may secondarily cause xerostomia. Chronic Kidney Disease with Hemodialysis Dental Management Prior to Dental Treatment Implementation of a multidisciplinary, patient-centered dental plan tailored to their individual needs upon communication with the nephrologist. This communication should include; (a) any systemic concerns (e.g., stage of renal disease, most recent blood tests, presence of systemic comorbidities, risk of excessivebleeding); (b) choice/dose/duration of current medications and medications suggested (and contraindicated) prior to, during, and after dental procedures (including the need for antibiotic prophylaxis); and (c) proposed duration and timing of treatment, anticipated results, time frame of healing, and post-therapeutic complications that could possibly develop. Dental Management Prior to Dental Treatment Implementation of a stress reduction protocol that includes morning dental appointments, a quiet calm environment to minimize the risk of stressful changes, and possible conscious sedation. Comprehensive intra- and extraoral examination, including hard tissue charting, periodontal examination, and intraoral pathology screening. Dental Management Prior to Dental Treatment A patient-centered oral hygiene care plan, including patient education, calculation of plaque, and evaluation of brushing and interdental flossing efficiency, should be developed and implemented. Daily use of antibacterial mouth rinses with essential oils or 0.12% chlorhexidine is recommended to minimize the risk of a fungal infection or in patients who are unable to follow a recommended oral hygiene protocol. Evaluate the need for topical fluoride therapy in patients with high caries risk, but remember that systemic delivery of fluoride for caries prophylaxis should be minimized due to its nephrotoxicity for patients with compromised renal function Dental Management Prior to Dental Treatment In patients presenting with halitosis, mechanical removal of dental biofilm, tongue coating, and bacteria, mouthwashes and patient education on proper oral hygiene should be used. If an invasive dental procedure is planned, a dentist should anticipate excessive bleeding during the procedure. Obtain a complete blood count and coagulation tests prior to any invasive dental treatment and ensure the availability of local and systemic hemostatic agents in the dental office. Dental Management During Dental Treatment The dentist should follow medication recommendations (including antibiotic prophylaxis) received from the patient’s nephrologist. If the patient is on warfarin, INR values should be obtained less than 1 hour prior to the procedure. Dental Management During Dental Treatment Patients who receive antibiotic prophylaxis and schedule multiple dental appointments should allow for an interval of 1–2 weeks between these appointments, and may need to use antibiotics from a different class to avoid resistance to it. If a patient presents with signs of chronic or active infection (e.g., dental caries, periodontal disease, abscesses, endodontic infection), these need to be treated as soon as possible. References • Michael Glick (ed.); Martin S. Greenberg (ed.); Peter B. Lockhart (ed.); Stephen J. Challacombe (ed.). Burket's Oral Medicine. 13th edition. Wiley-Blackwell. June 2021. ISBN: 9781119597780
