Cementum & Alveolar Bone

Dr. Mahmoud Mudalal

B.Sc. Dental surgery

M.Sc. Periodontology
Ph.D. Periodontology and Implantology
Asst. Professor at Arab American university
Member of ADEE.
Research fellow at Jilin Provincial Experimental School.
Google scholar. Mahmoud MUDALAL 24 citations.
Research Gate Ref #: 10.88.
 Aging and the Periodontium

• Effects of Aging on the Periodontium

• Effects of Aging on the Progression of Periodontal Diseases

• Aging and the Response to Treatment of the Periodontium

 Aging and the Periodontium
• Increased health awareness and improvements in preventive dentistry
have led to decreasing tooth loss for all age groups.
• The effects of this shift in tooth retention need to be considered carefully.
• In particular, increased life expectancy and greater health expectations
may lead to changes in demand from older individuals for periodontal
treatment and potentially a substantial increase in supportive periodontal
therapy.
 Effects of Aging on the Periodontium
• Gingival Epithelium
• Thinning and decreased keratinization of the gingival epithelium have been reported
with age.
• The significance of these findings could mean an increase in epithelial permeability
to bacterial antigens, a decreased resistance to functional trauma, or both.
• If so, such Changes may influence long-term periodontal outcomes.
• The effect of aging on the location of the junctional epithelium has been the subject
of much speculation.
• Some reports show migration of the junctional epithelium from its position in healthy
individuals (i.e., on the enamel) to a more apical position on the root surface, with
accompanying gingival recession. However, in other animal studies, no apical
migration has been noted. With continuing gingival recession, the width of the
attached gingiva would be expected to decrease with age, but the opposite appears to
be true.
• A, Normal relationship with the gingival margin 1 to 2 mm above the
cementoenamel junction.
• B, Wear of the incisal edge and continued tooth eruption. The gingival
margin remains in the same position as shown in A. Therefore, the root
surface is exposed, and clinical recession is evident. The width of the
attached gingiva has not changed.
• C, Wear of the incisal edge and continued tooth eruption. The gingival
margin has moved with the tooth; therefore, the entire dento-gingival
complex has moved coronally, with a resulting increase in the width of
the attached gingiva.
• D, No wear of incisal edge is evident. The gingiva has moved apically,
and clinical recession is evident. The width of attached gingiva is
reduced.
• (A) Overeruption with recession in an older individual (i.e., a 68-year-old
woman) with generalized recession and a history of previously treated
periodontitis. Note some overeruption of the lower anterior teeth and
wear of teeth related to oral hygiene measures.
• (B) Radiographs of the patient shown in A.
• (C) Overeruption without recession in an older individual (i.e., a 72-year-
old woman) with no periodontitis but marked lower incisor tooth wear
and overeruption. Note how the gingival margin has migrated coronally
with the erupting teeth.
• (D) Extensive recession in a younger individual (i.e., a 32-year-old man)
with marked recession and no history of periodontitis. The recession
has resulted from a combination of anatomically thin tissues and
toothbrush-related trauma.
 Gingival Connective Tissue
• Increasing age results in coarser and denser gingival connective tissues. Qualitative
and quantitative changes in collagen have been reported.
• These changes include an increased rate of conversion of soluble to insoluble
collagen, increased mechanical strength, and increased denaturing temperature.
• These results indicate increased collagen stabilization caused by changes in the
macromolecular conformation.
• Not surprisingly, an increased collagen content has been found in the gingivae of
older animals, despite a lower rate of collagen synthesis decreasing with age.
 Periodontal Ligament
• Changes in the periodontal ligament that have been reported with aging include
decreased numbers of fibroblasts and a more irregular structure, thus paralleling the
changes seen in the gingival connective tissues.
• Other findings include decreased organic matrix production, decreased epithelial cell
rests, and increased amounts of elastic fiber.
• Conflicting results have been reported for changes in the width of the periodontal
ligament in human and animal models.
• Although true variation may exist, this finding probably reflects the functional status
of the teeth in the studies: the width of the space will decrease if the tooth is
unopposed (i.e., hypofunction) or increase with excessive occlusal loading.
• Both scenarios can be anticipated as a result of tooth loss in this population.
• These effects may also explain the variability in studies that have reported qualitative
changes within the periodontal ligament.
 Cementum
• Some consensus regarding the effect of aging on cementum exists.
• An increase in cemental width is a common finding; this increase may be 5 to 10
times wider than in those of younger age.
• This finding is not surprising because deposition continues after tooth eruption. The
increase in width is greater apically and lingually.
• Although cementum has limited capacity for remodeling, an accumulation of
resorption bays explains the finding of increasing surface irregularity.
 Alveolar Bone
• Reports of morphologic changes in alveolar bone mirror age-related changes in other
bony sites.
• Specific to the periodontium are findings of a more irregular periodontal surface of
bone and the 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.
• Overriding the diverse observations of bony changes with age is the important
finding that the healing rate of bone in extraction sockets appears to be unaffected by
increasing age.
• Indeed, the success of Osseo integrated dental implants, which relies on intact bone
healing responses, does not appear to be age related.
 Bacterial Plaque
• Dento-gingival plaque accumulation has been suggested to increase with age.
• This may be explained by the increase in hard tissue surface area as a result of
gingival recession and the surface characteristics of the exposed root surface as a
substrate for plaque formation as compared with enamel.
• Other studies have shown no difference in plaque quantity with age. This
contradiction may reflect the different age ranges of experimental groups as variable
degrees of gingival recession and root surface exposure.
• For supragingival plaque, no real qualitative differences have been shown for plaque
composition.
• With regard to subgingival plaque, one study showed subgingival
flora to be similar to normal flora, whereas another study reported
increased numbers of enteric rods and pseudomonads in older
adults.
• It has been speculated that a shift occurs in the importance of
certain periodontal pathogens with age, specifically including an
increased role for Porphyromonas gingivalis and a decreased role
for Aggregatibacter actinomycetemcomitans. However,
differentiating true age-related effects from the changes in ecologic
determinants for periodontal bacteria will be difficult.
 Immune and Inflammatory Responses
• Advances in the study of the effects of aging on the immune response (i.e., immuno-
senescence) have altered the understanding of this phenomenon.
• In particular, more recent studies have set tighter controls on excluding individuals
with systemic conditions known to affect the immune response.
• As a result, age has been recognized as having much less effect on the alteration of
the host response than previously thought.
• Differences between younger and older individuals can be demonstrated for T and B
cells, cytokines, and natural killer cells, with increased inflammatory-type (M1)
macrophage subset gene expression (in a nonhuman primate model), but not for
polymorphonuclear cells.
• Age-related differences in the inflammatory response among individuals with
gingivitis have been clearly demonstrated and are discussed later in the coming
lectures.
 Effects of Aging on the Progression of
Periodontal Diseases
• In a classic experimental gingivitis study, subjects were rendered free of plaque and
inflammation through frequent professional cleaning. After this was achieved, the
subjects abstained from oral hygiene measures for periods of 3 weeks to allow
gingivitis to develop. In this experimental model, a comparison of developing
gingivitis between younger and older individuals demonstrated a greater
inflammatory response in older subjects, both in humans and in dogs. In the older age
group (i.e., 65 to 80 years), the findings included a greater amount of infiltrated
connective tissue, increased gingival crevicular fluid low, and an increased gingival
index.
• Other studies have not demonstrated differences between subjects; this finding may
be related to smaller differences between the ages of the younger and older
experimental groups. Intriguingly, 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.
• The phrase “getting long in the tooth” expresses a widespread belief that
age is inevitably associated with an increased loss of connective tissue
attachment.
• However, this observation may equally reflect cumulative exposure to a
number of potentially destructive processes. These exposures may
include plaque-associated periodontitis, long-term mechanical trauma
from toothbrushing, and iatrogenic damage from unfavorable restorative
dentistry or repeated scaling and root planing.
• The effects of these exposures act in one direction only (i.e., an increased
loss of attachment).
• The conclusions from these studies are strikingly consistent and show
that the effect of age is either nonexistent or provides a small and
clinically insignificant increased risk of loss of periodontal support.
Indeed, in comparison with the odds ratio of 20.52 for poor oral hygiene
status and periodontitis, the odds ratio for age was only 1.24, and
smoking was much more influential than age. Therefore, age has been
suggested to be not a true risk factor but rather a background or
associated factor for periodontitis. In addition, the clarification of a
genetic basis for susceptibility to severe forms of periodontitis underlines
the overriding importance of plaque, smoking, and susceptibility in
explaining most of the variations in periodontal disease severity among
individuals. Nevertheless, a longitudinal study of essentially untreated
periodontitis in an older adult (70 years old) Japanese population
indicated that 296 of 394 individuals (75%) had a least 1 site with 3 mm
or more loss of attachment over a 2-year period.
 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. Unfortunately, only a few
studies have directly compared such an approach among patients of
different age groups. The few studies that have done so clearly
demonstrate that, despite the histologic changes in the periodontium with
aging, no differences in response to nonsurgical or surgical treatment
have been shown for periodontitis. However, if plaque control is not
ideal, the continued loss of attachment is inevitable.
• Furthermore, without effective periodontal therapy, the progression of
disease may be faster with increasing age. Attempts to increase plaque
control by chemical means have also been reported.
• The biologic effects of aging have either no impact or
a minimal impact on an individual’s response to
periodontal treatment. However, other factors may
have a profound impact, including cognitive and
motor skills as well as medical history.