Periodontal Diseases

Periodontal diseases (also called periodontitis) are those diseases that affect one or more of

the periodontal tissues:

1. alveolar bone

2. periodontal ligament

3. cementum

4. gingiva

While many different diseases affect the tooth-supporting structures, plaque-induced inflammatory lesions

make up the vast majority of periodontal diseases[1] and have traditionally been divided into two

categories:[2]

1. gingivitis or

2. periodontitis .

Periodontitis is an infection of the periodontium—causing inflammation of the periodontal ligament,

gingiva, cementum, and alveolar bone. It usually presents as a worsening of gingivitis. Symptoms are rare

except with HIV or when abscesses develop, in which case pain and swelling are common. Diagnosis is

based on inspection, periodontal probing, and x-rays. Treatment involves dental cleaning that extends

under the gums and a vigorous home hygiene program. Advanced cases may require antibiotics and

surgery.

Etiology

Periodontitis usually develops when gingivitis, usually with abundant plaque and calculus beneath the

gingival margin, has not been adequately treated. In periodontitis, the deep pockets can harbor anaerobic

organisms that do more damage than those usually present in simple gingivitis. The gingiva progressively

loses its attachment to the teeth, periodontal pockets deepen, and bone loss begins. With progressive

bone loss, teeth may loosen, and gingiva recedes. Tooth migration is common in later stages.

Aggressive periodontitis describes a type of periodontal disease and includes two of the seven

classifications of periodontitis:[1]

1. Localized aggressive periodontitis (LAP)

2. Generalized aggressive periodontitis (GAP)

Aggressive periodontitis is much less common than chronic periodontitis and generally affects younger

patients than does the chronic form.[2][3]

The localized and generalized forms are not merely different in extent; they differ in etiology and

pathogenesis.

Characteristics

In contrast to chronic periodontitis, primary features that are common to both LAP and GAP are as

follows:[4]

except for the presence of periodontal disease, patients are otherwise healthy

rapid loss of attachment and bone destruction

familial aggregation

Moreover, aggressive periodontitis often presents with the following secondary features:[4]

Amounts of microbial deposits are inconsistent with the severity of the periodontal tissue destruction

elevated proportions of Aggregatibacter actinomycetemcomitans , and in some cases,

of Porphyromonas gingivalis as well

phagocyte abnormalities

hyperresponsive macrophage phenotype, including elevated levels of prostaglandin E2 (PGE2)

and interleukin 1β

progression of pathogenesis may be self limiting

[edit]Localized vs. generalized forms of aggressive periodontitis

The 1999 Consensus Report published by the American Academy of Periodontology permitted the

subdivision of aggressive periodontal disease into localized and generalized forms based on enough

individually specific features, as follows:[4]

Localized aggressive periodontitis

circumpubertal onset

robust serum antibody response to infective agents: the dominant serotype antibody is IgG2 [5]

localized first molar/incisor presentation

Generalized aggressive periodontitis

usually affects patients under 30 years of age

poor serum antibody response to infective agents

pronounced episodic nature of periodontal destruction

generalized presentation affecting at least 3 permanent teeth other than first molars and incisors

Severity of periodontal tissue destruction is subclassified in the same fashion as is chronic periodontitis.

[edit]Treatment

Treatment generally involves mechanical therapy (non-surgical or surgical debridement) in conjunction

with antibiotics. Several studies suggest that these types of cases respond best to a combination of

surgical debridement and antibiotics. Regenerative therapy with bone grafting procedures are often

selected in these cases due to the favorable morphology of the bony defects which result from the

disease.

Aggressive periodontitis: Several more rapidly progressive subtypes of chronic periodontitis exist,

collectively known as aggressive periodontitis. Aggressive periodontitis may develop as early as

childhood, sometimes before age 3 yr. Patients may have severe bone loss, even tooth loss, by age 20.

Neutrophil function may be defective in aggressive periodontitis; its clinical significance is unknown.

In one type of aggressive periodontitis that occurs in healthy adolescents (formerly called localized

juvenile periodontitis), patients often have significant colonization ofActinobacillus

actinomycetemcomitans. Typically, the signs of inflammation are minor. The disease is detected by

periodontal probing or x-rays, which show localized, deep (vertical) bone loss, commonly limited to the 1st

molars and incisors. Bone loss progresses faster than in adult periodontitis, often at a rate of 3 to

4 μm/day.

An uncommon type of aggressive periodontitis (formerly called prepubertal periodontitis) affects

deciduous teeth, usually shortly after eruption. Generalized acute proliferative gingivitis and rapid alveolar

bone destruction are its hallmarks. Patients also have frequent bouts of otitis media and are usually

diagnosed by age 4 yr. In some patients, the disease resolves before the permanent teeth erupt.

Treatment regimens are under study.

The prototypical aggressive periodontitis (formerly called rapidly progressive periodontitis) occurs in

patients aged 20 to 35 yr. It is often associated with A. actinomycetemcomitans,Porphyromonas

gingivalis, Eikenella corrodens, and many gram-negative bacilli, but cause and effect are not clear. Some

cases result from undiagnosed localized juvenile periodontitis or prepubertal periodontitis, but others

appear independently.

HIV-associated periodontitis is a particularly virulent, rapidly progressing disease. Clinically, it resembles

acute necrotizing ulcerative gingivitis (see Common Dental Disorders: Acute Necrotizing Ulcerative

Gingivitis (ANUG)) combined with rapidly progressive periodontitis. Patients may lose 9 to 12 mm of

attachment in as little as 6 mo.

Symptoms and Signs

Pain is usually absent unless an acute infection forms in one or more periodontal pockets or if HIV-

associated periodontitis is present. Impaction of food in the pockets can cause pain at meals. Abundant

plaque along with redness, swelling, and exudate are characteristic. Gums may be tender and bleed

easily, and breath may be foul.

Diagnosis Clinical evaluation

Sometimes dental x-rays

Inspection of the teeth and gingiva combined with probing of the pockets and measurement of their depth

are usually sufficient for diagnosis. Pockets deeper than 4 mm indicate periodontitis. Dental x-rays reveal

alveolar bone loss adjacent to the periodontal pockets.

Treatment Scaling and root planing

Sometimes oral antibiotics, antibiotic packs, or both

Surgery or extraction

For all forms of periodontitis, the first phase of treatment consists of thorough scaling and root planing (ie,

removal of diseased or toxin-affected cementum and dentin followed by smoothing of the root) to remove

plaque and calculus deposits. Thorough home oral hygiene is necessary. The patient is reevaluated after

3 wk. If pockets are no deeper than 4 mm at this point, the only treatment needed is regular cleanings.

If deeper pockets persist, systemic antibiotics can be used. A common regimen isamoxicillin

500 mg po qid for 10 days. In addition, a gel containing doxycycline

or microspheres of minocycline

can be placed into isolated recalcitrant pockets. These are resorbed in 2 wk.

Another approach is to surgically eliminate the pocket and recontour the bone so that the patient can

clean the depth of the sulcus (pocket reduction/elimination surgery). In selected situations, regenerative

surgery and bone grafting are done to encourage alveolar bone growth. Splinting of loose teeth and

selective reshaping of tooth surfaces to eliminate traumatic occlusion may be necessary. Extractions are

often necessary in advanced disease. Contributing systemic factors should be controlled before initiating

periodontal therapy.

Ninety percent of patients with HIV-associated periodontitis respond to irrigation of the sulcus with

povidone-iodine (which the dentist applies with a syringe), regular use of chlorhexidine mouth rinses, and

systemic antibiotics, usually metronidazole

250 mg po tid for 14 days.

Localized juvenile periodontitis requires periodontal surgery plus oral antibiotics (eg,amoxicillin

500 mg qid or metronidazole

250 mg tid for 14 days).

Localized

Localized Aggressive PeriodontitisClinical appearance: extreme bone loss around 1st molars and incisors; loose, drifting teeth; no plaque or inflammation; good OH

Etiology: Aa, large percentage of neutrophils with slow chemotactic response

Microbiology: AaHistopathology: neutrophils with slow chemotactic responseRadiographic features: extreme bone loss around 1st molars and incisors

Diagnosis: radiographs and probing; often younger than 20Treatment/Prognosis: mechanical debridement, systemic antibiotics (tetracycline), periodontal surgery

Generalized Aggressive PeriodontitisClinical appearance: affects most or all the teeth with 1st molars and incisors being the most severely involved; inflammation IS present with heavy plaque and calculus

Etiology: neutrophil chemotactic disorder

Microbiology: P. gingivalis, Eikenella corrodens, A. a

Diagnosis: generally younger than 20Treatment/Prognosis: improved OH, scaling and root planing, antibiotic therapy, periodontal surgery

Aggressive PeriodontitisClinical Appearance: severe inflammation, rapid bone loss, and early tooth loss

Etiology: white blood cell defects

Radiographic features: advanced bone loss

Treatment: responds poorly to conventional treatment such as scaling and root planing; antibiotics may help but it usually slows rather than stops diseasePrognosis: Poor; individuals with prepubertal gingivitis frequently become edentulous at an early ag

Chronic Periodontitis

Clinical Appearance: pockets

Etiology: plaque and calculus, disease activity/patient resistance

Microbiology: multibacterial; primary = Porphyromonas gingivalis

Histopathology: attachment loss, bone resorption

Radiographic features: horizontal bone loss

Diagnosis: probing depth

Treatment and prognosis: remove local etiologic factors, education, control of associated factors

[align=center] [/align]

Chronic periodontitis is a common disease of the oral cavity consisting of chronic inflammation of

the periodontal tissues that is caused by accumulation of profuse amounts of dental plaque.

Chronic periodontitis

Classification and external resources

ICD-10 K05.3

ICD-9 523.4

DiseasesDB ?

MeSH C07.465.714.533.324

Contents

[hide]

1 Diagnosis

2 Signs and symptoms

3 Pathology

4 Microbiology

5 Treatment

6 Adjunctive systemic antibiotic treatment

7 Locally delivered adjunctive antimicrobial treatment

8 Modulating the host response

9 Current controversies in chronic periodontal disease management

10 Cost/benefit analysis of treatment

11 Tentative links to other conditions

12 References

13 External links

[edit]Diagnosis

It is one of the seven destructive periodontal diseases as listed in the 1999 classification.[1]

[edit]Signs and symptoms

In the early stages, chronic periodontitis has few symptoms and in many individuals the disease has

progressed significantly before they seek treatment. Symptoms may include the following:

Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food (e.g.

apples) (though this may occur even in gingivitis, where there is no attachment loss)

Gum swelling that recurs

Halitosis , or bad breath, and a persistent metallic taste in the mouth

Gingival recession , resulting in apparent lengthening of teeth. (This may also be caused by heavy

handed brushing or with a stiff tooth brush.)

Deep pockets between the teeth and the gums (pockets are sites where the attachment has been

gradually destroyed by collagen-destroying enzymes, known as collagenases)

Loose teeth, in the later stages (though this may occur for other reasons as well)

Gingival inflammation and bone destruction are often painless. Patients sometimes assume that painless

bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing chronic

periodontitis in that patient.

Subgingival calculus is a frequent finding.

There is a slow to moderate rate of disease progression but the patient may have periods of rapid

progression ("bursts of destruction"). Chronic periodontitis can be associated with local predisposing

factors(e.g. tooth-related or iatrogenic factors). The disease may be modified by and be associated with

systemic diseases (e.g. diabetes mellitus, HIV infection) It can also be modified by factors other than

systemic disease such as smoking and emotional stress.

Major risk factors: Smoking, lack of oral hygiene with inadequate plaque biofilm control.

Measuring disease progression is carried out by measuring probing pocket depth (PPD) and bleeding

indices using a periodontal probe. Pockets greater than 3mm in depth are considered to be unhealthy.

Bleeding on probing is considered to be a sign of active disease. Discharge of pus, involvement of the

root furcation area and deeper pocketing may all indicate reduced prognosis for an individual tooth.

Age is related to the incidence of periodontal destruction: "...in a well-maintained population who practises

oral home care and has regular check-ups, the incidence of incipient periodontal destruction increases

with age, the highest rate occurs between 50 and 60 years, and gingival recession is the predominant

lesion before 40 years, while periodontal pocketing is the principal mode of destruction between 50 and

60 years of age."[2]

[edit]Pathology

Chronic periodontitis is initiated by Gram-negative tooth-associated microbial biofilms that elicit

a host response, which results in bone and soft tissue destruction. In response to endotoxin derived

fromperiodontal pathogens, several osteoclast-related mediators target the destruction of alveolar

bone and supporting connective tissue such as the periodontal ligament. Major drivers of this aggressive

tissue destruction are matrix metalloproteinases (MMPs), cathepsins, and other osteoclast-

derived enzymes.

[edit]Microbiology

There are two views of the microbiology of periodontitis: the specific plaque hypothesis and the non

specific plaque hypothesis.

The disease is associated with a variable microbial pattern.[3]

Anaerobic species of bacteria Porphyromonas gingivalis , Bacteroides forsythus , Treponema

denticola, Prevotella intermedia , Fusobacterium nucleatum , Eubacterium species have all been

implicated in chronic periodontitis.[4]

Microaerophile bacteria Actinomyces actinomycetemcomitans , Campylobacter rectus, and Eikenella

corrodens also may play a role in chronic periodontitis. [5]

[edit]Treatment

There is professional agreement among dentists that smoking cessation and good oral hygiene are key to

effective treatment and positive outcomes for patients.

The typical initial treatment known to be effective is scaling and root planing (SRP) to

mechanically debride the depths of the periodontal pocket and disturb the biofilm present. This is done

using a powered ultrasonic or sonic scaler or unpowered hand instruments. "In patients with chronic

periodontitis, subgingival debridement (in conjunction with supragingival plaque control) is an effective

treatment in reducing probing pocket depth and improving the clinical attachment level. In fact it is more

effective than supragingival plaque control alone".[6]

Full mouth disinfection protocols are favoured by some clinicians: "In patients with chronic periodontitis in

moderately deep pockets slightly more favourable outcomes for pocket reduction and gain in probing

attachment were found following FMD compared to control. However, these additional improvements

were only modest and there was only a very limited number of studies available for comparison, thus

limiting general conclusions about the clinical benefit of full-mouth disinfection."[7]

Open flap debridement is used by some practitioners particularly in deeper pocket areas. The advantages

of this approach is better visualization of the root surface to be cleaned. This must be weighed against the

risks of surgery. Open flap surgery is more effective than non-surgical periodontal therapy in deep

pocketing : "Both scaling and root planing alone and scaling and root planing combined with flap

procedure are effective methods for the treatment of chronic periodontitis in terms of attachment level

gain and reduction in gingival inflammation. In the treatment of deep pockets open flap debridement

results in greater PPD reduction and clinical attachment gain."[8]

Guided tissue regeneration (GTR) using PTFE membranes is favoured by some practitioners, despite its

cost.and complexity: "GTR has a greater effect on probing measures of periodontal treatment than open

flap debridement, including improved attachment gain, reduced pocket depth, less increase in gingival

recession and more gain in hard tissue probing at re-entry surgery. However there is marked variability

between studies and the clinical relevance of these changes is unknown. As a result, it is difficult to draw

general conclusions about the clinical benefit of GTR. Whilst there is evidence that GTR can demonstrate

a significant improvement over conventional open flap surgery, the factors affecting outcomes are unclear

from the literature and these might include study conduct issues such as bias. Therefore, patients and

health professionals need to consider the predictability of the technique compared with other methods of

treatment before making final decisions on use."[9]

Enamel matrix derivative (EMD) is favoured by some practitioners despite its high cost: "One year after its

application, EMD significantly improved probing attachment levels (1.1 mm) and probing pocket depth

reduction (0.9 mm) when compared to a placebo or control, however, the high degree of heterogeneity

observed among trials suggests that results have to be interpreted with great caution. In addition, a

sensitivity analysis indicated that the overall treatment effect might be overestimated. The actual clinical

advantages of using EMD are unknown. With the exception of significantly more postoperative

complications in the GTR group, there was no evidence of clinically important differences between GTR

and EMD. Bone substitutes may be associated with less gingival recession than EMD." [10]

[edit]Adjunctive systemic antibiotic treatment

Systemic antibiotics such as amoxicillin or metronidazole are sometimes used in addition to debridement

based treatments.

"Systemic antimicrobials in conjunction with scaling and root planing (SRP), can offer an additional benefit

over SRP alone in the treatment of periodontitis, in terms of clinical attachment loss (CAL) and probing

pocket depth (PPD) change, and reduced risk of additional CAL loss. However, differences in study

methodology and lack of data precluded an adequate and complete pooling of data for a more

comprehensive analyses. It was difficult to establish definitive conclusions, although patients with deep

pockets, progressive or 'active' disease, or specific microbiological profile, can benefit more from this

adjunctive therapy."[11]

[edit]Locally delivered adjunctive antimicrobial treatment

Chemical antimicrobials may be used by the clinician to help reduce the bacterial load in the diseased

pocket.

"Among the locally administered adjunctive antimicrobials, the most positive results occurred for

tetracycline, minocycline, metronidazole, and chlorhexidine. Adjunctive local therapy generally reduced

PD levels....Whether such improvements, even if statistically significant, are clinically meaningful remains

a question." [12]

Minocycline is typically delivered via slim syringe applicators. Chlorhexidine impregnated chips are also

available.

[edit]Modulating the host response

Sub-antimicrobial doses of doxycycline (SDD) have been used to alter host response to the periodontal

pathogens. This is believed to disrupt the action of matrix metalloproteinases and thus minimise host

mediated tissue destruction.

"The adjunctive use of SDD with SRP is statistically more effective than SRP alone in reducing PD and in

achieving CAL gain."[13]

[edit]Current controversies in chronic periodontal disease management

"There is no good evidence to show whether routine scale and polishing prevents chronic periodontitis."[14]

Lasers are increasingly being used in treatments for chronic periodontitis. However there is some

controversy over their use:

"No consistent evidence supports the efficacy of laser treatment as an adjunct to non-surgical periodontal

treatment in adults with chronic periodontitis."[15]

[edit]Cost/benefit analysis of treatment

"Costs for tooth retention via supportive periodontal therapy are relatively low compared with alternatives

(e.g. implants or bridgework) even in periodontally impaired teeth."[16]

=

[edit]Tentative links to other conditions

There is only very weak evidence linking to coronary heart disease.[17]

There is little evidence linking progression of periodontal disease to low birth weight or preterm birth:

"In these women with periodontitis and within this study's limitations, disease progression was not

associated with an increased risk for delivering a pre-term or a low birthweight infant."[18]

There is recently emerged evidence linking chronic periodontitis with head and neck squamous cell

carcinoma: "Patients with periodontitis were more likely to have poorly differentiated oral cavity SCC than

t

hose without periodontitis (32.8% versus 11.5%; P = 0.038)".[19]

References

1. ̂ Armitage, GC. "Development of a classification system for periodontal diseases and conditions." Ann

Perio 1999;4:1-6.

2. ̂ Heitz-Mayfield LJ, Schätzle M, Löe H, et al. (October 2003). "Clinical course of chronic periodontitis. II.

Incidence, characteristics and time of occurrence of the initial periodontal lesion". J. Clin.

Periodontol.30 (10): 902–8. PMID 14710770.

3. ̂ Moore WE, Holdeman LV, Cato EP, Smibert RM, Burmeister JA, Ranney RR (November

1983). "Bacteriology of moderate (chronic) periodontitis in mature adult humans". Infect. Immun. 42 (2):

510–5.PMID 6642641. PMC 264458.

4. ̂ Clinical Microbiology Reviews, October 2001, p. 727-752, Vol. 14, No. 4 0893-8512/01/$04.00+0 DOI:

10.1128/CMR.14.4.727-752.2001 Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis

and Treatment Walter J. Loesche1,2,* and Natalie S. Grossman2

5. ̂ Clinical Microbiology Reviews, October 2001, p. 727-752, Vol. 14, No. 4 0893-8512/01/$04.00+0 DOI:

10.1128/CMR.14.4.727-752.2001 Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis

and Treatment Walter J. Loesche1,2,* and Natalie S. Grossman2

6. ̂ Van der Weijden GA, Timmerman MF. "A systematic review on the clinical efficacy of subgingival

debridement in the treatment of chronic periodontitis". J. Clin. Periodontol. 29 (S3): 55–

71.doi:10.1034/j.1600-051X.29.s3.3.x.

7. ̂ Eberhard J, Jepsen S, Jervøe-Storm PM, Needleman I, Worthington HV (2008). "Full-mouth disinfection

for the treatment of adult chronic periodontitis". Cochrane Database Syst Rev (1):

CD004622.doi:10.1002/14651858.CD004622.pub210.1002/14651858.CD004622.pub2. PMID 18254056.

8. ̂ Heitz-Mayfield LJ, Trombelli L, Heitz F, Needleman I, Moles D (2002). "A systematic review of the effect of

surgical debridement vs non-surgical debridement for the treatment of chronic periodontitis". J. Clin.

Periodontol. 29 (Suppl 3): 92–102; discussion 160–2. PMID 12787211.

9. ̂ Needleman IG, Worthington HV, Giedrys-Leeper E, Tucker RJ (2006). "Guided tissue regeneration for

periodontal infra-bony defects". Cochrane Database Syst Rev (2):


10. ̂ Esposito M, Grusovin MG, Papanikolaou N, Coulthard P, Worthington HV (2009). "Enamel matrix

derivative (Emdogain(R)) for periodontal tissue regeneration in intrabony defects". Cochrane Database Syst

Rev (4):

CD003875. doi:10.1002/14651858.CD003875.pub310.1002/14651858.CD003875.pub3. PMID 19821315.

11. ̂ Herrera D, Sanz M, Jepsen S, Needleman I, Roldán S (2002). "A systematic review on the effect of

systemic antimicrobials as an adjunct to scaling and root planing in periodontitis patients". J. Clin.

Periodontol. 29 (Suppl 3): 136–59; discussion 160–2. PMID 12787214.

12. ̂ Bonito, AJ et al (August 2005). "Impact of Local Adjuncts to Scaling and Root Planing in Periodontal

Disease Therapy: A Systematic Review". Journal of Periodontology 76, No. 8.

13. ̂ Reddy MS, Geurs NC, Gunsolley JC (December 2003). "Periodontal host modulation with antiproteinase,

anti-inflammatory, and bone-sparing agents. A systematic review". Ann. Periodontol. 8 (1): 12–

37.doi:10.1902/annals.2003.8.1.12. PMID 14971246.

14. ̂ Beirne P, Worthington HV, Clarkson JE (2007). "Routine scale and polish for periodontal health in

adults". Cochrane Database Syst Rev (4):


15. ̂ Karlsson MR, Diogo Löfgren CI, Jansson HM (November 2008). "The effect of laser therapy as an adjunct

to non-surgical periodontal treatment in subjects with chronic periodontitis: a systematic review".J.

Periodontol. 79 (11): 2021–8. doi:10.1902/jop.2008.080197. PMID 18980508.

16. ̂ Pretzl B, Wiedemann D, Cosgarea R, et al. (August 2009). "Effort and costs of tooth preservation in

supportive periodontal treatment in a German population". J. Clin. Periodontol. 36 (8): 669–

76.doi:10.1111/j.1600-051X.2009.01409.x. PMID 19566541.

17. ̂ Hujoel PP (June 2002). "Does chronic periodontitis cause coronary heart disease? A review of the

literature". J Am Dent Assoc 133 (Suppl): 31S–36S. PMID 12085722.

18. ̂ Michalowicz BS, Hodges JS, Novak MJ, et al. (April 2009). "Change in periodontitis during pregnancy and

the risk of pre-term birth and low birthweight". J. Clin. Periodontol. 36 (4): 308–14.doi:10.1111/j.1600-

051X.2009.01385.x. PMID 19426177.

19. ̂ Tezal M, Sullivan MA, Hyland A, et al. (September 2009). "Chronic periodontitis and the incidence of head

and neck squamous cell carcinoma". Cancer Epidemiol. Biomarkers Prev. 18 (9): 2406–

12.doi:10.1158/1055-9965.EPI-09-0334. PMID 19745222.

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Periodontal Diseases