Drug – bio-affecting and body treating compositions – Preparations characterized by special physical form – Implant or insert
Reexamination Certificate
2003-04-02
2004-12-14
Spear, James M. (Department: 1615)
Drug, bio-affecting and body treating compositions
Preparations characterized by special physical form
Implant or insert
C424S400000, C424S422000, C424S434000
Reexamination Certificate
active
06830757
ABSTRACT:
BACKGROUND OF THE INVENTION
The present invention relates to a method for treating periodontal disease. Periodontal disease is characterized by a loss of supporting tissues of the teeth. In particular, periodontitis includes a loss of the periodontal ligament and a disruption of the ligament attachments to cementum, as well as reabsorption of alveola and bone. Along with a loss of tissue attachments, periodontal disease produces a migration of the epithelial attachments along the root surface and reabsorption of bone.
It is widely accepted that an initiation and progression of periodontal disease is dependent upon the presence of micro-organisms which are capable of causing the disease. At least three characteristics of periodontal micro-organisms have been identified which contribute to the ability of microbes to act as pathogens. A first characteristic is a capacity of the microbes to colonize. A second characteristic is an ability of the microbes to evade anti-bacterial host defense mechanisms. A third characteristic is an ability of the microbes to produce substances which directly initiate tissue destruction.
Two major periodontal disease pathogens,
A. actinomycetemcomitans
and
P. gingivalis
, are able to invade into the tissues.
A. actinomycetemcomitans
passes through epithelial cells into the underlying connective tissue while
P. gingivalis
invades and persists in epithelial cells.
It is believed that direct pathological effects of bacteria and effects of their products on the periodontium are significant during early stages of periodontal disease. Analysis of plaque samples from patients with increasingly severe levels of gingival inflammation reveals a succession of bacterial species with an increased capacity to directly induce an inflammatory response. For example, an increase in persistent levels of
Fusobacterium nucleatum
incites a mild gingivitis. A subsequent production of its metabolic by-products directly effects gingival vasculature. Resulting edema and an increase in production of, gingival crevicular fluid, GCF, provides an environment and nutrients that allow putative pathogens to flourish.
Bacteria such as
P. gingivalis
also produce enzymes such as proviasis, collagenase, and fibrinolysin that directly degrade surrounding tissues in superficial layers of the periodontium. In addition, this bacterium produces metabolic by-products such as H
2
S, ammonia and fatty acids that are toxic to surrounding cells. Furthermore, bacterial constituents such as lipopolysaccharide are capable of inducing bone reabsorption in vitro.
nce major protective elements of the periodontium have been overwhelmed by bacterial virulence mechanisms, several host-mediated destructive processes are initiated. Polymorphonucleocytes (PMNS), which normally provide protection can themselves contribute to tissue pathology. During a process of phagocytosis, PMNs typically spill some of the enzyme content extracellularly during a process known as degranulation. Some of the enzymes are capable of degrading the surrounding host tissues, such as collagen and basement membrane constituents, which contribute to tissue damage.
here is increasing evidence that the bulk of tissue destruction in established dental lesions is a result of the mobilization of the host tissues by an activation of monocytes, lymphocytes, and other host cells. Engagement of these cellular elements by bacterial factors, in particular bacterial lipopolysaccharide, is thought to stimulate production of both catabolic cytokines and inflammatory mediators such as arachidonic acid and metabolites, such as prostaglandin E
2
(PGE
2
). Such cytokines and inflammatory mediators, in turn, promote the release of tissue-derived enzymes. A summary of this reaction is described in an article,
“The Pathogenesis of Periodontal Diseases”, Periodontal, April
1999, Vol. 70, No. 4, pp. 457-470.
In some aspects, periodontal diseases are among the most unusual infections of human beings. One reason for this uniqueness is the unusual anatomic feature wherein a mineralized structure, a tooth, passes through an integument so that a portion of the tooth is exposed to an external environment while a portion is within connected tissues. This unusual aspect of the infection is described in an article entitled
“The Nature of Periodontal Diseases”
by S. Socransky et al. in
The Annals of Periodontology
, vol.2, No. 1, March 1997, pp. 4-10.
The tooth provides a surface for colonization by a diverse array of bacterial species. Bacteria attach to the tooth itself as well as to the epithelial surface of the gingival or periodontal pockets, and to underlying connective tissues. The outer layers of the tooth do not shed, and thus microbial colonization is facilitated. A situation is then established wherein micro-organisms colonize a relatively stable surface, which is the surface of the tooth, and are continually held in immediate proximity to soft tissues of the periodontium.
The presence of the tooth increases the complexity of the host-parasite relationship in a number of ways. The bacteria colonizing the tooth are by and large outside the body where they are less able to be controlled by mechanisms which operate within the tissues. The environment within a plaque is conducive to microbial survival, but it is unlikely to be particularly an effective environment for a host to seek out and destroy micro-organisms.
Factors such as pH, eH and proteolytic enzymes affect performance of host defense mechanisms. In addition, the tooth provides sanctuary in which micro-organisms hide, persist at low levels during treatment, and then re-emerge to cause further problems. Bacteria in dentin alluvials, which are flaws in the tooth, or areas which were demineralized by bacteria, are not easily approached by much larger host cells. In a similar manner, non-cellular host factors face diffusion barriers. Mechanical debridement, other than vigorous removal of tooth material, cannot reach organisms in the tooth. Chemotherapeutic agents also have difficulty in reaching the bacterial species. In particular, antimicrobial agents which require bacteria to multiply are adversely affected since the rate of growth is suspected to be very low.
One method for measuring the severity of periodontal disease is a technique of periodontal probing depth (PD). Measuring periodontal probing depth measures a loss of connective tissue attachments. A method of periodontal probing has been described in an article entitled
“Periodontal Probing: Probe-tip Diameter*”,
published by the School of Dentistry, Medical College of Georgia, Augusta, Ga.
Periodontal probing is performed when a periodontist places a probe into the sulcus or clinical pocket, and applies a force to move it apically into tissue along a tooth surface. The clinician applies pressure on the tissue and when the tissue exerts an opposite, equal pressure to the probe, displacement of the probe into the tissue will cease. The pressure exerted by the probe is directly proportional to force on the probe and inversely proportional to the area at the probe tip. With a round probe, a change in the tip diameter has a greater effect on pressure than does a similar change in the force. An increase in the probing force increases the pressure by a proportional amount. However, a relatively similar increase of the probe diameter reduces the pressure by a proportional amount which is squared. If the force is doubled (20 to 40 gramforce), the pressure is increased by a factor of 2. If the diameter is doubled (0.4 to 0.8 millimeters), the pressure is reduced by a factor of 4. The pressure is equal to the force applied in the probe/area at the tip-end=F/ur
2
=F/u(D/2)
2
: R=radius, D=diameter.
Positioning of the probe is shown in schematic cross-section in FIG.
1
. The probe
10
is inserted in an area between connective tissue
12
and dentin
14
, as is shown in FIG.
1
. The depth
16
of the probe
10
into that space is a measure of the severity of periodontal disease.
In early periodontitis, gums
Bennett Rachel M.
Northern Research Laboratories, Inc.
Schwegman Lundberg Woessner & Kluth P.A.
Spear James M.
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