Chapter 2 Aging and the

Periodontium

Effects of Aging on the Periodontium

Gingival thinning & decreased keratinization as the age increase

flattening of the rete pegs
Epithelium altered cell density
gingival recession is NOT an inevitanle physilogic process of aging but rather
be explained by the cumulative effects of inflammation & trauma in the
periodontium

Gingival increasing age = coarse & denser gingival connective tissues.

increase rate of conversion of soluble to insoluble collagen
Connective increased mechanical strength
Tissue increased denaturing temperature
increased collagen stabilization due to changes in the macromolecular
conformations

Periodontal decreased number of fibroblasts

more irregular structure (Similar w/ g.c.t)
Ligament decreased organic matrix production, epithelial rests and increased amounts
of elastic fibers.
cell proliferation decreases with age suggestinf an impairment of repair
potential.

Cementum increase in cemental width ( 5 to 10x with increasing age) - why? --> deposition
continues after tooth eruption.
increase in width is greater apically & lingually

Alveolar bone more irregular periodontal surface

less-regular insertion of collagen fibers
 Although age is a risk
factor for the bone mass reductions in individuals with osteoporosis, it is not
causative and therefore should be distinguished from physiologic aging
processes.

Bacterial Dentogingival plaque accumulation has been suggested to increase with age--
why? --> increased hard-tissue surface area due to gingival recession & the
Plaque surface characteristics of the exposed root surface.
In a study among 60-75 year olds the prevalence
of P. gingivalis, Treponema forsythia, Treponema denticola, A.
actinomycetemcomitans, and Prevotella intermedia were high and were NOT
clearly related to probing depth.

Immune & Differences between younger and older individuals can be demonstrated for T
and B cells, cytokines, and natural killer cells but not for polymorphonuclear
inflammatory cells and macrophage activity.
responses C-reactive protein (CRP) is an acute phase protein that is widely regarded as a
marker of inflammatory burden and response to bacterial infection-->maybe
increased in those with with progressive periodontitis and no other systemic
conditions.
Another modulator is Nutrition.
Lower serum folate in adults (Above 60) are associated with greater levels of
periodontitis.

EFFECTS OF AGING ON THE PROGRESSSION OF

PERIODONTAL DISEASES
Even at the baseline level of excellent gingival health before the commencement of
plaque accumulation, differences may exist between groups, with older individuals
demonstrating more inflammation (greater amount of infiltrated connective tissue,
increased gingival crevicular fluid flow, and an increased gingival index.

The phrase getting long in the tooth expresses a widespread belief that age is
inevitably associated with an increased loss of connective tissue attachment which
maybe due to exposure to potentitally destructive processes.

--> examples of exposure to: palque-associated periodontitis, chronic mechanical

trauma ( from toothbrushing), and iatrogenic damage from unfavorable restorative
dentistry (overhangs & ill fitting dentures), repeated scaling & root planing.

RISK FACTOR - defined as “any characteristic, behavior, or exposure with an

association to a particular disease.

--> it is not necessarily causal in nature (can be modified or not to reduce

initiation or progression of diesease.

modified causual risk factors: smoking, improved oral hygiene & etc.
non-modifiable risk factors : genetics
AGING AND THE RESPONSE TO TREATMENT OF THE
PERIODONTIUM
The successful treatment of periodontitis requires both meticulous home plaque control by the patient and meticulous supragingival and subgingival debridement by the therapist.

-->Without effective periodontal therapy, the progression of disease may be faster with increasing age.

-->Aging, may affect other aspects of the management of periodontal health (ex: risk of root caries)

__________
Chapter 3
CLASSIFICATIONS OF DISEASES AND CONDITIONS AFFECTING THE
PERIODONTIUM
--> Classification can be most consistently defined by the differences in the
clinical manifestations of diseases and conditions: they are clinically consistent
and require little (if any) clarification by scientific laboratory testing.
SIDE NOTES:

GINGIVITIS ASS. A result of an interaction between the microogranisms in the dental plaque
WITH PLAQUE ONLY biofilm & the tissues and the inflammatory cells of the host.
can be altered by the effects of: local factors, systemic factors, medications
and malnutrition.
examples of local contributing factors: tooth anatomic factors, dental
restorations & appliances, root fractures & cervical root resportion & cemental
tears.
Systemic factors (refer to the table above)-- these changes are most apparent
during pregnancy--> increase inflammation even in low presence of plaque.
Blood dyscrasias (ex: leukemia) --> gingival enlargement (spongy & swollen)
and bleeding.
Medication- results to induced gingival enlargement.
Examples of medications: anticonvulsant drugs ( such as phenytoin),
immunosuppressive drugs (such as cyclosporine), calcium channel blockers
(nifedipine, verapamil, diltiazem, & sodium valporate) and Oral contraceptives
(but may be reversed by discontinuation of use).

NON-PLAQUE Observed more frequently among: lower socioeconomic groups, in developing

INDUCED GINGIVAL countries & immunocompromised individuals.
Example: Benign mucous membrance pemphigoid -->sloughing* gingival
LESIONS
tissues leaving painful ulcerations of the gingiva.
Gingival diseases of specific bacterial origin are increasing in prevalence.
Mostly, as a result of sexually transmitted disease such as Gonorrhea (Nisseria
gonorrhoeae) and to a lesser degree Syphilis (Treponema pallidum)
Oral lesions may be a result of --> systemic infection or direct infection.
Gingivostomatitis -->rare entity that may present as an acute condition with
fever, malaise, and pain associated with acutely inflamed, diffuse, red, and
swollen gingiva with increased bleeding and occasional gingival abscess
formation.
Gingival infections have been associated with group A β-hemolytic
streptococcal infections.
Gingival diseases of viral origin caused commonly by: herpesviruses. Lesions
are frequently related to the reactivation of latent viruses.
Viral gingival diseases are treated with: topical or systemic antiviral drugs (ex:
acyclovir)
Fungal origin--> most common: candidiasis, caused by: Candida albicans,
characteristics: white patches on the gingiva, tonue, or oral mucous
membrane which can be removed by gauze and leave a red, bleeding surface.
genetic origin--> most clinically evident condition is: hereditary gingival
fibromatosis
Systemic conditions --> allergic reactions such as from: toothpastes,
mouthwashes, chewing gums and food. Histologically, shows a dense infiltrate
of eosinophilic cells.
Traumatic lesions may be self-inflicted & factitious* in origin. Examples of
traumatic lesions--> toothbrush trauma, iatrogenic trauma (caused by the
dentist), Peripheral ossifying fibroma (due to embedment of foreign body).
Foreign-body reactions example: amalgam into the gingiva creating an
amalgam tattoo. Abrasives during polishing procedures may also be
introduced.
PERIODONTITIS defined as “an inflammatory disease of the supporting tissues of the teeth caused
by specific microorganisms or groups of specific microorganisms, resulting in
progressive destruction of the periodontal ligament and alveolar bone with
increased probing depth formation, recession, or both.”

difference with gingivitis: with clinically detectable attachment loss

Clinical signs of inflammation—such as changes in color, contour, and consistency

as well as bleeding with probing—may not always be positive indicators of ongoing
attachment loss.

Clinically, more evident during the fourth decade of life

Early onset periodontitis was subclassified into: prepubertal, juvenile &
rapidly progressive forms (with localized or generalized distributions)

American Academy Forms of periodontitis:

of Periodontology
Chronic periodontitis
International
Aggressive Periodontitis (previously known as early-onset periodontitis)
Workshop for
Periodontitis as a manifestation of systemic disease
Classification of
Periodontal
Diseases, 1999
CHRONIC Most commmon form periodontitis
PERIODONTITIS most common in adults (above 35 y/o)
associated with accumulation of plaque & calculus ; slow to moderate rate
disease progression
May occur as localized diseases (less than 30% ) demonstrate attachment
& bone loss or generalized disease (if more than 30%)
may be described as by the severity of the disease. Slight ( 1-2mm of loss) ,
Moderate (3 to 4mm of loss) or Severe (5mm or more) clinical attachment
loss.

AGGRESSIVE Differs from chronic by: rapid rate of disease progression in an otherwise
PERIODONTITIS healthy individual.
previously classified as: early onset periodontitis
affects usually young individuals (during or shortly after puberty) & during
the 2nd or 3rd decades of life.

PERIODONTITIS AS A is the diagnosis to be used when the systemic condition is the major
MANIFESTATION OF predisposing factor and when local factors (e.g., large quantities of plaque
and calculus) are not clearly evident.
SYSTEMIC DISEASE
Papillon–Lefèvre syndrome (PLS) is an autosomal-recessive disorder
caused by mutations in the cathepsin C gene located on chromosome
11q14.
Significant causative factor: Aa
Clinical manifestations: severe aggressive periodontitis & diffuse
keratoderma on the palms and on the soles, knees, or both.
opportunistic periodontal pathogens such as Aggregatibacter
actinomycetemcomitans (Aa), Porphyromonas gingivalis, Tannerella
forsythia, Fusobacterium nucleatum, and Prevotella intermedia are
frequently identified among plaque samples from PLS patients.
What titer is typically elevated in with PLS? Serum immunoglobulin G titer
against Aa.
Sarcoidosis- chronic, cell-mediated, delayed-type hypersensitivty. Rarely
affects the oral cavity with incidence of occurence (in descending order)
lymph nodes, lips, soft palate, buccal mucosa, gingiva, tongue & bone.
Histologically, positive Kveim test.

BISPHOSPHATE- cause: prolonged use of Bisphosphonates

RELATED Bisphosphonates (BPs) are pyrophosphate analogs with a high affinity for
hydroxyapatite crystals.
OSTEONECROSIS OF
lesions may be asymptomatic, or they may present with pain, purulent
THE JAW
discharge, swelling, tooth mobility, and paresthesia, thereby culminating in
a reduced ability to eat and speak.
most frequent in : the mandible (65%), maxilla (26%) & both jaws (95%).
Frequency is higher in the POSTERIOR REGION of the jaw.
No treatment, discontinuance is not helpful.
NECROTIZING Acute
ULCERATIVE Predisposing factors: psychologuic stress, smoking, immunosuppression &
malnutrition.
GINGIVITIS (NUG)
treatment: antimicrobial therapy + plaque and calculus removal &
improved oral hygiene.

NECROTIZING consistent feature: loss of clinical attachment & alveolar bone

ULCERATIVE may be observed in patients with HIV Infections
manifests as: local ulceration & necrosis of gingival tissue with exposure of
PERIODONTITIS (NUP)
underlying bone, spontaneous bleeding & severe pain.
 PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS

ENDODONTIC- pulpal necrosis PRECEDES periodontal changes

PERIODONTAL Periapical lesion that originates with pulpal infection and necrosis may drain to the
oral cavity through the --> periodontal ligament or accessory canals
LESIONS
Clinically presents as: localized, deep, periodontal probing depth taht extends to
the apex of the tooth

PERIODONTAL- Scaling and root planing remove cementum and underlying dentin, which may lead
ENDODONTIC to chronic pulpitis through the bacterial penetration of dentinal tubules.

LESIONS

COMBINED occur when pulpal necrosis and a periapical

LESIONS lesion occur on a tooth that is also periodontally involved

TOOTH ANATOMIC FACTORS
Ex: Enamel pearls & cervical enamel projections
Cervical enamel projections found on : 15-24% of mandibular
molars and 9-25% of maxillary molars
associated with clinical attachment loss especially in the
FURCATION AREAS.

DENTAL RESTORATIONS AND common in restoration sor appliances located subgingivally.

APPLIANCES ex: onlays, crowns, fillings & orthodontic bands

caused by: trauma, restorative or endodontic procedures

ROOT FRACTURES

CERVICAL ROOT RESORPTION Can be seen in: Avulsed teeth that are reimplanted ----->
AND CEMENTAL TEARS due to development of anyklosis causing resorption
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