Periodontics. Fernando Suarez

Чтение книги онлайн.

СКАЧАТЬ infection and the number of pack-years.¹⁴

      Systemic effects

      Systemically, smoking can affect multiple components and mechanisms of the human immune response and subsequently the host response to periodontal pathogens. Smokers have been found to have a higher receptor activator of nuclear factor-κB ligand/osteoprotegerin (RANKL/OPG) ratio, which could partially explain the increased bone loss observed in smoking populations. This alteration in RANKL and OPG is observed not only in saliva¹⁵ but also in serum.¹⁶ Neutrophils constitute the first line of defense toward bacteria that accumulate in the gingival sulcus. Their function can be altered as a result of tobacco use.¹⁷ In later disease stages, antibody production also takes place. During that period, reduced levels of serum immunoglobulin G 2 (IgG2) are identified.¹⁸

      Treatment outcomes

      In the classic longitudinal studies performed at the University of Nebraska, periodontal patients were enrolled in a maintenance program and followed up for 6 years after receiving active treatment. Smokers demonstrated poorer response to surgical and nonsurgical treatment, having lower probing depth (PD) reduction and clinical attachment level (CAL) gain.¹⁹ When furcation sites were analyzed separately, smokers had 0.5 mm less CAL gain and 0.6 mm less PD reduction compared with nonsmokers.¹⁹ A noteworthy observation from a different publication by the same group is that smokers exhibited a similar percentage of sites with BOP as nonsmokers.²⁰ Other studies reported smokers having higher percentages of sites with BOP than nonsmokers with similar levels of oral hygiene.²¹ The inferior response of smokers to nonsurgical periodontal treatment is also observed in cases where local delivery of antibiotics is used as an adjunct to scaling and root planing.²²

      As mentioned previously, smoking negatively affects the response to surgical as well as nonsurgical periodontal treatment.^19,22,23 Guided tissue regeneration is negatively affected as well. Clinical studies performed in private practices in Italy concluded that smokers had approximately 3 mm less CAL gain 12 months postoperatively (2.1 ± 1.2 mm) compared with nonsmokers (5.2 ± 1.9 mm).²⁴ When followed up for an extended period of 5 years, stable treatment outcomes were associated with patients who were not smokers, who maintained adequate oral hygiene, and who complied with supportive periodontal treatment.²⁵ Similarly, soft tissue grafting procedures are negatively influenced by smoking habits.²⁶

      It should be noted that despite the fact that the treatment response following smoking cessation is comparable with nonsmokers, this does not reverse the detrimental effects of smoking that have already manifested.^21,27 Tomar and Asma²⁸ analyzed the data from the Third National Health and Nutrition Examination Survey (NHANES III). The sample consisted of more than 13,000 adults, and it was estimated that it is four times more likely for current smokers to have periodontitis compared with individuals who never smoked. When former smokers were analyzed separately, the ones who had quit smoking in the previous 2 years were more likely to be diagnosed with periodontitis, and this likelihood decreased gradually. Former smokers who quit smoking for at least 11 years were as likely to have periodontitis as those who had never smoked. According to this study, almost three-fourths of periodontitis cases in the United States (74.8%) are attributed to smoking.²⁸

      Ultimately, smoking increases the likelihood of tooth loss. McGuire and Nunn²⁹ discussed the prognosis and prediction of tooth loss and followed up with periodontal maintenance patients for 14 years. They estimated the risk for tooth loss to be increased by 2.9 times for heavy smokers (Box 4-2).

BOX 4-2 Link between smoking and periodontal status

      GTR, guided tissue regeneration; SRP, scaling and root planing.

      DIABETES MELLITUS

      According to the Centers for Disease Control and Prevention (CDC), an estimated 9.4% (30.3 million) of the U.S. population are diabetics, and almost 24% of this population (7.2 million) are undiagnosed.³⁰ The American Diabetes Association classifies diabetes based on its pathophysiology into the following categories:

       Type 1 (5% of diabetics): Caused by autoimmune destruction of the pancreatic β-cells. This results in inability of the pancreas to produce insulin.

       Type 2 (90%–95% of diabetics): Characterized by insulin resistance, eventually leading to loss of β-cell insulin secretion.

       Gestational (2%–10% of pregnancies): Onset usually during the second or third trimester of pregnancy. These individuals are more likely to develop Type 2 diabetes later in life.

       Other: Examples include diseases of the exocrine pancreas, and drug- or chemical-induced syndromes.

      Diabetes is considered another major risk factor for periodontal disease. The mechanisms that link diabetes to periodontal disease have been described as associated with the interaction of the advanced glycation end products (AGEs) with their receptor (RAGE). This interaction alters cell function, increases levels of reactive oxygen species, and increases the RANKL/OPG, therefore altering bone homeostasis and eventually leading to increased tissue destruction.³¹

      Local effects

      The composition of periodontal microbiota does not appear to be influenced by diabetes, according to the majority of the existing literature.³¹ Diabetics exhibit increased BOP, and this tendency increases as the level of diabetic control decreases.³² In a longitudinal study in Pima Indians, more than 2,200 subjects were enrolled and followed up for 2.5 years. The incidence of periodontitis was 2.6 times higher in diabetics compared with nondiabetics.³³ Similar findings were reported from an epidemiologic study of the same population, with diabetes increasing the risk for periodontal disease by three times.³⁴

      Treatment outcomes

      On the other hand, prediabetics or well-controlled diabetics are not at additional risk for periodontal disease.³⁵ The level of glycemic control has an impact on the outcome of the treatment. A favorable response is observed in well-controlled diabetics, similar to nondiabetic controls.³⁶

      The immunologic response of diabetics to bacterial plaque is similar to nondiabetics in terms of IgG levels, although differences can be observed in regard to the levels of E-selectin, vascular cell adhesion molecule-1 (VCAM-1), adiponectin, and plasminogen activator inhibitor-1.³⁷

      With regard to the effect of periodontal treatment on diabetic control, nonsurgical periodontal therapy can reduce the hemoglobin A1c (HbA1c) levels. However, this reduction may be considered insignificant, and it is not stable over time. The magnitude of the reduction is higher in Type 2 diabetics compared with Type 1 and when antibiotics were prescribed as an adjunct to nonsurgical treatment. Although the reduction of HbA1c following periodontal treatment reported from several studies can vary, based on the current evidence, it is anticipated to correspond to 0.3% to 0.4% less than the original value^38,39 (Box 4-3).

BOX 4-3 Link between diabetes and periodontal status

      PATHOGENIC СКАЧАТЬ