Complications and contraindications at the orthopedic treatment of generalized periodontitis. Indications, clinical technological techniques of immediate prosthesis designs.
There are two main groups of periodontal diseases: gingivitis and periodontitis. Gingivitis is recognised by gums that show classic signs of inflammation, redness and swelling, but without involvement of the periodontium. The periodon-tium includes the gingiva, cementum, periodontal ligaments, connective tissue, and the alveolar bone. Periodontitis occurs when inflammation spreads to the periodontium, causing one of the following conditions: (1) the gingiva detaches from the affected tooth along its root, creating a periodontal pocket; or (2) gingival recession, where the gingiva recedes along its root line, affecting the whole thickness of the gum. In both cases, alveolar bone loss hidden by ginvi-val inflammation is what matters most. When bone loss is extensive, the teeth can become loose and eventually fall out. Periodontal destruction is induced by the deleterious effects of inflammatory mediators occurring because of bacterial plaque build-up around the tooth. Periodontal diseases can be subdivided into 2 sub-groups: juvenile and adult. Periodontal diseases observed in young people are usually associated with neu-trophil dysfunction; in adults, they are caused mostly by an accumulation of bacterial plaque around the teeth and their roots. Certain lifestyles, health conditions or states of health, and systemic diseases are also factors that can increase the severity of periodontitis.
Gingivitis
There are two main groups of periodontal diseases: gingivitis and periodontitis. Gingivitis is recognised by gums that show classic signs of inflammation, redness and swelling, but without involvement of the periodontium. The periodon-tium includes the gingiva, cementum, periodontal ligaments, connective tissue, and the alveolar bone. Periodontitis occurs when inflammation spreads to the periodontium, causing one of the following conditions: the gingiva detaches from the affected tooth along its root, creating a periodontal pocket; or gingival recession, where the gingiva recedes along its root line, affecting the whole thickness of the gum. In both cases, alveolar bone loss hidden by ginvi-val inflammation is what matters most. When bone loss is extensive, the teeth can become loose and eventually fall out. Periodontal destruction is induced by the deleterious effects of inflammatory mediators occurring because of bacterial plaque build-up around the tooth. Periodontal diseases can be subdivided into 2 sub-groups: juvenile and adult. Periodontal diseases observed in young people are usually associated with neu-trophil dysfunction; in adults, they are caused mostly by an accumulation of bacterial plaque around the teeth and their roots. Certain lifestyles, health conditions or states of health, and systemic diseases are also factors that can increase the severity of periodontitis.
Why should physicians be concerned with periodontal diseases?
1. An accumulation of bacterial plaque around the teeth is the main aetiology involved in periodontal diseases; however, different lifestyles, systemic diseases, health statuses, as well as certain genetic factors can either enhance the risk of periodontal diseases or modify their prognosis.
2.Some periodontal diseases are caused by bacterial (linear gingival erythema), viral (primary herpetic gingivos-tomatitis) or fungal (histoplasmosis) infections, presenting an additional risk for the pathogen to be transmitted through direct contact with the mouth and saliva.Osteoporosis and periodontitis are diseases that affect a wide range of men and women in the worldwide, with incidence increasing with advancing age. Osteoporosis is a skeletal disorder characterized by compromising bone strength predisposing to increased risk of fracture, with bone strength characterized by bone density and bone quality.
3. In some cases, periodontal diseases may negatively affect a patient’s overall health.
4. The major risk factors associated with periodontal diseases (smoking, diabetes, oral hygiene, stress, etc.) are also associated with other conditions or systemic disease.
5. Some medications can affect the health of the periodontium.
6. Women are more susceptible to periodontal diseases because of the hormonal changes they experience during different stages of life: at puberty, during the menstrual cycle or pregnancy, when taking oral contraceptives, or during menopause. For example, during pregnancy, the immune response is weaker and concentrations of progesterone and oestrogen are at least.
2. Periodontitis.
ten-fold higher; consequently any accumulation of bacterial plaque, no matter how small, can induce a disproportionate inflammatory response in the periodon-tium. Therefore, it is important to encourage pregnant women and women who plan on becoming pregnant to maintain good dental hygiene.
Two risk factors of greater concern for periodontal diseases
Smoking
Smokers are afflicted more often with peri-odontitis than non-smokers and often experience a higher rate of bone loss. Conversely, smokers’ gums tend to bleed less when they brush due to the vasocon-strictive effect of tobacco, which masks the presence of periodontal disease. Moreover, smokers are exposed to a particularly destructive and painful type of periodontal disease, acute necrotizing ulcerative gingivitis (ANUG). Smoking may constitute a contraindication to gingival grafts and dental implants; in addition, prognosis of periodontal treatment in smokers is often less favourable.
Diabetes
Diabetes (types 1 and 2) increases the risk of periodontal diseases because the biochemical processes linked to diabetes reduce blood flow to the gums and blunt the immune response. Therefore, poorly controlled diabetes can enhance periodon-tal destruction in people with periodontitis.
The risk of smokers developing a periodontal disease is fivetimes higher than among non-smokers; the risk for a diabetic smoker is 20 times higher. Diabetic patients who show signs of microcomplications associated with diabetes (e.g. retinopathy) are more susceptible to periodontal diseases.
Two systemic complications: hypotheses
Cardiovascular diseases
Some studies suggest that having a periodontal disease can increase the risk of atherosclerosis, coronary disease, and myocardial infarction. At this time, four main mechanisms are suspected:
6. The direct effects of the infectious agents involved in periodontal diseases on atheroma formation;
7. The indirect effect of the immune response induced by a periodontal infection;
8. Common genetic predispositions between periodontal diseases and atherosclerosis;
9. Common risk factors linked to lifestyle. The production of protein such as C-reactive protein and fibrinogen seems to be particularly significant. Several pathogenic agents involved in periodontal diseases can also affect the heart, if bacteraemia occur; the classic example is infective endocarditis.
Preterm low-weight babies:
Some studies seem to indicate that periodontitis in a pregnant woman can affect the foetus’s health, especially if her periodontal condition worsens during her pregnancy.
Periodontitis is an inflammation of the supporting tissue of the teeth, usually leading to loss of bone and periodontal ligament and is a major cause of tooth loss and edentulousness in adults.
Periodontal diseases are associated with a number of chronic diseases including Osteoporosis.
Osteopenia and osteoporosis are systemic skeletal diseases characterized by low bone mass and microarchitectural deterioration with a consequent increase in bone fragility and susceptibility to fracture.
According to the World Health Organization, osteoporosis is considered to be present when bone mineral density (BMD) is 2.5 standard deviations (SD) below the young normal. Osteopenia is defined as bone density levels between 1 SD and 2.5 SD below normal BMD.
In the 3rd National Health and Nutrition Examination Survey (NHANES III) the prevalence of osteoporosis when assessed at the femoral neck was 20% of postmenopausal white women.
The risk factors for osteoporosis can be divided into non-modifiable and modifiable risk factors,
The non-modifiable include sex, age, early menopause, thin or small body frame, race, and heredity. Lack of calcium intake, lack of exercise, smoking, and alcohol are modifiable risk factors. Low bone mass, certain medications (corticosteroid or anticonvulsant), propensity to fall, and systemic diseases such as hyperparathyroidism are modifiable to some extent. The risk factors for osteoporosis include many risk factors associated with advanced periodontal disease. Since both osteoporosis and periodontal diseases are bone resorptive diseases, it has been hypothesized that osteoporosis could be a risk factor for the progression of periodontal disease. The data gathered on the mostly cross-sectional studies appears to indicate a relationship between systemic BMD and oral BMD. Additional data from ongoing longitudinal studies will further elaborate this relationship.
Menopause, osteoporosis and periodontal diseases Female life expectancy to 80 years old, 40 % of her life in menopause which is associated with decline in the hormonal levels due to decrease in the ovarian functions. All these hormonal changes will lead to psychological, oral and systemic health changes. Oral changes that can be seen may include: thinning of oral mucosa, desquamation of gingival epithelium, burning mouth, gingival recession, xerostomia and alveolar bone loss & ridge resorption.
Bone loss in women occurs most rapidly in the years immediately following menopause wheatural levels of estrogen are greatly reduced. In most women, bone mass reach its peak level at third decade of life and decline thereafter. This decline accelerate with the onset of menopause. While estimates the rate of menopausal bone loss may differ by population and measurement technology a rate on the order of 0.5% to 1.0% per year has been reported.
Association between Osteoporosis and periodontal diseases A growing body of literature has accumulated regarding the role of osteoporosis in the onset and progression of periodontal disease and tooth loss. The association between these two diseases is biologically plausible as well. However, most studies are crosssectional uncontrolled, consist of small samples, and are largely restricted to postmenopausal women. Cross-sectional studies have an inherent limitation in establishing causation, since bias, confounding, and temporality are difficult to establish and control. Loss of alveolar bone as a feature of periodontal disease may be easily confounded by other factors such as gender, hormone intake, smoking, race, age, stress and distress, diet, body mass, and exercise. Many of the studies to date inadequately address these issues. Most studies are relatively small and make control of confounding and assessment of effect modification difficult.
Potential mechanisms and biological aspects
Based upon our knowledge of osteopenia and periodontal disease and the risk factors that affect both, it is reasonable to propose the following hypothesis: periodontitis results from bacteria that produce factors which cause loss of collagenous support of the tooth, as well as loss of alveolar bone. Osteopenia results in loss of BMD throughout the body, including loss in the maxilla and mandible. The resulting local reduction of BMD in the jawbones would set the stage for more rapid alveolar crestal height loss since a comparable challenge of bacterial bone-resorbing factors could be expected to result in greater alveolar crestal loss than a non-osteopenic individual. There are, in addition, systemic risk factors such as smoking, diabetes, diet, and hormone levels that affect systemic bone loss and may also affect periodontitis.
Although periodontal disease has historically been thought to be the result of an infectious process, others have suggested that periodontal disease may be an early manifestation of generalized osteopenia. Evidence in support of this concept is limited and evaluation of the independent role of generalized osteopenia on periodontal disease requires further study. Bone loss associated with osteoporosis occurs when there is an imbalance between bone resorption and formation, favoring resorption. Calcium balance, vitamin D metabolism, estrogens, and aging are interrelated factors in the causation of osteoporosis. Chronic negative calcium balance reduces bone mineral content. Decrease in calcium intake and decrease in intestinal calcium absorption with age contribute to a negative calcium balance in older women. Both estrogen and vitamin D are known to affect intestinal calcium absorption. Vitamin D3 supplementation has been shown to reduce new vertebral fractures in postmenopausal women compared to women supplemented with calcium that contribute to bone loss include suboptimal skeletal development in early adulthood and age-related bone loss. Hormone dependent increases in bone resorption and accelerated loss of bone within 10 years after menopause have been reported to be the main pathogenic factors in primary osteoporosis in women. Estrogen deficiency appears to play a major role in osteopenia and accelerated bone loss, a concept which is supported by the higher prevalence of osteopenia in women than men. Also, a meta-analysis of the effect of estrogen replacement therapy on reduction of osteoporotic hip fractures in postmenopausal women estimated a 25% reduction in hip fracture in estrogen users compared to non-users, supporting a major role of estrogen in hip fracture and presumably osteoporosis prevention.
Why should physicians be concerned with periodontal diseases?
1. An accumulation of bacterial plaque around the teeth is the main aetiology involved in periodontal diseases; however, different lifestyles, systemic diseases, health statuses, as well as certain genetic factors can either enhance the risk of periodontal diseases or modify their prognosis.
2.Some periodontal diseases are caused by bacterial (linear gingival erythema), viral (primary herpetic gingivos-tomatitis) or fungal (histoplasmosis) infections, presenting an additional risk for the pathogen to be transmitted through direct contact with the mouth and saliva.Osteoporosis and periodontitis are diseases that affect a wide range of men and women in the worldwide, with incidence increasing with advancing age. Osteoporosis is a skeletal disorder characterized by compromising bone strength predisposing to increased risk of fracture, with bone strength characterized by bone density and bone quality.
In some cases, periodontal diseases may negatively affect a patient’s overall health.
10. The major risk factors associated with periodontal diseases (smoking, diabetes, oral hygiene, stress, etc.) are also associated with other conditions or systemic disease.
11. Some medications can affect the health of the periodontium.
12. Women are more susceptible to peri-odontal diseases because of the hormonal changes they experience during different stages of life: at puberty, during the menstrual cycle or pregnancy, when taking oral contraceptives, or during menopause. For example, during pregnancy, the immune response is weaker and concentrations of progesterone and oestrogen are at least
Periodontitis.
ten-fold higher; consequently any accumulation of bacterial plaque, no matter how small, can induce a disproportionate inflammatory response in the periodon-tium. Therefore, it is important to encourage pregnant women and women who plan on becoming pregnant to maintain good dental hygiene.
Two risk factors of greater concern for periodontal diseases
Smoking
Smokers are afflicted more often with peri-odontitis thaon-smokers and often experience a higher rate of bone loss. Conversely, smokers’ gums tend to bleed less when they brush due to the vasocon-strictive effect of tobacco, which masks the presence of periodontal disease. Moreover, smokers are exposed to a particularly destructive and painful type of periodontal disease, acute necrotizing ulcerative gingivitis (ANUG). Smoking may constitute a contraindication to gingival grafts and dental implants; in addition, prognosis of periodontal treatment in smokers is often less favourable.
Diabetes
Diabetes (types 1 and 2) increases the risk of periodontal diseases because the biochemical processes linked to diabetes reduce blood flow to the gums and blunt the immune response. Therefore, poorly controlled diabetes can enhance periodon-tal destruction in people with periodontitis.
The risk of smokers developing a periodontal disease is fivetimes higher than among non-smokers; the risk for a diabetic smoker is 20 times higher. Diabetic patients who show signs of microcomplications associated with diabetes (e.g. retinopathy) are more susceptible to periodontal diseases.
Two systemic complications: hypotheses
Cardiovascular diseases
Some studies suggest that having a peri-odontal disease can increase the risk of atherosclerosis, coronary disease, and myocardial infarction. At this time, four main mechanisms are suspected:
13. The direct effects of the infectious agents involved in periodontal diseases on atheroma formation;
14. The indirect effect of the immune response induced by a periodontal infection;
15. Common genetic predispositions between periodontal diseases and atherosclerosis;
16. Common risk factors linked to lifestyle. The production of protein such as C-reactive protein and fibrinogen seems to be particularly significant. Several pathogenic agents involved in periodontal diseases can also affect the heart, if bacteraemia occur; the classic example is infective endocarditis.
Preterm low-weight babies:
Some studies seem to indicate that peri-odontitis in a pregnant woman can affect the foetus’s health, especially if her peri-odontal condition worsens during her pregnancy.
•When should patient check?
•When lifestyles, health conditions, and systemic diseases predispose a patient to periodontal diseases or when the reason for medical consultation involves a bucco-dental problem.
•When a patient has not seen a dentist for about 12 months and there are signs that he or she may have a periodontal disease, or when a newly diagnosed condition increases the patient’s risk of developing periodontal diseases. In the latter case, it is also important to inform the patient of the additional risks of periodontal diseases.
All cases of periodontitis evolve from gingivitis; however, gingivitis does not necessarily develop into periodontitis. Clinical signs of gingivitis are inflammation of the gums and gums that bleed easily. Gingival recession, periodontal pockets, the destruction of interdental gingival papilla, and increasingly loose teeth are all clinical signs of periodontitis. Tartar detection is of prime importance since it is directly involved in the pathogenesis of periodontal diseases.
Periodontitis is an inflammation of the supporting tissue of the teeth, usually leading to loss of bone and periodontal ligament and is a major cause of tooth loss and edentulousness in adults (Fig.1).
Periodontal diseases are associated with a number of chronic diseases including Osteoporosis.
Osteopenia and osteoporosis are systemic skeletal diseases characterized by low bone mass and microarchitectural deterioration with a consequent increase in bone fragility and susceptibility to fracture.
According to the World Health Organization, osteoporosis is considered to be present when bone mineral density (BMD) is 2.5 standard deviations (SD) below the young normal. Osteopenia is defined as bone density levels between 1 SD and 2.5 SD below normal BMD.
In the 3rd National Health and Nutrition Examination Survey (NHANES III) the prevalence of osteoporosis when assessed at the femoral neck was 20% of postmenopausal white women.
The risk factors for osteoporosis can be divided into non-modifiable and modifiable risk factors,
The non-modifiable include sex, age, early menopause, thin or small body frame, race, and heredity. Lack of calcium intake, lack of exercise, smoking, and alcohol are modifiable risk factors. Low bone mass, certain medications (corticosteroid or anticonvulsant), propensity to fall, and systemic diseases such as hyperparathyroidism are modifiable to some extent (Fig.3). The risk factors for osteoporosis include many risk factors associated with advanced periodontal disease. Since both osteoporosis and periodontal diseases are bone resorptive diseases, it has been hypothesized that osteoporosis could be a risk factor for the progression of periodontal disease. The data gathered on the mostly cross-sectional studies appears to indicate a relationship between systemic BMD and oral BMD. Additional data from ongoing longitudinal studies will further elaborate this relationship.
Menopause, osteoporosis and periodontal diseases Female life expectancy to 80 years old, 40 % of her life in menopause which is associated with decline in the hormonal levels due to decrease in the ovarian functions. All these hormonal changes will lead to psychological, oral and systemic health changes. Oral changes that can be seen may include: thinning of oral mucosa, desquamation of gingival epithelium, burning mouth, gingival recession, xerostomia and alveolar bone loss & ridge resorption.
Bone loss in women occurs most rapidly in the years immediately following menopause wheatural levels of estrogen are greatly reduced. In most women, bone mass reach its peak level at third decade of life and decline thereafter. This decline accelerate with the onset of menopause. While estimates the rate of menopausal bone loss may differ by population and measurement technology a rate on the order of 0.5% to 1.0% per year has been reported.
Association between Osteoporosis and periodontal diseases A growing body of literature has accumulated regarding the role of osteoporosis in the onset and progression of periodontal disease and tooth loss. The association between these two diseases is biologically plausible as well. However, most studies are crosssectional uncontrolled, consist of small samples, and are largely restricted to postmenopausal women. Cross-sectional studies have an inherent limitation in establishing causation, since bias, confounding, and temporality are difficult to establish and control. Loss of alveolar bone as a feature of periodontal disease may be easily confounded by other factors such as gender, hormone intake, smoking, race, age, stress and distress, diet, body mass, and exercise. Many of the studies to date inadequately address these issues. Most studies are relatively small and make control of confounding and assessment of effect modification difficult.
Potential mechanisms and biological aspects
Based upon our knowledge of osteopenia and periodontal disease and the risk factors that affect both, it is reasonable to propose the following hypothesis: periodontitis results from bacteria that produce factors which cause loss of collagenous support of the tooth, as well as loss of alveolar bone. Osteopenia results in loss of BMD throughout the body, including loss in the maxilla and mandible. The resulting local reduction of BMD in the jawbones would set the stage for more rapid alveolar crestal height loss since a comparable challenge of bacterial bone-resorbing factors could be expected to result in greater alveolar crestal loss than
non-osteopenic individual. There are, in addition, systemic risk factors such as smoking, diabetes, diet, and hormone levels that affect systemic bone loss and may also affect periodontitis.
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Although periodontal disease has historically been thought to be the result of an infectious process, others have suggested that periodontal disease may be an early manifestation of generalized osteopenia. Evidence in support of this concept is limited and evaluation of the independent role of generalized osteopenia on periodontal disease requires further study. Bone loss associated with osteoporosis occurs when there is an imbalance between bone resorption and formation, favoring resorption. Calcium balance, vitamin D metabolism, estrogens, and aging are interrelated factors in the causation of osteoporosis. Chronic negative calcium balance reduces bone mineral content. Decrease in calcium intake and decrease in intestinal calcium absorption with age contribute to a negative calcium balance in older women. Both estrogen and vitamin D are known to affect intestinal calcium absorption. Vitamin D3 supplementation has been shown to reduce new vertebral fractures in postmenopausal women compared to women supplemented with calcium that contribute to bone loss include suboptimal skeletal development in early adulthood and age-related bone loss. Hormone dependent increases in bone resorption and accelerated loss of bone within 10 years after menopause have been reported to be the main pathogenic factors in primary osteoporosis in women. Estrogen deficiency appears to play a major role in osteopenia and accelerated bone loss, a concept which is supported by the higher prevalence of osteopenia in women than men. Also, a meta-analysis of the effect of estrogen replacement therapy on reduction of osteoporotic hip fractures in postmenopausal women estimated a 25% reduction in hip fracture in estrogen users compared to non-users, supporting a major role of estrogen in hip fracture and presumably osteoporosis prevention.
Treatment of osteoporosis and periodontitis
Regarding the treatment of osteoporosis include decrease the risk factors through many treatment options such as adding protective factors of a Ca & vit. D rich diet + supplementation, weight bearing exercises, hormonal replacement therapy (HRT)-(ERT), drug therapy such as: alendronate (Fosamax®), calcitonin, selective estrogen receptor modulators and parathyroid hormone.
HRT as one of the treatment modalities for osteoporosis had been showed that patient on HRT show regaining bone mass to pre menopause level & in preventing / reversing postmenopausal osteoporotic changes in long bones & spine and has a beneficial effect on tooth loss, mandibular bone density & gingival bleeding.
Clinical consideration and management of periodontal disease for an osteoporisis patient If the patient is osteoporosis susceptible and due to the changes in alveolar bone level or oral manifestation for a menopause woman; close monitoring of periodontal maintenance, informing the patient regarding the potential risks of hormone depleting on the oral tissue and consulting the patient’s physician about the current medication & the replacements to treat osteoporosis.
Every treatment modality in periodontal therapy can be done for osteoporotic patient from scaling and root planing, different periodontal and implant surgery so we can say from the scientific evidences that osteoporosis is not a contraindication for different periodontal surgery (guided tissue regeneration and implant) in spite of the lack for more controlled prolonged studies in that field (Fig.5)
Regarding dental Implant osteoporosis is not likely a risk factor for failure of osseointegrated implants, dental implant placement in edentulous area aid in maintaining the height & density of alveolar bone. osteoporotic bone does not heal differently than more dense bone and the prognosis of osseointegrated implants can be improved in O.P patient who received treatment such as (Fosamax®) (Fig.6)
New evidences and precautions for oseoporotic patient who are on certain medication and need a huge periodontal and implant’s surgical intervention Ruggiero and colleagues reported in the August 2004 issue of the Journal of Oral and Maxillofacial Surgery the observation of an osteonecrosis syndrome reminiscent of osteoradionecrosis in certain patients taking bisphosphonate drugs. Patients developed osteoradionecrosis-like lesions soon after extraction of teeth for periodontal, endodontic, or prosthetic reasons; from 2001 to 2003, they saw 63 cases, of which approximately two-thirds of the osteonecrosis cases occurred in the mandible. All patients had been receiving various forms of bisphosphonate therapy (primarily zoledronic acid and pamidronate) for a variety of metastatic cancers. Also in CHICAGO – April 11, 2006 – The patient of a periodontist in private practice in New Orleans, LA, developed osteonecrosis of the jaw (ONJ), a condition that can cause severe, often irreversible and debilitating damage to the jaw, following periodontal surgical therapy. Two years prior to surgery, the patient had started receiving IV bisphosphonate therapy, or bone-sparing drugs commonly used in the treatment of osteoporosis and metastatic bone cancer to help decrease associated pain and fractures, following treatment for breast carcinoma.
So it will be wise enough after all these continuous observation to start with a small periodontal surgical intervention for those patient who are osteoporotic on intravenous bisphosphenate therapy or bone spring drugs and see the prognosis and the healing before we go for more advances and complicated surgical interventions).
Conclusion
From the literature we had, it appeared that there is an association of osteporosis with onset and progression of periodontal diseases in humans, also the studies revealed that Low bone mass independently associated with loss of alveolar crest height & tooth loss.
1.The limitations of the studies that investigate the aspects of the relation between osteoporosis and periodontal diseases include: small sample size 2.Limited control of other profounding factors 3.V arying definitions of periodontal diseases & O.P.
Finally there is a demanding issue to better understanding and investigation for the potential mechanisms between periodontal diseases and systemic problems including osteoporosis.
Gingivitis and periodontitis are the 2 major forms of infamma-tory diseases affecting the periodontium. Their primary etiology is bacterial plaque, which can initiate destruction of the gingi-val tissues and periodontal attachment apparatus. Gingivitis is infammation of the gingiva that does not result in clinical attachment loss. Periodontitis is infammation of the gingiva and the adjacent attachment apparatus and is characterized by loss of connective tissue attachment and alveolar bone. Each of these diseases may be subclassifed based upon etiology, clinical presentation, or associated complicating factors.
Gingivitis is a reversible disease. Therapy is aimed primarily at reduction of etiologic factors to reduce or eliminate infam-mation, thereby allowing gingival tissues to heal. Appropriate supportive periodontal maintenance that includes personal and professional care is important in preventing re-initiation of infammation.
Therapeutic approaches for periodontitis fall into 2 major categories: 1) anti-infective treatment, which is designed to halt the progression of periodontal attachment loss by removing etiologic factors; and 2) regenerative therapy, which includes anti-infective treatment and is intended to restore structures destroyed by disease. Essential to both treatment approaches is the inclusion of periodontal maintenance procedures.
Infammation of the periodontium may result from many causes (eg, bacteria, trauma). However, most forms of gingivitis and periodontitis result from the accumulation of tooth-adherent microorganisms. Prominent risk factors for development of chronic periodontitis include the presence of
specifc subgingival bacteria, tobacco use, diabetes, age, and male gender. Furthermore, there is evidence that other factors can contribute to periodontal disease pathoge-nesis: environmental, genetic, and systemic (eg, diabetes).
This paper primarily reviews the treatment of plaque-induced gingivitis and chronic periodontitis, but there might be some situations where the described therapies will not resolve disease or arrest disease progression. Furthermore, the treatments discussed should not be deemed inclusive of all possible therapies, or exclusive of methods of care reasonably directed at obtaining good results. The ultimate decision regarding the appropriateness of any specifc procedure must be made by the practitioner in light of the circumstances presented by an individual patient.
Plaque-induced Gingivitis
Therapy for individuals with chronic gingivitis is initially directed at reduction of oral bacteria and associated calcifed and noncalcifed deposits. Patients with chronic gingivitis, but without signifcant calculus, alterations in gingival morphology, or systemic diseases that affect oral health, may respond to a therapeutic regimen consisting of improved personal plaque control alone. The periodontal literature documents the short-and long-term effects following self-treatment of gingivitis by personal plaque control. However, while it may be possible under controlled conditions to remove most plaque with a variety of mechanical oral hygiene aids, many patients lack the motivation or skill to attain and maintain a plaque-free state for signifcant periods of time. Clinical trials also indicate that self-administered plaque control programs alone, without periodic professional reinforcement, are inconsistent in providing long-term inhibition of gingivitis.
Many patients with gingivitis have calculus or other associated local factors (eg, defective dental restorations) that interfere with personal oral hygiene and the ability to remove bacterial plaque. An acceptable therapeutic result for these individuals is usually obtained when personal plaque control measures are performed in conjunction with professional removal of plaque, calculus, and other local contributing factors.
Removal of dental calculus is accomplished by scaling and root planing procedures using hand, sonic, or ultrasonic instruments. The therapeutic objective of scaling and root planing is to remove plaque and calculus to reduce subgingival bacteria below a threshold level capable of initiating clinical infammation.The success of instrumentation is determined by evaluating the periodontal tissues following treatment and during the maintenance phase of therapy.
The use of topical antibacterial agents to help reduce bacterial plaque may be benefcial for the prevention and treatment of gingivitis in some patients.
A number of these agents in oral rinses and dentifrices have been tested in clinical trials. However, to be accepted by the American Dental Association (ADA) Council on Dental Therapeutics as an effective agent for the treatment of gingivitis, a product must reduce plaque and demonstrate effective reduction of gingival infammation over a period of at least 6 months. The agent must also be safe and not induce adverse side effects.
Three medicaments have been given the ADA Seal of Acceptance for the control of gingivitis. The active ingredients of one product are thymol, menthol, eucalyptol, and methyl salicylate. Active ingredients in the other two are chlorhexidine digluconate and triclosan. If properly used, the addition of a topical anti-plaque agent to a gingivitis treatment regimen for patients with defcient plaque control will likely result in reduction of gingivitis. However, experimental evidence indicates that penetration of topically applied agents into the gingival crevice is minimal.31 Therefore, these agents are useful for the control of supragingival, but not subgingival plaque. Among individuals who do not perform excellent oral hygiene, supra-gingival irrigation with and without medicaments is capable of reducing gingival infammation beyond that normally achieved by toothbrushing alone. This effect is likely due to the fushing out of subgingival bacteria.
If gingivitis remains following the removal of plaque and other contributing local factors, thorough evaluation should be undertaken of systemic factors (eg, diabetes, pregnancy, etc.). If such conditions are present, gingival health may be attained once the systemic problem is resolved and plaque control is maintained.
Acute Periodontal Diseases
Necrotizing ulcerative gingivitis (NUG) is associated with specifc bacterial accumulations occurring in individuals with lowered host resistance. NUG usually responds rapidly to the reduction of oral bacteria by a combination of personal plaque control and professional debridement. If lymphadenopathy or fever accompanies oral symptoms, administration of systemic antibiotics may be indicated. The use of chemotherapeutic rinses by the patient may be benefcial during the initial treatment stages. After the acute infammation of the NUG lesion is resolved, additional intervention may be indicated to prevent disease recurrence or to correct resultant soft tissue deformities. Necrotizing ulcerative periodontitis (NUP) manifests as rapid necrosis and destruction of the gingiva and periodontal attachment apparatus. It may initiate gingival bleeding and pain, and it usually represents an extension of necrotizing ulcerative gingivitis in individuals with lowered host resistance. NUP has been reported among both HIV-positive and negative individuals, but its true prevalence is unknown. Management of NUP involves debridement which may be combined with irrigation with antiseptics (eg, povidone iodine), antimicrobial mouth rinses (eg, chlorhexidine), and administration of systemic antibiotics. There is also evidence that HIV-immune defciency may be associated with severe loss of periodontal attachment that does not necessarily present clinically as an ulcerative lesion.40 Although not an acute disease, linear gin-gival erythema (LGE) occurs in some HIV-infected individuals and does not appear to respond to conventional scaling, root planing, and plaque control. Antibiotic therapy should be used in HIV-positive patients with caution due to the possibility of inducing opportunistic infections.
The oral manifestations of a primary herpes simplex virus type I infection often include gingivitis. By the time gingivitis is present, patients are usually febrile, in pain, and have lymph-adenopathy. Diagnosis is generally made from the clinical appearance of the oral soft tissues. Although not performed routinely, a viral culture may provide defnitive identifcation of the infective agent. In otherwise healthy patients, treatment for herpetic gingivitis consists of palliative therapy. The infection is self-limiting and usually resolves in 7 to 10 days. Systemic antiviral therapy with acyclovir is appropriate for immunocompromised patients with herpetic gingivitis.
Gingival Enlargement
Chronic gingival infammation may result in gingival enlargement. This overgrowth of gingiva may be exaggerated in patients with genetic or drug-related systemic factors (eg, anticonvul-sants, cyclosporine and calcium channel blocking drugs). Among individuals taking phenytoin, gingival overgrowth may be minimized with appropriate personal oral hygiene and professional maintenance. However, root debridement in patients with gingival overgrowth often does not return the periodontium to normal contour. The residual overgrowth may not only complicate the patient’s ability to adequately clean the dentition, but it may also present esthetic and functional problems.
For patients with gingival overgrowth, the modifcation of tissue topography by surgical recontouring may be undertaken to create a maintainable oral environment. Postoperative management following tissue resection is important. The benefts of surgical reduction may be lost due to rapid proliferation of the tissues during the post-therapy phase. Recurrence is common in many patients with drug-induced gingival overgrowth. For these patients, consultation with the patient’s physician is advisable to determine if it is possible to use an alternative drug therapy that does not induce gingival overgrowth. If not, then repeated surgical and/or non-surgical intervention may be required.
Chronic Periodontitis
Appropriate therapy for patients with periodontitis varies considerably with the extent and pattern of attachment loss, local anatomical variations, type of periodontal disease, and therapeutic objectives. Periodontitis destroys the attachment apparatus of teeth resulting in periodontal pocket formation and alteration of normal osseous anatomy. The primary objectives of therapy for patients with chronic periodontitis are to halt disease progression and to resolve infammation. Therapy at a diseased site is aimed at reducing etiologic factors below the threshold capable of producing breakdown, thereby allowing repair of the affected region. Regeneration of lost peri-odontal structures can be enhanced by specifc procedures. However, many variables responsible for complete regeneration of the periodontium are unknown and research is ongoing in this area.
Scaling and Root Planing
The benefcial effects of scaling and root planing combined with personal plaque control in the treatment of chronic peri-odontitis have been validated. These include reduction of clinical infammation, microbial shifts to a less pathogenic subgingival fora, decreased probing depth, gain of clinical attachment, and less disease progression.
Scaling and root planing procedures are technically demanding and time-consuming. Studies show that clinical conditions generally improve following root planing; nonetheless, some sites still do not respond to this therapy. The addition of gingival curettage to root planing in the treatment of generalized chronic periodontitis with shallow suprabony pockets does not signifcantly reduce probing depth or gain clinical attachment beyond that attained by scaling and root planing alone. The following factors may limit the success of treatment by root planing: root anatomy (eg, concavities, furrows etc.), furcations, and deep probing depths.
Several weeks following the completion of root planing and efforts to improve personal plaque control, re-evaluation should be conducted to determine the treatment response. Several factors must be considered at sites that continue to exhibit signs of disease. If the patient’s daily personal plaque control is not adequate to maintain gingival health, then additional instruction and motivation in personal plaque control and/or the use of topical chemotherapeutics (eg, mouthrinses, local drug delivery devices) may be indicated. Anatomical factors that can limit the effectiveness of root instrumentation or limit the patient’s ability to perform personal plaque control (eg, deep probing depths, root concavities, furcations) may require additional therapy including surgery. Host response may also have an effect on treatment outcome and patients with systemic conditions (eg, diabetes, pregnancy, stress, AIDS, immunodefcien-cies, and blood dyscrasias) may not respond well to therapy that is directed solely at controlling local factors. In such patients, it is important that attempts be made to control the contributing systemic factors.
Pharmacological Therapy
Pharmacotherapeutics may have an adjunctive role in the management of periodontitis in certain patients. These ad-junctive therapies are categorized by their route of administration to diseased sites: systemic or local drug delivery.
Systemic Drug Administration
Numerous investigations have assessed the use of systemic antibiotics to halt or slow the progression of periodontitis or to improve periodontal status. The adjunctive use of systemically delivered antibiotics may be indicated in the following situations: patients with multiple sites unresponsive to mechanical debridement, acute infections, medically compromised patients, presence of tissue-invasive organisms and ongoing disease progression. The administration of antibiotics for the treatment of chronic periodontitis should follow accepted pharmacological principles including, when appropriate, iden-tifcation of pathogenic organisms and antibiotic sensitivity testing.
Considerable research efforts have focused on systemic application of host modulating agents such as non-steroidal anti-infammatory drugs (NSAIDS) and subantimicrobial dose doxycycline. Investigators have reported some beneft when these medications are incorporated into treatment proto-cols.Recently [year 2000], the United States Food and Drug Administration (FDA) approved the use of a systemically delivered collagenase inhibitor consisting of a 20-mg capsule of doxycycline hyclate as an adjunct to scaling and root planing for the treatment of periodontitis. Benefts included a statistically signifcant reduction in probing depths, a gain in clinical attachment levels and a reduction in the incidence of disease progression. Overall, the data suggest that use of subantimi-crobial dose doxycycline as an adjunct to scaling and root planing provides defned but limited improvement in periodontal status.
It is important to consider the potential benefts and side effects of systemic pharmacological therapy. Benefts may include the ability to treat patients unresponsive to conventional therapy or an individual with multiple sites experiencing recurrent periodonitits. In contrast, potential risks associated with systemically administered antibiotics include development of resistant bacterial strains,85 emergence of opportunistic infections, and possible allergic sensitization of patients. With regard to the prolonged administration of NSAIDS, harmful effects may include gastrointestinal upset and hemorrhage, renal and hepatic impairment, central nervous system disturbances, inhibition of platelet aggregation, prolonged bleeding time, bone marrow damage, and hypersensitivity reactions. At present, the incidence of negative side effects reported after root planing with or without administration of subantimicrobial dose doxycy-cline has been similar. In general, since patients with chronic periodontitis respond to conventional therapy, it is unnecessary to routinely administer systemic medications such as antibiotics, NSAIDS, or subantimicrobial dosing with doxycycline.
Local Delivery
Controlled delivery of chemotherapeutic agents within peri-odontal pockets can alter the pathogenic fora and improve clinical signs of periodontitis. Local drug delivery systems provide several benefts; the drug can be delivered to the site of disease activity at a bactericidal concentration and it can facilitate prolonged drug delivery. The FDA has approved the use of an ethylene vinyl acetate fber that contains tetracy-cline, a gelatin chip that contains chlorhexidine93 and a minocycline polymer formulation as adjuncts to scaling and root planing. The FDA has also approved doxycycline hyclate in a bioabsorbable polymer gel as a stand-alone therapy for the reduction of probing depths, bleeding upon probing, and gain of clinical attachment.
Local delivery systems have potential limitations and benefts. If used as a monotherapy, problems associated with local delivery can include allergic reaction, possible inability to disrupt bioflms, and failure to remove calculus. The benefts include the ease of application, selectively targeting a limited number of diseased sites that were unresponsive to conventional therapy, and possibly enhanced treatment results at specifc locations. Local delivery modalities have shown benefcial clinical improvements with regard to probing depth reduction and gain in clinical attachment.91-94 Furthermore, there are limited data to suggest that local delivery of antibiotics may also be benefcial in preventing recurrent attachment loss in the absence of maintenance therapy.
Utilization of antibiotics at an individual site will depend on the discretion of the treating therapist after consultation with the patient. The greatest potential of local delivery devices may be to enhance therapy at sites that do not respond to conventional treatment. Ultimately, the results of local drug delivery must be evaluated with regard to the magnitude of improvement that can be attained relative to disease severity. A more complete review of local drug delivery can be found in the American Academy of Periodontology position paper The Role of Controlled Drug Delivery for Periodontitis.
Surgical Therapy
Surgical access to facilitate mechanical instrumentation of the roots has been utilized to treat chronic periodontitis for decades. A surgical approach to the treatment of periodontitis is utilized in an attempt to: 1) provide better access for removal of etiologic factors; 2) reduce deep probing depths; and 3) regenerate or reconstruct lost periodontal tissues.
Clinical trials indicate that both surgical and nonsurgical approaches can be effective in achieving stability of clinical attachment levels. Flap refection is capable, however, of increasing the effcacy of root debridement, especially at sites with deep probing depths or furcations.
Nevertheless, complete calculus removal, even with surgical access, may not always be achieved. The addition of osseous resection during surgical procedures appears to produce greater reduction of probing depth due to gingival reces-sion, particularly in furcations. Regardless of the type of therapy, furcated teeth are problematic since they are still more likely to lose clinical attachment than nonfurcated teeth. While these overall fndings are helpful, the practitioner should base specifc decisions for therapy on fndings for each individual patient.
Regenerative Surgical Therapy
The optimal goal of therapy for individuals who have lost a signifcant amount of periodontal attachment is regeneration of lost tissues. While root debridement in combination with plaque control has demonstrated effcacy in resolving infam-mation and arresting periodontitis, healing typically results in the formation of a long junctional epithelium with remodeling of the alveolus. Similarly, surgical debride-ment alone does not induce signifcant amounts of new connective tissue attachment. However, some bone fll may occur in selected sites.
Clinical trials suggest that obtaining new periodontal attachment or regenerating lost tissues is enhanced by the use of adjunctive surgical technique devices and materials. Chemical agents that modify the root surface, while promoting new attachment, have shown variable results when used in humans. Bone grafting and guided tissue regeneration (GTR) techniques, with or without bone replacement grafts, may be successful when used at selected sites with advanced attachment loss. The use of biologically engineered tissue inductive proteins (eg, growth factors, extracellular matrix proteins, and bone morphogenic proteins) to stimulate periodontal or osseous regeneration has also shown promise. Literature reviews on periodontal regeneration and mucogingival therapy provide additional information regarding these therapies.
Regenerative therapy and other treatment modalities can be affected by several risk factors (eg, diabetes and tobacco use) which can diminish periodontal treatment outcomes. In this regard, cigarette smoking is associated with a high risk for progressive periodontitis and treatment for periodontitis may be less effective in smokers thaon-smokers. These factors are reviewed in more depth in the Academy’s position paper Tobacco Use and the Periodontal Patient. To maximize effective prevention and treatment of periodontitis, patients should be encouraged to stop smoking and to stop using smokeless tobacco.
Occlusal Management
Several studies indicated that excessive occlusal forces do not initiate plaque-induced periodontal disease or connective tissue attachment loss (periodontitis). However, other investigations suggest that tooth mobility may be associated with adverse effects on the periodontium and affect the response to therapy with respect to gaining clinical attachment. With regards to treatment, occlusal therapy may aid in reducing tooth mobility and gaining some bone lost due to traumatic occlusal forces. Occlusal equilibration also may be used to ameliorate a variety of clinical problems related to occlusal instability and restorative needs. Clinicians should use their judgment as to whether or not to perform an occlusal adjustment as a component of periodontal therapy based upon an evaluation of clinical factors related to patient comfort, health and function.
Periodontal Maintenance Procedures
Periodic monitoring of periodontal status and appropriate maintenance procedures should be part of the long-term treatment plan for managing chronic periodontitis. Although experimental studies have demonstrated very successful treatment outcomes when patients are professionally maintained at 2-week intervals, such a program is impractical for most chronic periodontitis patients. Therefore, to maximize successful therapeutic outcomes, patients must maintain effective daily plaque control. It also appears that in-offce periodontal maintenance at 3 to 4 month intervals can be effective in maintaining most patients.4 A more comprehensive review on this subject can be found in the American Academy of Periodontology’s position paper entitled
Every treatment modality in periodontal therapy can be done for osteoporotic patient from scaling and root planing, different periodontal and implant surgery so we can say from the scientific evidences that osteoporosis is not a contraindication for different periodontal surgery (guided tissue regeneration and implant) in spite of the lack for more controlled prolonged studies in that field.
Regarding dental Implant osteoporosis is not likely a risk factor for failure of osseointegrated implants, dental implant placement in edentulous area aid in maintaining the height & density of alveolar bone. osteoporotic bone does not heal differently than more dense bone and the prognosis of osseointegrated implants can be improved in O.P patient who received treatment such as (Fosamax®).
New evidences and precautions for oseoporotic patient who are on certain medication and need a huge periodontal and implant’s surgical intervention Ruggiero and colleagues reported in the August 2004 issue of the Journal of Oral and Maxillofacial Surgery the observation of an osteonecrosis syndrome reminiscent of osteoradionecrosis in certain patients taking bisphosphonate drugs. Patients developed osteoradionecrosis-like lesions soon after extraction of teeth for periodontal, endodontic, or prosthetic reasons; from 2001 to 2003, they saw 63 cases, of which approximately two-thirds of the osteonecrosis cases occurred in the mandible. All patients had been receiving various forms of bisphosphonate therapy (primarily zoledronic acid and pamidronate) for a variety of metastatic cancers. Also in CHICAGO – April 11, 2006 – The patient of a periodontist in private practice in New Orleans, LA, developed osteonecrosis of the jaw (ONJ), a condition that can cause severe, often irreversible and debilitating damage to the jaw, following periodontal surgical therapy. Two years prior to surgery, the patient had started receiving IV.
bisphosphonate therapy, or bone-sparing drugs commonly used in the treatment of osteoporosis and metastatic bone cancer to help decrease associated pain and fractures, following treatment for breast carcinoma.
So it will be wise enough after all these continuous observation to start with a small periodontal surgical intervention for those patient who are osteoporotic on intravenous bisphosphenate therapy or bone spring drugs and see the prognosis and the healing before we go for more advances and complicated surgical interventions).
Conclusion
From the literature we had, it appeared that there is an association of osteporosis with onset and progression of periodontal diseases in humans, also the studies revealed that Low bone mass independently associated with loss of alveolar crest height & tooth loss.
1.The limitations of the studies that investigate the aspects of the relation between osteoporosis and periodontal diseases include: small sample size 2.Limited control of other profounding factors 3.V arying definitions of periodontal diseases & O.P.
Finally there is a demanding issue to better understanding and investigation for the potential mechanisms between periodontal diseases and systemic problems including osteoporosis.
Gingivitis and periodontitis are the 2 major forms of infamma-tory diseases affecting the periodontium. Their primary etiology is bacterial plaque, which can initiate destruction of the gingi-val tissues and periodontal attachment apparatus. Gingivitis is infammation of the gingiva that does not result in clinical attachment loss. Periodontitis is infammation of the gingiva and the adjacent attachment apparatus and is characterized by loss of connective tissue attachment and alveolar bone. Each of these diseases may be subclassifed based upon etiology, clinical presentation, or associated complicating factors.
Gingivitis is a reversible disease. Therapy is aimed primarily at reduction of etiologic factors to reduce or eliminate infam-mation, thereby allowing gingival tissues to heal. Appropriate supportive periodontal maintenance that includes personal and professional care is important in preventing re-initiation of infammation.
Therapeutic approaches for periodontitis fall into 2 major categories: 1) anti-infective treatment, which is designed to halt the progression of periodontal attachment loss by removing etiologic factors; and 2) regenerative therapy, which includes anti-infective treatment and is intended to restore structures destroyed by disease. Essential to both treatment approaches is the inclusion of periodontal maintenance procedures.4
Infammation of the periodontium may result from many causes (eg, bacteria, trauma). However, most forms of gingivitis and periodontitis result from the accumulation of tooth-adherent microorganisms. Prominent risk factors for development of chronic periodontitis include the presence of
specifc subgingival bacteria, tobacco use, diabetes, age, and male gender. Furthermore, there is evidence that other factors can contribute to periodontal disease pathoge-nesis: environmental, genetic, and systemic (eg, diabetes).
This paper primarily reviews the treatment of plaque-induced gingivitis and chronic periodontitis, but there might be some situations where the described therapies will not resolve disease or arrest disease progression. Furthermore, the
treatments discussed should not be deemed inclusive of all possible therapies, or exclusive of methods of care reasonably directed at obtaining good results. The ultimate decision regarding the appropriateness of any specifc procedure must be made by the practitioner in light of the circumstances presented by an individual patient.
Plaque-induced Gingivitis
Therapy for individuals with chronic gingivitis is initially directed at reduction of oral bacteria and associated calcifed and noncalcifed deposits. Patients with chronic gingivitis, but without signifcant calculus, alterations in gingival morphology, or systemic diseases that affect oral health, may respond to a therapeutic regimen consisting of improved personal plaque control alone.16 The periodontal literature documents the short-and long-term effects following self-treatment of gingivitis by personal plaque control. However, while it may be possible under controlled conditions to remove most plaque with a variety of mechanical oral hygiene aids, many patients lack the motivation or skill to attain and maintain a plaque-free state for signifcant periods of time. Clinical trials also indicate that self-administered plaque control programs alone, without periodic professional reinforcement, are inconsistent in providing long-term inhibition of gingivitis.
Many patients with gingivitis have calculus or other associated local factors (eg, defective dental restorations) that interfere with personal oral hygiene and the ability to remove bacterial plaque. An acceptable therapeutic result for these individuals is usually obtained when personal plaque control measures are performed in conjunction with professional removal of plaque, calculus, and other local contributing factors.
Removal of dental calculus is accomplished by scaling and root planing procedures using hand, sonic, or ultrasonic instruments. The therapeutic objective of scaling and root planing is to remove plaque and calculus to reduce subgingival bacteria below a threshold level capable of initiating clinical infammation.The success of instrumentation is determined by evaluating the periodontal tissues following treatment and during the maintenance phase of therapy.
The use of topical antibacterial agents to help reduce bacterial plaque may be benefcial for the prevention and treatment of gingivitis in some patients.
A number of these agents in oral rinses and dentifrices have been tested in clinical trials.28 However, to be accepted by the American Dental Association (ADA) Council on Dental Therapeutics as an effective agent for the treatment of gingivitis, a product must reduce plaque and demonstrate effective reduction of gingival infammation over a period of at least 6 months. The agent must also be safe and not induce adverse side effects.
Three medicaments have been given the ADA Seal of Acceptance for the control of gingivitis. The active ingredients of one product are thymol, menthol, eucalyptol, and methyl salicylate. Active ingredients in the other two are chlorhexidine digluconate and triclosan.29 If properly used, the addition of a topical anti-plaque agent to a gingivitis treatment regimen for patients with defcient plaque control will likely result in reduction of gingivitis.30 However, experimental evidence indicates that penetration of topically applied agents into the gingival crevice is minimal.31 Therefore, these agents are useful for the control of supragingival, but not subgingival plaque. Among individuals who do not perform excellent oral hygiene, supra-gingival irrigation with and without medicaments is capable of reducing gingival infammation beyond that normally achieved by toothbrushing alone. This effect is likely due to the fushing out of subgingival bacteria.
If gingivitis remains following the removal of plaque and other contributing local factors, thorough evaluation should be undertaken of systemic factors (eg, diabetes, pregnancy, etc.). If such conditions are present, gingival health may be attained once the systemic problem is resolved and plaque control is maintained.
Acute Periodontal Diseases
Necrotizing ulcerative gingivitis (NUG) is associated with specifc bacterial accumulations occurring in individuals with lowered host resistance. NUG usually responds rapidly to the reduction of oral bacteria by a combination of personal plaque control and professional debridement. If lymphadenopathy or fever accompanies oral symptoms, administration of systemic antibiotics may be indicated. The use of chemotherapeutic rinses by the patient may be benefcial during the initial treatment stages. After the acute infammation of the NUG lesion is resolved, additional intervention may be indicated to prevent disease recurrence or to correct resultant soft tissue deformities. Necrotizing ulcerative periodontitis (NUP) manifests as rapid necrosis and destruction of the gingiva and periodontal attachment apparatus. It may initiate gingival bleeding and pain, and it usually represents an extension of necrotizing ulcerative gingivitis in individuals with lowered host resistance. NUP has been reported among both HIV-positive and negative individuals, but its true prevalence is unknown. Management of
NUP involves debridement which may be combined with irrigation with antiseptics (eg, povidone iodine), antimicrobial mouth rinses (eg, chlorhexidine), and administration of systemic antibiotics. There is also evidence that HIV-immune defciency may be associated with severe loss of periodontal attachment that does not necessarily present clinically as an ulcerative lesion.40 Although not an acute disease, linear gin-gival erythema (LGE) occurs in some HIV-infected individuals and does not appear to respond to conventional scaling, root planing, and plaque control. Antibiotic therapy should be used in HIV-positive patients with caution due to the possibility of inducing opportunistic infections.
The oral manifestations of a primary herpes simplex virus type I infection often include gingivitis. By the time gingivitis is present, patients are usually febrile, in pain, and have lymph-adenopathy. Diagnosis is generally made from the clinical appearance of the oral soft tissues. Although not performed routinely, a viral culture may provide defnitive identifcation of the infective agent. In otherwise healthy patients, treatment for herpetic gingivitis consists of palliative therapy. The infection is self-limiting and usually resolves in 7 to 10 days. Systemic antiviral therapy with acyclovir is appropriate for immunocompromised patients with herpetic gingivitis.
Gingival Enlargement
Chronic gingival infammation may result in gingival enlargement. This overgrowth of gingiva may be exaggerated in patients with genetic or drug-related systemic factors (eg, anticonvul-sants, cyclosporine and calcium channel blocking drugs). Among individuals taking phenytoin, gingival overgrowth may be minimized with appropriate personal oral hygiene and professional maintenance. However, root debridement in patients with gingival overgrowth often does not return the periodontium to normal contour. The residual overgrowth may not only complicate the patient’s ability to adequately clean the dentition, but it may also present esthetic and functional problems.
For patients with gingival overgrowth, the modifcation of tissue topography by surgical recontouring may be undertaken to create a maintainable oral environment. Postoperative management following tissue resection is important. The benefts of surgical reduction may be lost due to rapid proliferation of the tissues during the post-therapy phase. Recurrence is common in many patients with drug-induced gingival overgrowth. For these patients, consultation with the patient’s physician is advisable to determine if it is possible to use an alternative drug therapy that does not induce gingival overgrowth. If not, then repeated surgical and/or non-surgical intervention may be required.
Chronic Periodontitis
Appropriate therapy for patients with periodontitis varies considerably with the extent and pattern of attachment loss, local anatomical variations, type of periodontal disease, and therapeutic objectives. Periodontitis destroys the attachment apparatus of teeth resulting in periodontal pocket formation and alteration of normal osseous anatomy. The primary objectives of therapy for patients with chronic periodontitis are to halt disease progression and to resolve infammation. Therapy at a diseased site is aimed at reducing etiologic factors below the threshold capable of producing breakdown, thereby allowing repair of the affected region. Regeneration of lost peri-odontal structures can be enhanced by specifc procedures. However, many variables responsible for complete regeneration of the periodontium are unknown and research is ongoing in this area.
Scaling and Root Planing
The benefcial effects of scaling and root planing combined with personal plaque control in the treatment of chronic periodontitis have been validated. These include reduction of clinical infammation, microbial shifts to a less pathogenic subgingival fora, decreased probing depth, gain of clinical attachment, and less disease progression.
Scaling and root planing procedures are technically demanding and time-consuming. Studies show that clinical conditions generally improve following root planing; nonetheless, some sites still do not respond to this therapy. The addition of gingival curettage to root planing in the treatment of generalized chronic periodontitis with shallow suprabony pockets does not signifcantly reduce probing depth or gain clinical attachment beyond that attained by scaling and root planing alone. The following factors may limit the success of treatment by root planing: root anatomy (eg, concavities, furrows etc.), furcations, and deep probing depths.
Several weeks following the completion of root planing and efforts to improve personal plaque control, re-evaluation should be conducted to determine the treatment response. Several factors must be considered at sites that continue to exhibit signs of disease. If the patient’s daily personal plaque control is not adequate to maintain gingival health, then additional instruction and motivation in personal plaque control and/or the use of topical chemotherapeutics (eg, mouthrinses, local drug delivery devices) may be indicated. Anatomical factors that can limit the effectiveness of root instrumentation or limit the patient’s ability to perform personal plaque control (eg, deep probing depths, root concavities, furcations) may require additional therapy including surgery. Host response may also have an effect on treatment outcome and patients with systemic conditions (eg, diabetes, pregnancy, stress, AIDS, immunodefcien-cies, and blood dyscrasias) may not respond well to therapy that is directed solely at controlling local factors. In such patients, it is important that attempts be made to control the contributing systemic factors.
Pharmacological Therapy
Pharmacotherapeutics may have an adjunctive role in the management of periodontitis in certain patients. These adjunctive therapies are categorized by their route of administration to diseased sites: systemic or local drug delivery.
Systemic Drug Administration
Numerous investigations have assessed the use of systemic antibiotics to halt or slow the progression of periodontitis or to improve periodontal status. The adjunctive use of systemically delivered antibiotics may be indicated in the following situations: patients with multiple sites unresponsive to mechanical debridement, acute infections, medically compromised patients, presence of tissue-invasive organisms and ongoing disease progression. The administration of antibiotics for the treatment of chronic periodontitis should follow accepted pharmacological principles including, when appropriate, identifcation of pathogenic organisms and antibiotic sensitivity testing.
Considerable research efforts have focused on systemic application of host modulating agents such as non-steroidal anti-infammatory drugs (NSAIDS) and subantimicrobial dose doxycycline. Investigators have reported some beneft when these medications are incorporated into treatment proto-cols.Recently [year 2000], the United States Food and Drug Administration (FDA) approved the use of a systemically delivered collagenase inhibitor consisting of a 20-mg capsule of doxycycline hyclate as an adjunct to scaling and root planing for the treatment of periodontitis. Benefts included a statistically signifcant reduction in probing depths, a gain in clinical attachment levels and a reduction in the incidence of disease progression. Overall, the data suggest that use of subantimi-crobial dose doxycycline as an adjunct to scaling and root planing provides defned but limited improvement in periodontal status.
It is important to consider the potential benefts and side effects of systemic pharmacological therapy. Benefts may include the ability to treat patients unresponsive to conventional therapy or an individual with multiple sites experiencing recurrent periodonitits. In contrast, potential risks associated with systemically administered antibiotics include development of resistant bacterial strains,85 emergence of opportunistic infections, and possible allergic sensitization of patients. With regard to the prolonged administration of NSAIDS, harmful effects may include gastrointestinal upset and hemorrhage, renal and hepatic impairment, central nervous system disturbances, inhibition of platelet aggregation, prolonged bleeding time, bone marrow damage, and hypersensitivity reactions. At present, the incidence of negative side effects reported after root planing with or without administration of subantimicrobial dose doxycy-cline has been similar. In general, since patients with chronic periodontitis respond to conventional therapy, it is unnecessary to routinely administer systemic medications such as antibiotics, NSAIDS, or subantimicrobial dosing with doxycycline.
Local Delivery
Controlled delivery of chemotherapeutic agents within peri-odontal pockets can alter the pathogenic fora and improve clinical signs of periodontitis. Local drug delivery systems provide several benefts; the drug can be delivered to the site of disease activity at a bactericidal concentration and it can facilitate prolonged drug delivery. The FDA has approved the use of an ethylene vinyl acetate fber that contains tetracy-cline, a gelatin chip that contains chlorhexidine and a minocycline polymer formulation as adjuncts to scaling and root planing. The FDA has also approved doxycycline hyclate in a bioabsorbable polymer gel as a stand-alone therapy for the reduction of probing depths, bleeding upon probing, and gain of clinical attachment.
Local delivery systems have potential limitations and benefts. If used as a monotherapy, problems associated with local delivery can include allergic reaction, possible inability to disrupt bioflms, and failure to remove calculus. The benefts include the ease of application, selectively targeting a limited number of diseased sites that were unresponsive to conventional therapy, and possibly enhanced treatment results at specifc locations. Local delivery modalities have shown benefcial clinical improvements with regard to probing depth reduction and gain in clinical attachment.91-94 Furthermore, there are limited data to suggest that local delivery of antibiotics may also be benefcial in preventing recurrent attachment loss in the absence of maintenance therapy.
Utilization of antibiotics at an individual site will depend on the discretion of the treating therapist after consultation with the patient. The greatest potential of local delivery devices may be to enhance therapy at sites that do not respond to conventional treatment. Ultimately, the results of local drug delivery must be evaluated with regard to the magnitude of improvement that can be attained relative to disease severity. A more complete review of local drug delivery can be found in the American Academy of Periodontology position paper The Role of Controlled Drug Delivery for Periodontitis.
Surgical Therapy
Surgical access to facilitate mechanical instrumentation of the roots has been utilized to treat chronic periodontitis for decades. A surgical approach to the treatment of periodontitis is utilized in an attempt to: 1) provide better access for removal of etiologic factors; 2) reduce deep probing depths; and 3) regenerate or reconstruct lost periodontal tissues.
Clinical trials indicate that both surgical and nonsurgical approaches can be effective in achieving stability of clinical attachment levels. Flap refection is capable, however, of increasing the effcacy of root debridement, especially at sites with deep probing depths or furcations.
Nevertheless, complete calculus removal, even with surgical access, may not always be achieved. The addition of osseous resection during surgical procedures appears to produce greater reduction of probing depth due to gingival reces-sion, particularly in furcations. Regardless of the type of therapy, furcated teeth are problematic since they are still more likely to lose clinical attachment than nonfurcated teeth. While these overall fndings are helpful, the practitioner should base specifc decisions for therapy on fndings for each individual patient.
Regenerative Surgical Therapy
The optimal goal of therapy for individuals who have lost a signifcant amount of periodontal attachment is regeneration of lost tissues. While root debridement in combination with plaque control has demonstrated effcacy in resolving infam-mation and arresting periodontitis, healing typically results in the formation of a long junctional epithelium with remodeling of the alveolus. Similarly, surgical debride-ment alone does not induce signifcant amounts of new connective tissue attachment. However, some bone fll may occur in selected sites.
Clinical trials suggest that obtaining new periodontal attachment or regenerating lost tissues is enhanced by the use of adjunctive surgical technique devices and materials. Chemical agents that modify the root surface, while promoting new attachment, have shown variable results when used in humans. Bone grafting and guided tissue regeneration (GTR) techniques, with or without bone replacement grafts, may be successful when used at selected sites with advanced attachment loss. The use of biologically engineered tissue inductive proteins (eg, growth factors, extracellular matrix proteins, and bone morphogenic proteins) to stimulate periodontal or osseous regeneration has also shown promise. Literature reviews on periodontal regeneration and mucogingival therapy provide additional information regarding these therapies.
Regenerative therapy and other treatment modalities can be affected by several risk factors (eg, diabetes and tobacco use) which can diminish periodontal treatment outcomes. In this regard, cigarette smoking is associated with a high risk for progressive periodontitis and treatment for periodontitis may be less effective in smokers thaon-smokers. These factors are reviewed in more depth in the Academy’s position paper Tobacco Use and the Periodontal Patient. To maximize effective prevention and treatment of periodontitis, patients should be encouraged to stop smoking and to stop using smokeless tobacco.
Occlusal Management
Several studies indicated that excessive occlusal forces do not initiate plaque-induced periodontal disease or connective tissue attachment loss (periodontitis). However, other investigations suggest that tooth mobility may be associated with adverse effects on the periodontium and affect the response to therapy with respect to gaining clinical attachment. With regards to treatment, occlusal therapy may aid in reducing tooth mobility and gaining some bone lost due to traumatic occlusal forces. Occlusal equilibration also may be used to ameliorate a variety of clinical problems related to occlusal instability and restorative needs. Clinicians should use their judgment as to whether or not to perform an occlusal adjustment as a component of periodontal therapy based upon an evaluation of clinical factors related to patient comfort, health and function.
Immediate denture
An immediate denture is a complete denture or partial denture inserted on the same day, immediately following the removal of natural teeth.
There are several advantages of an immediate denture. The most important factor is that you will never need to appear in public without teeth. It is also easier to duplicate the shape, color and arrangement of your natural teeth while some are still present in your mouth. When an immediate denture is inserted at the time of extraction, it will act as a Band-Aid to protect the tissues and reduce bleeding. An immediate denture will allow you to establish your speech patterns early. You will not have to learn to speak without a denture in place and then later relearn to speak with a new denture. An immediate denture will also allow you to chew better than without any teeth and minimize facial distortion that may occur when teeth are removed.
The biggest disadvantage is the increased cost. Another disadvantage is that you cannot always see how the denture will look before the teeth are extracted and the immediate denture is inserted. Also, initially, an immediate denture does not always fit as accurately as a conventional denture, which is made after the tissues have healed for six to eight weeks following extractions, and without wearing a denture.
An immediate denture is initially more expensive than a conventional denture because additional time is needed for construction. A surgical stent (a guide for recontouring tissues after extraction) is ofteecessary and more follow-up visits are needed for adjustments and re-fitting. A soft temporary reline material will be utilized for re-fitting your denture when it becomes loose during the healing process. After the soft tissues have healed and shrinkage of the underlying bone has occurred (about six months following extractions), the immediate denture must be finalized by a permanent reline or new denture. At this time, you will be charged for either a reline or a new denture, depending on your choice.
Your doctor will discuss with you the pros and cons of a permanent reline versus making a new denture, to help you make a decision. A major advantage to making a new denture is that the immediate denture can be a spare denture if the new denture breaks, is misplaced, or has to be repaired or relined in our laboratory. If the immediate denture is relined, it will usually need to be left overnight while it is permanently relined in the laboratory.
Not everyone is a candidate for an immediate denture. Some people may be advised against this treatment, due to general health conditions, or because of specific oral problems.
Four to five visits may be necessary for the fabrication phase of an immediate denture, plus any preliminary surgery. For patients requiring a complete immediate denture, the back teeth are often extracted six to eight weeks prior to the fabrication phase. This allows the extraction sites to heal and a better-fitting immediate complete denture to be fabricated.
The fabrication phase consists of impressions, bite records, tooth selection and try-in of the back teeth. On the day of delivery, you will be seen in oral surgery for extraction of the appropriate teeth, followed immediately by the insertion of the immediate denture.
Reevaluation
Multiple clinical studies have shown that non-surgical scaling and root planing is usually successful if the periodontal pockets are shallower than 4–5 mm (See articles by Stambaugh RV, Int J Periodontics Rest Dent, 1981 or Waerhaug J, J Periodontol, 1978). It is necessary for the dentist or hygienist to perform a reevaluation 4–6 weeks after the initial scaling and root planing, to determine if the patient’s oral hygiene has improved and inflammation has regressed. Probing should be avoided at 4–6 weeks, and an analysis by gingival index should determine the presence or absence of inflammation. Three monthly reevaluation of periodontal therapy should involve periodontal charting as a better indication of the success of treatment, and to see if other courses of treatment can be identified. Pocket depths of greater than 5-6mm which remain after initial therapy, with bleeding upon probing, indicate continued active disease and will very likely lead to further bone loss over time. This is especially true in molar tooth sites where furcations (areas between the roots) have been exposed.
Surgery
If non-surgical therapy is found to have been unsuccessful in managing signs of disease activity, periodontal surgery may be needed to stop progressive bone loss and regenerate lost bone where possible. There are many surgical approaches used in treatment of advanced periodontitis, including open flap debridement, osseous surgery, as well as guided tissue regeneration and bone grafting. The goal of periodontal surgery is access for definitive calculus removal and surgical management of bony irregularities which have resulted from the disease process to reduce pockets as much as possible. Long-term studies have shown that in moderate to advanced periodontitis, surgically treated cases often have less further breakdown over time and when coupled with a regular post-treatment maintenance regimen are successful iearly halting tooth loss iearly 85% of patients.
Maintenance
Once successful periodontal treatment has been completed, with or without surgery, an ongoing regimen of “periodontal maintenance” is required. This involves regular checkups and detailed cleanings every three months to prevent re-population of periodontitis-causing microorganism, and to closely monitor affected teeth so that early treatment can be rendered if disease recurs. Usually periodontal disease exists due to poor plaque control, therefore if the brushing techniques are not modified, a periodontal recurrence is probable.
Alternative treatments
Periodontitis has an inescapable relationship with subgingival calculus (tartar). The first step in any procedure is to eliminate calculus under the gum line, as it houses destructive anaerobic microorganisms that consume bone, gum and cementum (connective tissue) for food.
Most alternative “at-home” gum disease treatments involve injecting anti-microbial solutions, such as hydrogen peroxide, into periodontal pockets via slender applicators or oral irrigators. This process disrupts anaerobic microorganism colonies and is effective at reducing infections and inflammation when used daily. A number of potions and elixirs that are functionally equivalent to hydrogen peroxide are commercially available but at substantially higher cost. However, such treatments do not address calculus formations, and so are short-lived, as anaerobic microorganism colonies quickly regenerate in and around calculus.
Additionally, Periodontitis can be treated in a noninvasive manner by means of Periostat, an FDA-approved, orally-administered drug that has been shown to reduce bone loss. Its mechanism of action in part involves inhibition of Matrix metalloproteinases (such as collagenase), which degrade the extracellular matrix under inflammatory conditions. This ultimately can lead to reduction of aveolar bone-loss in patients with periodontal disease (as well as patients without periodontitis).
Prognosis
Dentists and dental hygienists measure periodontal disease using a device called a periodontal probe. This is a thin “measuring stick” that is gently placed into the space between the gums and the teeth, and slipped below the gum-line. If the probe can slip more than 3 millimeters below the gum-line, the patient is said to have a gingival pocket if no migration of the epithelial attachment has occurred or a periodontal pocket if apical migration has occurred. This is somewhat of a misnomer, as any depth is in essence a pocket, which in turn is defined by its depth, i.e., a 2 mm pocket or a 6 mm pocket. However, it is generally accepted that pockets are self-cleansable (at home, by the patient, with a toothbrush) if they are 3 mm or less in depth. This is important because if there is a pocket which is deeper than 3 mm around the tooth, at-home care will not be sufficient to cleanse the pocket, and professional care should be sought. When the pocket depths reach 6 and 7 mm in depth, the hand instruments and cavitrons used by the dental professionals may not reach deeply enough into the pocket to clean out the microbic plaque that cause gingival inflammation. In such a situation the bone or the gums around that tooth should be surgically altered or it will always have inflammation which will likely result in more bone loss around that tooth. An additional way to stop the inflammation would be for the patient to receive subgingival antibiotics (such as minocycline) or undergo some form of gingival surgery to access the depths of the pockets and perhaps even change the pocket depths so that they become 3 mm or less in depth and can once again be properly cleaned by the patient at home with his or her toothbrush.
If a patient has 7 mm or deeper pockets around their teeth, then they would likely risk eventual tooth loss over the years. If this periodontal condition is not identified and the patient remains unaware of the progressive nature of the disease then, years later, they may be surprised that some teeth will gradually become loose and may need to be extracted, sometimes due to a severe infection or even pain.
According to the Sri Lankan tea labourer study, in the absence of any oral hygiene activity, approximately 10% will suffer from severe periodontal disease with rapid loss of attachment (>2 mm/year). 80% will suffer from moderate loss (1–2 mm/year) and the remaining 10% will not suffer any loss.
Periodontitis is very common, and is widely regarded as the second most common disease worldwide, after dental decay, and in the United States has a prevalence of 30–50% of the population, but only about 10% have severe forms.
Like other conditions that are intimately related to access to hygiene and basic medical monitoring and care, periodontitis tends to be more common in economically disadvantaged populations or regions. Its occurrence decreases with higher standard of living. In Israeli population, individuals of Yemenite, North-African, South Asian, or Mediterranean origin have higher prevalence of periodontal disease than individuals from European descent.
There are 2 types of Dental Splints:
Fixed Dental Splints
Removable Dental Splints
Immediate Dentures
High-quality Immediate Dentures
Dr. Bruce Goldman of the Dental Design Center has over 25 years of experience dealing in custom dentures – including immediate dentures designed to go in place immediately following tooth extraction.
With our own lab right on the premises, we can provide you with immediate service so that you never have to go without a natural smile in public. We can take a cast of your mouth prior to tooth extraction, so that you have a new set of teeth waiting for you from the start.
More information on Immediate Dentures is included below, while information on our other services is contained elsewhere on our website.
To schedule an appointment for a consultation call 561-967-8666 or to schedule an appointment online.
“Dr Goldman has fixed a nightmare. He made me a full set of dentures, and they look and feel great!!! This is a great office.” – R.Z.
“My original upper plate never did adhere. I had it 40 years when Dr. Goldman made me a new one. I was amazed at the perfect fit and how it actually adhered. The fit was so perfect, I never needed an adjustment. Excellent work!” – A.R.
An immediate denture is what it says. It is placed immediately after the teeth have been extracted. It cannot and will not function or feel like a denture placed over healed oral tissue. It does provide a certain amount of function and esthetics for the patient.
Approximately 6 months after receiving your immediate dentures, the dentures will have to be rebased, relined or a new denture will have to be made.
As a note, there is no such thing as a “permanent denture” as your mouth will continue to change shape over time. Well-made dentures can last you 5 to 10 years, but they may need to be adjusted or re-made depending on the healing process.
Perhaps the most important advantage of immediate dentures is that you never need to appear in public without any teeth. Other advantages include:
1. The form, size and arrangement of your natural teeth can more closely be duplicated when some teeth remain in your mouth.
2. When immediate dentures are inserted, they act as a bandage and help to reduce bleeding.
3. Immediate dentures protect the tissues at the sensitive extraction sites from irritation which might result from the tongue and food. This can mean less discomfort for you than with conventional denture construction.
4. Immediate dentures can enable you to establish your speech patterns more easily. You do not have to learn to speak without teeth and then re-learn once dentures are made.
5. With immediate dentures you can chew better than you could without teeth during the normal waiting period for conventional dentures.
6. If dentures do not replace the natural teeth within a short time, the cheeks tend to fall in.
7. If you remain without teeth for some time, you may develop oral habits that will interfere with your ability to learn how to use dentures properly.
Like any other procedure, the insertion of immediate dentures does have limitations, of which you should be aware. There are some people for whom immediate dentures are not advisable because of their general health or specific oral problems.
1. More office visits are required during the first few months, to watch for changes in the gums and in the mouth function. Also the original good fit and occlusion of the denture will be lost as healing takes place. This is normal.
2. Because of changes in the tissues after removal of the teeth, immediate dentures usually need to be re-fitted by a dentist within several (usually six) months. This involves additional expense. In some cases new dentures must be made.
3. In the areas where the last remaining teeth will be removed, immediate dentures will not always fit quite as accurately as conventional dentures made at a later date, after gums have healed.
4. Because some of your teeth are still in place, you cannot see how the dentures will look in your mouth until after the natural teeth have been removed.
5. Immediate dentures are usually more expensive because of the additional time required for their construction.
1. For the first 24 hours, DO NOT REMOVE the denture. The denture will control the bleeding and actually cause minimal discomfort.
2. Some swelling is to be expected after extractions. To keep the swelling to a minimum, and to help stop the bleeding, hold an ice pack to the areas of the jaw where teeth have been extracted. 15 minutes on, and 15 minutes off.
3. For discomfort take Tylenol, or the medication the doctor may prescribe.
4. Remove the denture 4 or 5 times a day after the first day, and rinse the mouth with warm salt water. Do this for the first week. You may sleep with the denture.
5. If sutures were placed, you will return in 1 week to remove them.
6. You should eat soft foods for the 1st week, then gradually determine what you can handle.What you once ate with ease, may now be very difficult.
7. For the first 1-2 weeks, up to 1000 mg of vitamin C a day will promote and aid healing of the mouth. Refraining from alcohol consumption and cigarette smoking would also be beneficial.
8. You WILL find that a denture adhesive will be necessary to help hold the denture in place.
9. If you develop any sore spots, call the office so that we may take care of it as soon as p
10. ractical.
