Periodontitis
(Pyorrhea)
Pathophysiology
Periodontitis usually develops when gingivitis, usually with abundant plaque and calculus (a concretion of bacteria, food residue, saliva, and mucus with calcium and phosphate salts) beneath the gingival margin, has not been adequately treated. In periodontitis, deep pockets form in the periodontal tissue and can harbor anaerobic organisms that do more damage than those usually present in simple gingivitis. Colonizing organisms include Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Eikenella corrodens, and many gram-negative bacilli.
The organisms trigger chronic release of inflammatory mediators, including cytokines, prostaglandins, and enzymes from neutrophils and monocytes. The resulting inflammation affects the periodontal ligament, gingiva, cementum, and alveolar bone. The gingiva progressively loses its attachment to the teeth, bone loss begins, and periodontal pockets deepen. With progressive bone loss, teeth may loosen, and gingiva recedes. Tooth migration is common in later stages, and tooth loss can occur.
Risk Factors
Modifiable risk factors that contribute to periodontitis include
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Plaque
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Diabetes (especially type 1)
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Emotional stress
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Vitamin C deficiency (scurvy)
Addressing these conditions can improve the treatment outcomes of periodontitis.
Classification
The American Academy of Periodontology's (AAP) 2017 reclassification of periodontal diseases and conditions now distinguishes 3 forms of periodontitis:
Other AAP designations are abscesses of the peridontium, periodontitis associated with endodontic lesions, and developmental or acquired deformities and conditions.
Periodontal abscesses are accumulations of pus that usually occur in pre-existing pockets, sometimes related to impacted foreign material. Tissue may be rapidly destroyed, risking tooth loss.
Periodontitis associated with endodontic lesions involves a communication between the pulp and periodontal tissues.
In developmental or acquired deformities and conditions, faulty occlusion, causing an excessive functional load on teeth, plus the requisite plaque and gingivitis may contribute to progression of a particular type of periodontitis characterized by angular bony defects.
Necrotizing periodontitis
Necrotizing periodontitis is a particularly virulent, rapidly progressing disease characterized by
In some patients, inflammation also involves the oral cavity, causing necrotizing stomatitis.
Necrotizing periodontitis typically occurs in patients with an impaired immune system and thus is often called HIV-associated periodontitis because HIV is a common cause. Clinically, it resembles acute necrotizing ulcerative gingivitis combined with generalized aggressive periodontitis. Patients may lose 9 to 12 mm of attachment in as little as 6 months.
Periodontitis as a direct manifestation of systemic disease
Periodontitis as a direct manifestation of systemic disease is considered in patients who have inflammation disproportionate to plaque or other local factors and who also have a systemic disease. However, distinguishing whether a disease is causing periodontitis or contributing to plaque-induced periodontitis is often difficult.
Systemic diseases associated with hematologic disease that can manifest as periodontitis include
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Acquired neutropenia
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Lazy leukocyte syndrome
Systemic diseases associated with genetic disorders that can manifest as periodontitis include
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Familial and cyclic neutropenia
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Leukocyte adhesion deficiency syndromes
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Papillon-Lefèvre syndrome
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Histiocytosis syndromes
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Infantile genetic agranulocytosis
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Ehlers-Danlos syndrome (types IV and VIII)
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Cohen syndrome
Periodontitis
The previous (1999) classification distinguished between chronic and aggressive periodontitis. However, although the age, rate of onset and severity of periodontitis vary significantly, the underlying pathophysiology is now recognized to be similar and current evidence does not support such a distinction. Disease severity is now classified as stage I through IV, and rate of progression as grade A through C.
Periodontitis can begin anywhere between early childhood and older adulthood. About 85% of the population is affected to a mild degree, but the most advanced cases are seen in < 5% of the population.
Important severity factors include
Symptoms and Signs
Pain is usually absent unless an acute infection forms in one or more periodontal pockets or if HIV-associated periodontitis is present. Impaction of food in the pockets can cause pain at meals. Abundant plaque along with redness, swelling, and exudate are characteristic. Gums may be tender and bleed easily, and breath may be foul. As teeth loosen, particularly when only one third of the root is in the bone, chewing becomes painful.
Diagnosis
Treatment
Treatment of modifiable risk factors such as poor oral hygiene, diabetes, and smoking improves outcomes.
For all forms of periodontitis, the first phase of treatment consists of thorough scaling (professional cleaning with hand or ultrasonic instruments) and root planing (removal of diseased or toxin-affected cementum and dentin followed by smoothing of the root) to remove plaque and calculus deposits. Thorough home oral hygiene is necessary and includes careful brushing and flossing to help clean. It may include chlorhexidine swabs or rinses. A therapist should help teach the patient how to do these procedures. The patient is reevaluated after 3 weeks. If pockets are no deeper than 4 mm at this point, the only treatment needed is regular cleanings. Sometimes a flap of gum tissue is made to allow access for scaling and planing of deeper parts of the root.
If deeper pockets persist, systemic antibiotics can be used. A common regimen is amoxicillin 500 mg orally 3 times a day for 10 days. In addition, a gel containing doxycycline or microspheres of minocycline can be placed into isolated recalcitrant pockets. These drugs are resorbed in 2 weeks.
Another approach is to surgically eliminate the pocket and recontour the bone (pocket reduction/elimination surgery) so that the patient can clean the depth of the normal crevice (sulcus) between the tooth and gingiva. In certain patients, regenerative surgery and bone grafting are done to encourage alveolar bone growth. Splinting of loose teeth and selective reshaping of tooth surfaces to eliminate traumatic occlusion may be necessary. Extractions are often necessary in advanced disease. Contributing systemic factors should be controlled before initiating periodontal therapy.
Ninety percent of patients with necrotizing ulcerative periodontitis due to HIV (HIV-associated periodontitis) respond to combined treatment with scaling and planing, irrigation of the sulcus with povidone-iodine (which the dentist applies with a syringe), regular use of chlorhexidine mouth rinses, and systemic antibiotics, usually metronidazole 250 mg orally 3 times a day for 14 days.
Localized aggressive periodontitis requires periodontal surgery plus oral antibiotics (eg, amoxicillin 500 mg 4 times a day or metronidazole 250 mg 3 times a day for 14 days).
Key Points
Drugs Mentioned In This Article
| Drug Name | Select Trade |
|---|---|
povidone-iodine |
Povidone-iodine |
metronidazole |
FLAGYL |
amoxicillin |
AMOXIL |
minocycline |
MINOCIN |
doxycycline |
PERIOSTAT, VIBRAMYCIN |
