Periodontics
DENTALELLE TUTORING
The Periodontium
AB, alveolar bone; AC,
alveolatrcrest; AM, alveolar
mucosa; AP, alveolar process; CB,
compact bone of alveolar bone
proper; CEJ, cemento-enamel
junction; CT, connective tissue; DEJ,
dentino-enamel junction; ES, enamel
space; G, gingiva; GE, gingival
epithelium; GG, gingival groove; GM,
gingival margin; GS, gingival
sulcus; JE, junctional
epithelium; MGJ, mucogingival
junction; MS, marrow space; OE,
oral epithelium; PDL, periodontal
ligament; RCE, radicular (root)
cementum; SE, sulcular epithelium;
Incisor
AB, alveolar bone; C, incisive canal; CE,
cementum; F, foramen;
G, gingiva; MGJ, mucogingival junction; PDL,
periodontal ligament
Periodontium
 Composed of:
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Gingiva
Cementum
Alveolar Bone
Periodontal Ligament
Gingiva
 The gingiva is the keratinized mucosa that surrounds
the teeth. It forms a collar around each tooth, that
ranges in width from1 to 9 mm. The narrowest zone
of the gingiva is usually found on the buccal surface
of the mandibular canine to first premolar region.
 The widest zone is often located on the lingual
aspect of the last mandibular molar. The gingiva is
attached in part to the cementum of the tooth and in
part to the alveolar process. The gingiva is composed
of masticatory mucosa.
Features
 In light-skinned individuals the gingiva can be readily distinguished
from the adjacent dark red alveolar mucosa by its lighter pink
color. Its apical border, that separates it from the adjacent alveolar
mucosa, is the mucogingival junction. A similar tissue relationship
can be seen on the lingual aspect of the mandible.
 In dark-skinned persons the gingiva may contain melanin pigment
to a greater extent than the adjacent alveolar mucosa. The melanin
pigment is synthesized in specialized cells, the melanocytes, located
in the basal layer of the epithelium. The melanin is produced as
granules, themelanosomes, that are stored within the cytoplasm of
the melanocytes, as well as the cytoplasm of
adjacent keratinocytes. Melanocytes are embryologically derived
from neural crest cells that eventually migrate into the
epithelium. If pigmented gingiva is surgically resected, it will often
heal with little or no pigmentation. Therefore, surgical procedures
should be designed so as to preserve the pigmented tissues.
The Gingiva
 The most coronal portion of the gingiva is the gingival
margin. The term marginal gingiva refers to that portion of the
gingiva that is located close to the gingival margin.
 The gingival sulcus is the shallow groove between the marginal
gingiva and the tooth.
 The gingival groove is an indentation that parallels the oral or
vestibular surface of the gingival margin. It is located at about the
same level as the apical border of the junctional
epithelium. Note: its level does not correspond to that of the
bottom of the gingival sulcus. It is only present occasionally. Its
presence or absence is not related to gingival
health. Inflammation may cause the tissues to swell and mask its
presence.
Free and Attached
 Clinicians sometime use the
terms "free" and "attached" gingiva. Although these terms
may have some clinical relevance, they are anatomically
incorrect. The determination as to whether the gingiva is
"free" or "attached" is made by probing the gingival sulcus
with a periodontal probe.
 This instrument will frequently penetrate the junctional
epithelium beyond the sulcus bottom, particularly in the
presence of inflammation. This results in the clinical
impression that the marginal gingiva is detached from the
tooth to a much greater degree than is the case.
Anatomically. "Attached" gingiva refers to the portion of the
gingiva apical to the "free" gingiva which is firmly bound to
the underlying tooth and alveolar process.
Parts of the Gingiva
Interdental
 The gingiva that occupies the interdental spaces coronal
to the alveolar crest is the interdental gingiva. It is
composed of a pyramidal interdental papilla in the
incisor region.
 In the posterior region it is composed of an oral and a
vestibular papilla (P) joined by an interdental
"col" (C). The interdental gingiva is attached to the tooth
by junctional epithelium (JE) coronally and by
connective tissue fibers apically (not shown). The most
coronal portion of the interdental gingiva is lined
with sulcular epithelium (SE)
Oral Epithelium
 It is the stratified, squamous keratinizing epithelium, that lines the
vestibular and oral surfaces of the gingiva. It extends from the
mucogingival junction to the gingival margin, except for the palatal
surface where it blends with the palatal epithelium.
 The oral epithelium consists of a basal layer (stratum basale, SB), a
spinous layer (stratum spinosum, SS), a granular layer (stratum
granulosum, SG) and a cornified layer (stratum corneum, SC). It is
designed primarily for protection against mechanical injury during
mastication.
 Resistance to mechanical injury is mediated primarily by the
numerous intercellular junctions, mostly desmosomes, that hold the
cells tightly together and the cornified layer. The cornified layer and
the relatively narrow intercellular spaces also contribute to the
relative lack of permeability.
 The oral epithelium is connected to the underlying connective tissue of the lamina
propria by an irregular interface. This interface consists of finger-like projections of
connective tissue from the papillary layer extending into depressions on the
undersurface of the epithelium. These depressions are located between the
interconnected Rete ridges that form the undersurface of the epithelium. Crosssections of these ridges, as seen in histological sections are sometimes referred to
as Rete pegs.
 Transmission electron micrograph of the junction between a basal cell of the
gingival oral epithelium and the connective tissue of the underlying lamina
propria. The epithelial cell (EC) contains widely dispersed cytoplasmic filaments,
also known as tonofilaments.
 The epithelial cell membrane facing the lamina propria is studded with
numerous hemidesmosomes (HD) and is connected to it by a basal lamina(BL). The
basal lamina consists of an electron-dense layer, the lamina densa (LD) and an
electron-lucent layer, the lamina lucida (LL). The lamina densa is composed of an
afibrillar type of collagen, type IV collagen. The lamina lucida is composed of
laminin and other glycoproteins. Anchoring fibrils (AF), composed of type VII
collagen, extend from the undersurface of the lamina densa into the lamina propria.
Sulcular Epithelium
 It is the stratified, squamous epithelium, non-keratinized or para
keratinized, that is continuous with the oral epithelium and lines
the lateral surface of the sulcus. Apically, it overlaps the coronal
border of the junctional epithelium, a structural design that
minimizes ulceration of the epithelial lining in this region. This
epithelium shares many of the characteristics of the oral epithelium
(Fig. 10), including good resistance to mechanical forces and
relative impermeability to fluid and cells.
The overall structure of the sulcular epithelium resembles that of
the oral epithelium, except for the surface layer that is less
keratinized than its counterpart in the oral epithelium. This
incomplete type of keratinization is referred to
as parakeratinization. CT, gingival connective tissue; GS,
gingival sulcus; PKE, parakeratinized epithelial layer.
Junctional Epithelium
 It is the stratified non-keratinizing epithelium, that surrounds the tooth like a collar
with a cross-section resembling a thin wedge. It is attached by one broad surface to
the tooth and by the other to the gingival connective tissue. The junctional
epithelium has 2 basal laminas, one that faces the tooth (internal basal lamina) and
one that faces the connective tissue (external basal lamina). The proliferative cell
layer responsible for most cell divisions is located in contact with the connective
tissue, i.e. next to the external basal lamina.
 The desquamative (shedding) surface of the junctional epithelium is located at its
coronal end, which also forms the bottom of the gingival sulcus.
 The junctional epithelium is more permeable than the oral or sulcular epithelium. It
serves as the preferential route for the passage of bacterial products from the sulcus
into the connective tissue and for fluid and cells from the connective tissue into the
sulcus.
 The term epithelial attachment: refers to the attachment apparatus, i.e. the internal
basal lamina and hemidesmosomes, that connects the junctional epithelium to the
tooth surface. This term is not synonymous with junctional epithelium which refers
to the entire epithelium.
 Segment of junctional epithelium (JE) from an area just apical to the gingival
sulcus. The width of the junctional epithelium may consist of as many as 30 cells in
the sulcus region to as few as one cell in its most apical portion. The intercellular
spaces between the cells of the junctional epithelium are wider than in the oral or
sulcular epithelia. This is due in part to the lower density of intercellular junctions
between the cells of the junctional epithelium. The density of junctions is
approximately one third of that in the oral and sulcular epithelium.
 This section is unusual by the absence of inflammatory cells in the connective
tissue adjacent to the epithelium.
 Transmission electronmicrograph of normal, uninflamed junctional epithelium
(JE). The cells are orientated with their long axis parallel to the tooth surface. The
intercellular spaces are relatively narrow. The epithelium is attached to the enamel
by an internal basal lamina (IBL) and to the connective tissue (CT) by the external
basal lamina (EBL). ES, enamel space.

The cytoplasm of the junctional epithelium contain dispersed tonofilaments, but
lack tonofibrils. Under normal circumstances these cells do not undergo
keratinization.
 Transmission electronmicrograph of junctional epithelium in inflamed gingiva.
Note the marked distension of the intercellular spaces by polymorphonuclear
leucocytes (PMN) that are migrating from the connective tissue toward the
gingival sulcus (located toward the top of the micrograph). Fluid exudate from the
connective tissue also flows into the sulcus through the enlarged intercellular
spaces. The spaces enlarge in part through rupture of the desmosomal junctions
and in part because they become distended by inflammatory cells and fluid.

The bi-directional arrows indicate that the junctional epithelium (JE) is the most
permeable portion of the gingival epithelia. Soluble substances can diffuse from the
oral cavity into the underlying gingival connective tissue (CT), while both fluids and
cells can travel through the junctional epithelium from the connective tissue into the
gingival sulcus (S) on their way to the oral cavity.
 Because of its permeability to bacterial products and other assorted antigens
originating in the oral cavity, the connective tissue adjacent to the junctional
epithelium tends to become infiltrated with chronic inflammatory cells, primarily
lymphocytes and plasma cells. OE, oral epithelium; SE, sulcular epithelium.
Gingival Connective Tissue
 The gingival connective tissue is composed of gingival fibers, ground
substance, and cells, including neural and vascular elements.
The bulk of the gingival connective tissue is composed of a dense,
predominantly collagenous matrix that contains collagen fibers running in
recognized fiber groups. These are referred to as the principal fibers of
the gingival connective tissue. The dense gingival connective tissue is
referred to as a lamina propria. It consists of the papillary layer, finger-like
projections of connective tissue that are contained within depressions on
the undersurface of the overlying epithelium, and the reticular layer,
located between the epithelial undersurface and the root surface or
adjacent alveolar process.
 At its junction with the lining mucosa, in the region delineated by
the mucogingival junction, the lamina propria becomes continuous with
the much looser and elastic connective tissue of the alveolar submucosa.
 The major components of the gingival connective
tissue include the fibers, the ground substance or
intercellular matrix, assorted cells, blood and
lymphatic vessels, and nerves. The ground substance
occupies the space between cells, fibers and
neurovascular elements.
 Its major constituents are water, glycoproteins
and proteoglycans. The ground substance permits
the diffusion of biological substances between
various structural elements.
Gingival Fibers
 Most of the fibers are composed of collagen, with
minor contributions
from elastic fibers and oxytalan fibers.
 Elastic and oxytalan fibers are generally confined to
perivascular regions, although oxytalan fibers are
also found as thin fiber bundles within collagen-rich
regions like the lamina propria.
Gingival Fibers - Collagen
 Transmission electron micrograph of gingival connective tissue
showing the intercellular junctions (ICJ) between cytoplasmic
strands from adjacent fibroblasts. The fibroblasts form an
interconnected network of cells, the intercellular spaces of which are
filled with fibers and ground substance, the jelly-like material in
which the fibers are embedded. The fibroblasts are responsible for
the production of the fibers and ground substance. They are also
capable of removing fibers and ground substance during remodeling
of the gingival tissues.
 Most of the fibers in gingival connective tissue are composed
of collagen. The bulk of the collagen is type I collagen, the most
abundant form of collagen in the human body. The structural unit
of type I collagen is a typically striated fibril with a characteristic
banding pattern that repeats every 64 nm. The banding results
from the packing arrangement of the collagen molecules that make
up the individual fibril
Fibrils
 Type I collagen fibrils are normally organized into
bundles of fibrils, or fibers. They are found throughout
the lamina propria.
 Type III collagen fibers are thinner than the type I fibers
and tend to be found close to basal laminas of vascular
channels and epithelial tissues. They stain readily with
silver stains and probably account for most of the
argyrophilic (silver stained) fibers seen in silver-stained
sections.
 They are also known as reticular fibers.
Gingival Fibers - Other
 Type VII collagen is found as anchoring fibrils, located in
intimate contact with epithelial basal laminas. In addition to
the fibrillar forms of collagen mentioned above, type IV
collagen, an amorphous form of collagen, is found in the basal
laminas of the epithelial lining and blood vessel walls,
primarily in the lamina densa.
 The other fiber types found in the periodontium are elastic
fibers and oxytalan fibers. Elastic fibers are rather scarce
in the lamina propria. They are a more common constituent
of the lining submucosa. They consist of 2 major components,
microfibrils made of fibrillin and the amorphous
component elastin. The latter provides the fiber with its
elastic properties.
 Note that elastic fibers consist of 2 distinct structural
entities, a microfibrillar component (MF) composed of
the protein fibrillin, and an amorphous component (AE)
that is composed of elastin, the protein that gives the
fibers their elastic properties. As elastic fibers mature,
the ratio of elastin to fibrillin increases. In the gingiva,
most elastic fibers are immature and poorly developed.
Oxytalan fibers are a fiber type related to elastic fibers.
They appear to consist of the microfibrillar component
only, thereby resembling very immature elastic fibers.
Fiber Groups
 These are largely composed of collagenous
fibers. The dentogingival fibers (A) insert into the supracrestal root
cementum and fan out into the adjacent connective
tissue. The dentoperiosteal fibers (B) insert into the supracrestal root
cementum and blend with the periosteal covering of the adjacent alveolar
process. The alveologingival fibers (C) insert into the alveolar crest and
fan out into the adjacent gingival connective
tissue. The circumferential fibers (D) follow a circular course around
individual dental units.
 The semicircular fibers (E) insert on the approximal surfaces of a tooth
and follow a semicircular course to insert on the opposite side of the same
tooth. The transgingival fibers (F) insert into the approximal surface of
a tooth and fan out toward the oral or vestibular
surface. The intergingival (G) fibers course along the oral or vestibular
surfaces of the dental arch. The transseptal fibers (H) course from one
approximal tooth surface to the approximal surface of the adjacent tooth.
Gingival Cells
 The major cellular elements in the gingival connective tissue
include:
 Fibroblasts, macrophages, mast cells, osteoblasts and osteoblast precursor
cells, cementoblasts and cementoblast precursor
cells, osteoclasts and odontoclasts, assorted inflammatory cells, and cells
that make up vascular channels and nerves. Inflammatory cells
include polymorphonuclear leucocytes, lymphocytes and plasma cells.
 Under normal circumstances they may be found in small numbers, as
isolated cells. In the presence of inflammation they can be found in large
numbers, often as dense cellular aggregates that have replaced the fibrous
elements in the connective tissue. The connective tissue also contains
undifferentiated ectomesenchymal cells that serve as a replacement source
for more differentiated cells, primarily fibroblasts.
 Fibroblasts are irregularly shaped cells responsible
for the synthesis of various connective tissue fibers
and the ground substance in which they are
imbedded. They are also responsible for the removal
of these structural elements. Therefore these cells
play a key role in the maintenance and remodeling of
the connective tissue.
Vessels and Nerves
 (i) Blood supply:
 The gingival blood supply originates from blood vessels in the
periodontal ligament, the marrow spaces of the alveolar process and
supraperiosteal blood vessels. These vessels in turn supply major
capillary plexuses that are located in the connective tissue adjacent
to the oral epithelium and the junctional epithelium.
 (ii) Lymphatics:
 The gingival tissues are supplied with lymphatic vessels that drain
principally to submaxillary lymph nodes.
 (iii) Nerves:
 Branches of the trigeminal nerve provide sensory and
proprioceptive functions. In addition, autonomic nerve endings are
associated with the vasculature.
Connective Tissue – Epithelial Interactions
 The interaction of connective tissues and adjacent epithelia have a significant effect
on epithelial tissue differentiation. The dense lamina propria found under the
masticatory mucosa is largely responsible for the maintenance of the stratified
squamous keratinizing epithelium that covers it. Likewise, the loose
connective tissue that supports the non-keratinizing lining epithelium is largely
responsible for the absence of keratinization in this epithelium.
 If a tissue graft consisting of lamina propria is taken from the masticatory mucosa of
the hard palate and is transplanted to a region lacking an adequate covering of
keratinizing mucosa, it will induce the epithelium that grows over it to keratinize,
even if the epithelium originates from an adjacent, non-keratinized mucosal
surface.
 This property of the connective tissue to modulate the differentiation of the
overlying epithelium is taken advantage of in reconstructive surgical
procedures. For example, a palatal connective tissue graft can be transplanted
subepithelially to a zone lacking keratinized mucosa, where it will induce the
overlying epithelium to differentiate into a keratinized epithelium.
Periodontal Ligament
Supportive
 The periodontal ligament serves primarily
a supportive function by attaching the tooth to the
surrounding alveolar bone proper. This function is mediated
primarily by the principal fibers of the periodontal ligament
that form a strong fibrous union between the root cementum
and the bone. The periodontal ligament also serves as a
shock-absorber by mechanisms that provide resistance to
light as well as heavy forces.
 Light forces are cushioned by intravascular fluid that is
forced out of the blood vessels. Moderate forces are also
absorbed by extravascular tissue fluid that is forced out of the
periodontal ligament space into the adjacent marrow
spaces. The heavier forces are taken up by the principal
fibers.
Remodeling
 The periodontal ligament also serves a
major remodeling function by providing cells that are
able to form as well as resorb all the tissues that make up
the attachment apparatus, i.e. bone, cementum and the
periodontal ligament
 Undifferentiated ectomesenchymal cells, located around
blood vessels, can differentiate into the specialized cells
that form bone (osteoblasts), cementum
(cementoblasts), and connective tissue fibers
(fibroblasts). Bone- and tooth-resorbing cells
(osteoclasts and odontoclasts) are generally
multinucleated cells derived from blood-borne
macrophages.
Sensory and Nutritive
 The periodontal ligament also serves
a sensory function. The myelinated dental nerves that
perforate the fundus of the alveoli rapidly lose their
myelinated sheath as they branch to supply both the pulp and
periodontal ligament. The periodontal ligament is richly
supplied with nerve endings that are primarily receptors for
pain and pressure.
 Finally, the periodontal ligament provides
a nutritive function that maintains the vitality of its various
cells. The ligament is well-vascularized, with the major blood
supply originating from the dental arteries that enter the
ligament through the fundus of the
alveoli. Major anastomoses exist between blood vessels in the
adjacent marrow spaces and the gingiva.
Cementum
Cementum
 Cementum may be found both on the root as well as the crowns of teeth. It may also
vary in its structure. Some forms of cementum may be cellular, while others are
not. Some have a fibrillar collagenous matrix, while others do not.
 Cementum may be classified in the following ways:
Radicular cementum: The cementum that is found on the root surface.
Coronal cementum: The cementum that forms on the enamel covering the crown.
Cellular cementum: Cementum containing cementocytes in lacunae within the
cementum matrix.
Acellular cementum: Cementum without any cells in its matrix.
Fibrillar cementum: Cementum with a matrix that contains well-defined fibrils
of type I collagen.
Afibrillar cementum: Cementum that has a matrix devoid of detectable type I
collagen fibrils. Instead, the matrix tends to have a fine, granular consistency.
 Extrinsic fiber cementum: Cementum that contains primarily extrinsic
fibers, i.e. Sharpey's fibers that are continuous with the principal fibers of
the periodontal ligament. Since the fibers were originally produced by
periodontal ligament fibroblasts, they are considered "extrinsic" to the
cementum. These fibers are orientated more or less perpendicularly to the
cementum surface and play a major role in tooth anchorage.

Intrinsic fiber cementum: Cementum that contains primarily
intrinsic fibers, i.e. fibers produced by cementoblasts and that are
orientated more or less parallel to the cementum surface. This form of
cementum is located predominantly at sites undergoing repair, following
surface resorption. It plays no role in tooth anchorage.

Mixed fiber cementum: Cementum that contains a mixture of
extrinsic and intrinsic fiber cementum.
Types
 1. Acellular, afibrillar cementum
 This cementum is mostly composed of mineralized matrix, without
detectable collagen fibrils or cementocytes. It is produced
exclusively by cementoblasts. It is typically found as coronal
cementum on human teeth.
 2. Acellular, extrinsic fiber cementum
 This type of cementum has a matrix of well-defined, type I collagen
fibrils. The fibrils are part of the, densely packed Sharpey's fibers,
that are continuous with the principal fibers of the periodontal
ligament. Because of their dense packing, the individual Sharpey's
fibers that form the bulk of the matrix may no longer be identifiable
as individual fibers within the cementum layer. This cementum,
which is acellular, is located in the cervical two-thirds of the root
of human teeth. It plays a major role in tooth anchorage.
 3. Cellular, intrinsic fiber cementum
 This cementum contains cementocytes in a matrix composed almost exclusively of
intrinsic fiber cementum. It is located almost exclusively at sites of cementum
repair. It plays no part in tooth anchorage. However, it may be covered over by
extrinsic or mixed fiber cementum, both of which are able to provide new
anchorage.
 4. Cellular, mixed fiber cementum
 It is found on the apical third of the root and in furcations (i.e. between roots). In
these locations, the rate of cementum formation is usually more rapid than in the
cervical region. The mineralized, extrinsic collagen fibers (Sharpey's fibers) run a
more irregular course than in acellular, extrinsic fiber cementum. Intrinsic fibers
are found interspersed among the extrinsic fibers of the cementum matrix, so that
individual Sharpey’s fibers are more readily identifiable than in extrinsic fiber
cementum. Cementoblasts are trapped in hollow chambers (or lacunae) where they
become cementocytes.
 The thickness of radicular cementum increases with age. It is thicker apically than
cervically. Thickness may range from 0.05 to 0.6 mm.
Bone
General
 The alveolar process is the portion of the jawbone that contains
the teeth and the alveoli in which they are suspended. The
alveolar process rests on basal bone. Proper development of the
alveolar process is dependent on tooth eruption and its
maintenance on tooth retention. When teeth fail to develop (e.g.
anodontia), the alveolar process fails to form. When all teeth are
extracted, most of the alveolar process becomes involuted, leaving
basal bone as the major constituent of the jawbone. The remaining
jawbone, therefore, is much reduced in height.
 The alveolar process is composed of an outer and inner cortical
plate of compact bone that enclose the spongiosa, a compartment
composed of spongy bone ( also called trabecular or cancellous
bone).
 It is important to distinguish between the terms "alveolar process"
and "alveolar bone" .
Alveolar Bone/Alveolar Process
 The alveolar bone proper lines the alveolus (or
tooth housing) which is contained within the
alveolar process. It is composed of a thin plate of
cortical bone with numerous perforations ( or
cribriform plate) that allow the passage of blood
vessels between the bone marrow spaces and the
periodontal ligament.
 The coronal rim of the alveolar bone forms the
alveolar crest, which generally parallels the cementoenamel junction at a distance of 1-2 mm apical to it
Fenestration
 Where roots are prominent and the overlying bone
very thin, the bone may actually resorb locally,
creating a window in the bone through which the
root can be seen. This window-like defect in the
bone is referred to as a fenestration (F)
Dehiscence
 In some cases, as shown in this figure, the rim of
bone between the fenestration and the alveolar crest
may disappear altogether and produce a defect
known as a dehiscence (D). Awareness of these
defects is important when surgical flaps are reflected,
as the exposure of such defects during surgery may
aggravate their severity.
Bone Formation
 Bone is produced by osteoblasts (OB) that are found in the
periosteum, endosteum and periodontal ligament adjacent to
bone-forming surfaces. These specialized cells originate from
less differentiated precursor cells close to the bone. These
cells are in turn derived from undifferentiated
ectomesenchymal cells found in the periosteum, endosteum
and the periodontal ligament.
 During bone formation, osteoblasts become incorporated into
bone as osteocytes (OC) that are completely surrounded by
bone. The chamber in which they are trapped is called
a lacuna (plur. lacunae). Osteocytes remain connected to
osteoblasts and other osteocytes by cytoplasmic processes that
run through small canals in the bone, or canaliculi (C).
Osteon
 Cortical plate of compact bone in the mandible. The mandible
is enveloped by a well-developed cortex of compact bone. The
bulk of the compact bone consists of cylindrical units of bone,
the osteons or Haversian systems (HS).
 Each osteon has a central canal, the Haversian canal that
houses a blood vessel. Haversian canals are linked to one
another and the periphery of the cortex by Volkman canals
that course perpendicularly to the Haversian canals. The
outer and inner layers of the cortex consist of parallel lamellae
of compact bone, called the external (ECL) and internal
circumferential lamellae. The bone that fills the spaces
between adjacent osteons is the interstitial bone.
CLASSIFICATION OF
PERIODONTAL DISEASES
Gingival Diseases…
Gingival Diseases
 Dental plaque-induced gingival diseases*
 1. Gingivitis associated with dental plaque only
 a. without other local contributing factors
 b. with local contributing factors (See VIII A)
Systemic Factors
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Gingival diseases modified by systemic factors
a. associated with the endocrine system
1) puberty-associated gingivitis
2) menstrual cycle-associated gingivitis
 3) pregnancy-associated
 a) gingivitis
 b) pyogenic granuloma
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4) diabetes mellitus-associated gingivitis
b. associated with blood dyscrasias
1) leukemia-associated gingivitis
2) other
Medications
 Gingival diseases modified by medications
 a. drug-influenced gingival diseases
 1) drug-influenced gingival enlargements
 2) drug-influenced gingivitis
 a) oral contraceptive-associated gingivitis
 b) other
Malnutrition
 Gingival diseases modified by malnutrition
 a. ascorbic acid-deficiency gingivitis
 b. other
Non-plaque induced
 1. Gingival diseases of specific bacterial origin
 a. Neisseria gonorrhea-associated lesions
 b. Treponema pallidum-associated lesions
 c. streptococcal species-associated lesions
 d. other
Viral Origin
 Gingival diseases of viral origin
 a. herpesvirus infections
 1) primary herpetic gingivostomatitis
 2) recurrent oral herpes
 3) varicella-zoster infections
 b. other
Fungal Origin
 Gingival diseases of fungal origin
 a. Candida-species infections
 1) generalized gingival candidiasis
 b. linear gingival erythema
 c. histoplasmosis
 d. other
Genetic Origin
 Gingival lesions of genetic origin
 a. hereditary gingival fibromatosis
 b. other
Systemic Conditions
 a. mucocutaneous disorders
 1) lichen planus
 2) pemphigoid
 3) pemphigus vulgaris
 4) erythema multiforme
 5) lupus erythematosus
 6) drug-induced
 7) other
Continued
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b. allergic reactions
1) dental restorative materials
a) mercury
b) nickel
c) acrylic
d) other
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2) reactions attributable to
a) toothpastes/dentifrices
b) mouth rinses/mouthwashes
c) chewing gum additives
d) foods and additives
3) other
Traumatic and Foreign
 Traumatic lesions (factitious, iatrogenic,
 accidental)
 a. chemical injury
 b. physical injury
 c. thermal injury
 7. Foreign body reactions
 8. Not otherwise specified (NOS)
Periodontal Diseases…
Chronic and Aggressive
 Chronic Periodontitis†
 A. Localized
 B. Generalized
 III. Aggressive Periodontitis†
 A. Localized
 B. Generalized
Perio - Systemic
 Periodontitis as a Manifestation of Systemic
 Diseases
 A. Associated with hematological disorders
 1. Acquired neutropenia
 2. Leukemia's
 3. Other
Continued
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B. Associated with genetic disorders
1. Familial and cyclic neutropenia
2 Down syndrome
3. Leukocyte adhesion deficiency syndromes
4. Papillon-Lefèvre syndrome
5. Chediak-Higashi syndrome
6. Histiocytosis syndromes
7. Glycogen storage disease
8. Infantile genetic agranulocytosis
9. Cohen syndrome
10. Ehlers-Danlos syndrome (Types IV and VIII)
11. Hypophosphatasia
12. Other
 C. Not otherwise specified (NOS)
Necrotizing
 Necrotizing Periodontal Diseases
 A. Necrotizing ulcerative gingivitis (NUG)
 B. Necrotizing ulcerative periodontitis (NUP)
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VI. Abscesses of the Periodontium
A. Gingival abscess
B. Periodontal abscess
C. Pericoronal abscess
 VII. Periodontitis Associated With Endodontic Lesions
 A. Combined periodontics-endodontic lesions
Developmental or Acquired
 VIII. Developmental or Acquired Deformities and
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Conditions
A. Localized tooth-related factors that modify or
predispose
to plaque-induced gingival diseases/periodontitis
1. Tooth anatomic factors
2. Dental restorations/appliances
3. Root fractures
4. Cervical root resorption and cemental tears
Continued
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Mucogingival deformities and conditions around teeth
1. Gingival/soft tissue recession
a. facial or lingual surfaces
b. interproximal (papillary)
2. Lack of keratinized gingiva
3. Decreased vestibular depth
4. Aberrant frenum/muscle position
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5. Gingival excess
a. pseudo pocket
b. inconsistent gingival margin
c. excessive gingival display
d. gingival enlargement (See I.A.3. and I.B.4.)
6. Abnormal color
Continued
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C. Mucogingival deformities and conditions on edentulous
ridges
1. Vertical and/or horizontal ridge deficiency
2. Lack of gingiva/keratinized tissue
3. Gingival/soft tissue enlargement
4. Aberrant frenum/muscle position
5. Decreased vestibular depth
6. Abnormal color
 D. Occlusal trauma
 1. Primary occlusal trauma
 2. Secondary occlusal trauma
Please Remember…
 Can be further classified on the basis of extent and
severity. As a general guide…
 Extent can be characterized as Localized = ≤30%
of sites involved and Generalized = >30% of sites
involved.
 Severity can be characterized on the basis of the
amount of clinical attachment loss (CAL) as follows:
Slight = 1 or 2 mm CAL, Moderate = 3 or 4 mm
CAL, and Severe = ≥5 mm CAL.
The Gingival Index
 The Gingival Index, published by Löe in 1967,
scores a 0 for no visible signs of inflammation a 1 for
slight change in color and texture, a 2 for noticeable
inflammation and bleeding upon probing and a 3 for
overt inflammation and spontaneous bleeding.
 The Plaque Index, published by Silness & Löe in
1964, scores plaque deposits on a 0-3 scale where 0
indicates that plaque is absent, 1 indicates plaque
detected by gingival marginal probing, 2 indicates
visible plaque and 3 indicates a lot of plaque.
Inflammation
 The presence or absence of inflammation have been
clinically assessed by gingival redness, suppuration,
bleeding on probing (BOP), measurements of
gingival temperature and gingival crevicular fluid
(GCF) and supragingival plaque.
 Further measures of success include maintaining
and improving periodontal comfort, esthetics and
function.
Current Health is Important
 The patient’s current, and historic periodontal health
and plaque control status serves as a baseline when
setting goals.
 The presence, absence, history, extent and
severity of periodontal diseases indicate the need
for various therapies.
ORA
 The Oral Risk Assessment (ORA) and Early Intervention
System provide a methodology to organize patient
“CARE”:
• Collection of relevant medical and dental information
• Assessment and assimilation of the collected
information
• Recommendation of professional therapies and home
care procedures and products
• Evaluation of treatment and healthcare outcomes
Health Implications
 The patient’s current systemic health also impacts
the setting of periodontal health goals. Systemic
conditions, infections, anomalies, trauma, etc.
contribute to gingival and periodontal diseases.
 For example, diabetes, endocrine effects,
medications, malnutrition, hematologic disorders,
genetic disorders as well as other systemic
considerations may affect oral health.
Remember the Anatomy
 The alveolar process is the portion of the mandible
and the maxilla that supports the teeth. Tooth
attachment is attained by the alveolar bone, the root
cementum and the periodontal membrane.
 Compact bone lines the alveolus, or tooth socket, and
is seen radiographically as the lamina dura.
Cancellous bone, containing bone trabeculae, is
found between the tooth sockets.
The Bone
The Bone
 Bone is often thought to be a static structure, but it
actually is continuously remodeling through actions
of osteoclasts (bone resorbing cells) and
osteoblasts (bone-building cells) and their
products, under the influence of parathyroid
hormone (PTH), vitamin D, estrogens,
glucocorticoids, growth hormone, thyroid hormone
and other factors such as cytokines, a unique family
of growth factors.
Remodeling the Bone
 Remodeling is accomplished in the trabecular bone
of the alveolar process, and elsewhere, by a team of
cells that dissolves a pit-like area in bone and then
fills it with new bone. This team of cells is called the
Basic Multicellular Unit (BMU).
 Bone is remodeled through a sequence of steps that
may take as much as 200 days, as follows:
Origination
 Origination is the phase during which a BMU
originates following an initiating “event” such as micro
damage, mechanical stress, exposure to one or more of a
group of biological factors, or even at random.
 The immune response begins in reaction to one of these
events. Cytokines and other growth factors, such as
parathyroid hormone (PTH), insulin-like growth factors
(IGF), interleukin-1 (IL-1), interleukin-6 (IL-6) and
tumor necrosis factor (TNF), are important in the
Origination phase.
Continued
 IL-1 may be the most important factor in the immune
response. Its function is to enhance the activation of Tcells in response to antigen. IL-6 is produced by
fibroblasts and other cells. IL-6 enhances glucocorticoid
syntheses. Overall it augments the response of immune
cells to other cytokines.
 Tumor Necrosis Factor-α (TNF- α), like IL-1, is a major
immune response-modifying cytokine produced mainly
by activated macrophages. The presence of TNF induces
osteoclast formation.
 Factors such as estrogen can reduce occurrence of
the Origination phase, thereby reducing the rate and
occurrence of bone resorption.
 Biologically mediated strategies for improving bone
growth in periodontitis patients work to modify the
effects of factors that promote bone resorption or to
boost the effects of the factors that promote bone
growth.
Osteoclast Recruitment
 The lining cells that were activated during Origination
secrete RANK-ligand, which may remain bound to the
cell surface. Preosteoclasts are activated by RANK-ligand
(RANKL) and then differentiate into mature osteoclasts
which develop a ruffled border and resorb bone.
 Osteoprotegerin (OPG) can act to bind the RANK-ligand
which reduces its effect. RANK-ligand is a potent bonebuilding agent. Osteoclasts are more effective at
resorbing bone when RANK-ligand’s effect is reduced.
Resorption
 Bone is resorbed by the mature osteoclasts for approximately two
weeks at a given location until the osteoclasts undergo preprogrammed cell death.
 New osteoclasts are continuously activated as the BMU travels.
Integrins and interleukins are immune factors that can act to
increase osteoclast activity. Integrins are cell surface receptors that
bind ligands and reduce their bone-building effect.
 Estrogen, calcitonin, interferon and TGF can reduce bone
resorption during this phase. Calcitonin works in opposition to
parathyroid hormone and can reduce its role in bone resorption.
Similarly bisphosphonates, such as risedronate sodium inhibit
osteoclast mediated bone resorption thereby reducing net bone loss.
Osteoblast Recruitment
 Osteoblasts are derived from bone marrow stromal
cells and are attracted by bone-derived growth
factors, (including Cbfa1, BMP’s, IGF, PTH, and
others) and perhaps the remains of the selfdestructed osteoclasts. Cbfa1 activates the bonespecific protein, osteocalcin.
 Bone morphogenetic proteins (BMPs) induce new
bone formation by stimulating proliferation and
migration of undifferentiated bone cell precursors.
Osteoid Formation and Mineralization
 Osteoblasts start the process of bone-building by
secreting layers of osteoid to slowly refill the cavity, as
well as growth factors (including TGF-beta, BMP’s and
IGF) and proteins. The presence of glucocorticoids may
retard osteoid formation.
Mineralization
 The osteoid begins to mineralize utilizing calcium and
phosphate when it is approximately 6 microns thick.
Mineralization is controlled by osteoblast activity. The
presence of pyrophosphate may reduce mineralization.
Mineral Maturation
 Bone density increases over months after the cavity
has been filled with bone because the mineral
crystals become more closely packed.
Quiescence
 During quiescence, some osteoblasts become lining
cells which help regulate ongoing calcium release
from the bones. Other osteoblasts become osteocytes
which remain in bone, connected by long cell
processes, which can sense functional stress on the
bone.
Bone Loss based on Morphology
 Bone lost to chronic periodontitis can create bone defects
with varying characteristics.
 For example, intra bony defects can have 1, 2 or 3
walls, they can be wide or narrow; and they can be
shallow or deep. In general, deep and narrow defects
with more bony walls have the greatest and most
predictable chance for successful gain in attachment
following periodontal surgery. Other factors strongly
influencing the chances for attachment gains include the
patient’s local, behavioral and systemic conditions and
characteristics. Plaque control, smoking, systemic
conditions clearly affect surgical outcomes.
Treatment
 The goals of achieving and maintaining periodontal
health lead to the endpoint of obtaining a healthy
and functional dentition for life.
 We track progress towards that endpoint by
assessing the health of the periodontal attachment
apparatus structures. Therapeutic options are
evaluated by the degree to which those outcomes are
met, as well as with the relative costs (measured in
dollars, time, morbidity, comfort, esthetics, etc.)
required to achieve them.
Continued
 All therapies which assist in limiting the deleterious
effects of the host response to periodontal pathogens can
be considered bone-preserving, as well as toothpreserving therapeutic options. The most effective
therapies may be those most under-rated in the
minds of some dental professionals. Adequate plaque
control by the patient and routine scaling and root
planing and adjunctive therapies in the general practice
and periodontal practice are essential to attain and
maintain periodontal health for most patients.
 Surgical therapies complement non-surgical therapies to
provide a range of valuable options.
The least invasive options are key!
 This is often accomplished through non-surgical
periodontal treatment, including scaling and root
planing (a careful cleaning of the root surfaces to remove
plaque and tartar from deep periodontal pockets and to
smooth the tooth root to remove bacterial toxins),
followed by adjunctive therapy such as systemic and local
delivery antimicrobials and host modulation, as needed
and on a case by- case basis.
 Most Periodontists would agree that after scaling and
root planing, many patients do not require any further
active treatment, including surgical therapy.
Antiseptics
 Antiseptics, delivered via rinsing and irrigation, have
been shown to be effective in controlling gingivitis,
but not periodontitis.
 The agents generally are not retained at the site long
enough for their antimicrobial effect to provide a
measurable benefit to pocket depth and/or
attachment levels.
Antimicrobials Delivered Locally
 Controlled clinical trials have consistently shown
that locally-delivered sustained-release
antimicrobials, along with scaling and root planing,
have been shown to provide a clinically and
statistically significant increase in the percentage of
patients achieving predetermined periodontal
benefits, than does scaling and root planing alone.
 Some trials have also shown that an agent alone can
reduce probing depths as much as SRP alone.
Continued
 Generally, it is agreed that these agents provide better
outcomes than SRP alone in sites where patient access
for plaque control might otherwise be limited; i.e.
wherever pocket depths are 2 mm or greater. Improved
outcomes can be obtained with these products during
both active and maintenance therapy.
 Bacterial resistance to antibiotic therapies have not been
reported, but resistance concerns can be avoided by the
use the locally-delivered sustained-release antimicrobial
containing chlorhexidine, an antiseptic rather than an
antibiotic which is not known to induce the emergence of
resistant strains
Products
 Examples of these products which have been
in the U.S. include tetracycline fibers, chlorhexidine
chip, doxycycline polymer, and minocycline
microspheres.
 A recent 3 month phase II clinical trial found that 0.4%
moxifloxacin gel, a fourth-generation fluoroquinolone,
administered in a single subgingival administration
adjunctive to scaling and root planning, resulted in
additional pocket depth reduction compared with scaling
and root planing plus a placebo gel.
Continued
 Moxifloxacin is a broad spectrum antimicrobial active
against aerobic and anaerobic bacteria. These results
would need to be confirmed in a phase III clinical trial.
Phase II trials generally assess efficacy and dose response
prior to designing a larger phase III trial.
 Phase III studies are generally randomized controlled
multicenter trials on larger groups of patients. The goals
of a phase III trial usually compares efficacy as compared
to the current gold standard treatment.
 Another recent 9 month clinical trial indicated that
microsphere formulation of doxycycline provide both a
more sustained release and a high initial drug
concentration as compared with doxycycline gel.
 All three groups (scaling and root planing alone,
doxycycline microspheres and doxycycline gel) showed
improvements in relative attachment levels at 9 months.
The group receiving scaling and root planing plus
doxycycline microspheres showed significantly greater
gain in relative attachment levels than the other
groups.21 Again further research is needed comparing
other agents and delivery systems.
Systemic Antibiotics
 Disrupting the biofilm mechanically is the gold
standard for reducing disease.
 Systemic antibiotics help prevent recolonization and
reorganization of the biofilm after the biofilm has
been disrupted.
 Many studies evaluate the effect of different
antibiotics in conjunction with scaling and root
planing.
Tetracycline
 Tetracycline administered as an adjunct to scaling and root
planing has shown a pocket reduction greater than
scaling and root planing alone.
 Mean pocket depth reductions were between 0.2 mm and 0.8
mm greater than scaling and root planing alone at six months
(2.2 mm to 3.1 mm total reduction) in pockets 4 mm to 6 mm.
 Mean clinical attachment level gain at six months was 0.04
mm to 0.3 mm better than scaling alone (1.06 mm to 1.7 mm
net gain). If surgical outcomes are included in the metaanalysis, then tetracycline with scaling and root planing with
or without replaced flap surgery has a net attachment benefit
over the intervention alone of 0.41 mm with a P = 0.003.
Metronidazole
 Metronidazole alone has shown a mean PD change over
scaling and root planing alone ranging from -.02 mm to
0.41 mm (0.46mm to 1.83 mm reduction in PD),
however, these differences in pocket depth were
shown not to have reached statistical
significance.
 Clinical attachment level changes in patients taking
metronidazole ranged .2 mm to 1.2 mm difference from
SRP alone (0.43 mm to 2.45 mm). Metronidazole with
amoxicillin after scaling and root planing in patients with
chronic periodontitis mean difference in clinical
attachment from scaling and root planing alone of 0.46
mm to 0.9 mm.
Augmentin
 Augmentin with scaling and root planing have not
shown to be effective in changes in PD at one year vs
SRP alone.
 Cal levels in Augmentin ranged in difference from
SRP alone by 0.16 mm to 1.3 mm (1 mm to 2.18 mm
total).
Clindamycin
 Clindamycin with SRP had CAL levels 1.6 mm better
than SRP alone in sites 6 mm or greater (3 mm
change) and 1.4 mm better than SRP alone overall
(1.7 mm change).
 Changes in PD ranged from 0.2 mm to 2.3 mm
between studies
Azithromycin
 Azithromycin and SRP showed a 0.3 mm increase in PD
over SRP alone at one year, whereas in sites initially 5
mm or greater, azithromycin showed 0.8 mm better than
SRP alone.
 In sites with 6 mm or greater pocket depth, azithromycin
and SRP had CAL gain over SRP alone of 0.9 mm at one
year.
 The microbiologic makeup of the subgingival biofilm at
one year after SRP and azithromycin had significantly
less red complex bacteria. Within one year all other
bacterial changes had reverted to near baseline.
Abscesses of the Periodontium
Types
 Periodontitis related abscess: When acute
infections originate from a biofilm ( in the deepened
periodontal pocket)
 Non-Periodontitis related abscess: When the
acute infections originate from another local source.
eg. Foreign body impaction, alteration in root
integrity
Acute
 The abscess develops in a short period of time and lasts
for a few days or a week. An acute abscess often presents
as a sudden onset of pain on biting and a deep throbbing
pain in a tooth in which the patient has been tending to
clench. The gingiva becomes red, swollen and tender.
 In the early stages, there is no fluctuation or pus
discharge, but as the disease progresses, the pus and
discharge from the gingival crevice become evident.
Associated lymph node enlargement maybe present.
Chronic
 This is the condition that lasts for a long time and
often develops slowly. In the chronic stages, a nasty
taste and spontaneous bleeding may accompany
discomfort.
 The adjacent tooth is tender to bite on and is
sometimes mobile. Pus may be present as also may
be discharges from the gingival crevice or from a
sinus in the mucosa overlying the affected root. Pain
is usually of low intensity.
Microbiology
Rods
 Streptococcus viridans is the most common isolate in the
exudate of periodontal abscesses when aerobic
techniques are used. It has been reported that the
microorganisms that colonize the periodontal abscesses
are primarily Gram negative anaerobic rods.
 Although they are not found in all cases of periodontal
abscesses, high frequencies of Porphyromonas
gingivalis, Prevotella intermedia, Fusobacterium
nucleatum, Campylobacter rectus, and
Capnocytophagaspp have been reported.
A.A?
 Actinobacillus actinomycetemcomitans is not usually
detected. The disappearance of Porphyromonas gingivalis from the
abscessed sites after treatment suggests a close association of this
microorganism with abscess formation.
 Spirochetes have been found as the predominant cell type in
periodontal abscesses when assessed by darkfield microscopy.
Strains of Peptostreptococcus, Streptococcus milleri (S. anginosus
and S. Inter medius), Bacteroides capillosus, Veillonella, B. fragilis,
and Eikenella corrodens have also been isolated.
 Overall, studies have noted that the microbiotas found in abscesses
are similar to those in deep periodontal pockets.
Periodontal Abscesses
 1. Porphyromonas gingivalis-55-100%
 2. Prevotella intermedia- 25-100%
 3. Fusobacterium nucleatum -44-65%
 4. Actinobacillus actinomycetemcomitans-25%
 5. Camphylobacter rectus- 80%
 6. Prevotella melaninogenica-22%
What happens…
 After the infiltration of pathogenic bacteria to the
periodontium, the bacteria and/or bacterial products
initiate the inflammatory process, consequently
activating the inflammatory response. Tissue
destruction is caused by the inflammatory cells and
their extracellular enzymes.
 An inflammatory infiltrate is formed, followed by the
destruction of the connective tissue, the encapsulation of
the bacterial mass and pus formation. The lowered tissue
resistance and the virulence as well as the number of
bacteria present, determine the course of infection. The
entry of bacteria into the soft tissue wall initiates the
formation of the periodontal abscess.
How does an Abscess develop?
 Changes in the composition of the microflora, bacterial virulence or in
host defences could also make the pocket lumen inefficient to drain the
increased suppuration.
 Closure of the margins of the periodontal pockets may lead to the extension
of the infection into the surrounding tissues, due to the pressure of the
suppuration inside the closed pocket.
 Fibrin secretions leading to the local accumulation of pus, may favour the
closure of the gingival margin to the tooth surface.
 Tortuous periodontal pockets are especially associated with furcation
defects. These can eventually become isolated and can favour the formation
of an abscess.
 After procedures like scaling where the calculus is dislodged and pushed
into the soft tissue.
Also…
 Periodontal abscesses can also develop in the absence of
periodontitis, due to the following causes:
 Impaction of foreign bodies (such as a piece of dental floss, a
popcorn kernel, a piece of a toothpick, fishbone, or an
unknown object).
 Infection of lateral cysts
 Local factors affecting the morphology of the root may
predispose to periodontal abscess formation. (The presence of
cervical cemental tears has been related to rapid progression
of periodontitis and the development of abscesses).
Other Factors Associated with an Abscess
 Post non-surgical therapy periodontal abscess (Abscess may occur
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during the course of active non-surgical therapy)
Post scaling periodontal abscess. eg. Due to the presence of a small
fragment of the remaining calculus that may obstruct the pocket
entrance or when a fragment of the calculus is forced into the deep,
non-inflamed portion of the tissue
Post surgical periodontal abscess -when the abscess occurs
immediately following periodontal surgery. It is often due to the
incomplete removal of the subgingival calculus
Perforation of the tooth wall by an endodontic instrument.
The presence of a foreign body in the periodontal tissue (eg. Suture
/ pack)
Post antibiotic periodontal abscess -treatment with systemic
antibiotics without subgingival debridement in patients with
advanced perio may cause abscess formation.
Diagnosis
 Diagnosis depends on many factors – and whether
pain is present will differentiate from an acute or
chronic abscess.
 Asking if the client smokes is very important – as
this could delay healing time for the periodontal
abscess or gum disease in general.
 Everything needs to be examined included the lesion,
oral hygiene, clients medical and dental history,
mobility, pus, swelling, redness, etc.
How to Confirm
 Radiographs –
 There are several dental radiographical techniques which are
available (periapicals, bitewings and OPG) that may reveal
either a normal appearance of the interdental bone or evident
bone loss, ranging from just a widening of the periodontal
ligament space to pronounced bone loss involving most of the
affected cases.
 Intra oral radiographs, like periapical and vertical bite-wing
views, are used to assess marginal bone loss and the perapical
condition of the tooth which is involved. A gutta percha point
which is placed through the sinus might locate the source of
the abscess.
Vitality Test
 The Pulp Vitality Test –
 The Pulp vitality test, like thermal or electrical tests,
could be used to assess the vitality of the tooth and
the subsequent ruling out of the concomitant pulpal
infections.
Microbial and Lab Testing
 Microbial Test -
 Samples of pus from the sinus/ abscess or that which is
expressed from the gingival sulcus could be sent for
culture and for sensitivity tests. Microbial tests can also
help in implementing the specific antibiotic courses.
 Lab Testing  Lab tests may also be used to confirm the diagnosis. The
elevated numbers of the blood leukocytes and an increase
in the blood neutrophils and monocytes may be
suggestive of an inflammatory response of the body to
bacterial toxins in the periodontal abscess.
Other
 Others  Multiple periodontal abscesses are usually associated
with increased blood sugar and with an altered
immune response in diabetic patients.
 Therefore, the assessment of the diabetic status
through the testing of random blood glucose, fasting
blood glucose or glycosylated haemoglobin levels is
mandatory to rule out the aetiology of the
periodontal abscess.
Types
Gingival Abscess
 Features that differentiate the gingival abscess from
the periodontal abscess are:
 i. History of recent trauma;
 ii. Localisation to the gingiva;
 iii. No periodontal pocketing
Periapical Abscess
 Periapical abscess can be differentiated by the
following features:
 i. Located over the root apex
 ii. Non-vital tooth, heavily restored or large filling
 iii. Large caries with pulpal involvement.
 iv. History of sensitivity to hot and cold food
 v. No signs / symptoms of periodontal diseases.
 vi. Periapical radiolucency on intraoral radiographs.
Perio-Endo
 PERIO-ENDO LESION
 i. Severe periodontal disease which may involve the furcation
 ii. Severe bone loss close to the apex, causing pulpal infection
 iii. Non-vital tooth which is sound or minimally restored
 ENDO-PERIO LESION
 Endo-perio lesion can be differentiated by:
 i. Pulp infection spreading via the lateral canals into the
periodontal pockets.
 ii. Tooth usually non-vital, with periapical radiolucency
 iii. Localised deep pocketing
Cracked Tooth Syndrome
 Cracked tooth Syndrome can be differentiated by:
 i. History of pain on mastication
 ii. Crack line noted on the crown.
 iii. Vital tooth
 iv. Pain upon release after biting on cotton roll,
rubber disc or
 tooth sleuth
 v. No relief of pain after endodontic treatment
Root Fracture
 Root fracture can be differentiated by the presence of:
 i. Heavily restored crown
 ii. Non-vital tooth with mobility
 iii. Post crown with threaded post
 iv. Possible fracture line and halo radiolucency around
the root which are visible in periapical radiographs
 v. Localised deep pocketing, normally one site only
 vi. Might need an open flap exploration to confirm
diagnosis
Treatment
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1. Local measures
i. Drainage
ii. Maintain drainage
iii. Eliminate cause
 2. Systemic measures in conjunction with the

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local measures
The management of a patient with periodontal abscess
can divided into three stages:
i. Immediate management
ii. Initial management
iii. Definitive therapy
Antibiotics
 Antibiotics are prescribed empirically before the microbiological
analysis and before the antibiotic sensitivity tests of the pus and
tissue specimens. The empirical regimens are dependent on the
severity of the infection.




The common antibiotics which are used are:
1. Phenoxymethylepenicillin 250 -500 mg qid 5/7 days
2. Amoxycillin 250 - 500 mg tds 5-7 days
3. Metronidazole 200 - 400 mg tds 5-7 days

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If allergic to penicillin, these antibiotics are used:
1. Erythromycin 250 –500 mg qid 5-7 days
2. Doxycyline 100 mg bd 7-14 days
3. Clindamycin 150-300 mg qid 5-7 days
Initial Therapy - Acute
 a. The irrigation of the abscessed pocket with saline
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or antiseptics
b. When present, the removal of foreign bodies
c. Drainage through the sulcus with a probe or light
scaling of the tooth surface
d. Compression and debridement of the soft tissue
wall
e. Oral hygiene instructions
f. Review after 24-48 hours; a week later, the
definitive treatment should be carried out.
Periodontal
 The treatment options for periodontal abscess under
initial therapy:
 1. Drainage through pocket retraction or incision
 2. Scaling and root planning
 3. Periodontal surgery
 4. Systemic antibiotics
 5. Tooth removal
Conclusion
 The occurrence of periodontal abscesses in patients who are under
supportive periodontal treatment has been frequently described.
 Early diagnosis and appropriate intervention are extremely
important for the management of the periodontal abscess, since this
condition can lead to the loss of the involved tooth. A single case of
a tooth diagnosed with periodontal abscess that responds
favourably to adequate treatment does not seem to affect its
longevity.
 In addition, the decision to extract a tooth with this condition
should be taken, while taking into consideration, other factors such
as the degree of clinical attachment loss, the presence of tooth
mobility, the degree of furcation involvement, and the patient’s
susceptibility to periodontitis due to the associated systemic
conditions.