ALVEOLAR BONE
And it’s associated pathologies
By the student : Mustafa Waly Hussain
Stage : 4th
Group : D
A Brief Introduction
The alveolar process is a major component of the tooth-
supporting apparatus and is comprised of alveolar bone proper,
cortical alveolar bone, alveolar crest, and trabecular bone. The
alveolar process develops along with the dentition and
undergoes resorption following extraction of teeth. With the
advent of dental implant-supported rehabilitation,
understanding and preserving the alveolar bone has become
more imperative than ever before. In order to achieve the same,
knowledge about applied biology, composition, microstructure,
and anatomic, clinical, and radiographic features of alveolar
bone is essential.
The Alveolar Process
COMPOSITION
Inorganic matrix
Alveolar bone is 67% inorganic material by weight. The inorganic
material is composed mainly of the minerals calcium and
phosphate. The mineral content is mostly in the form of calcium
hydroxyapatite crystals.
Organic matrix
The remaining alveolar bone is organic material (33%). The
organic material consists of collagen and non-collagenous
material. The cellular component of bone consists of
osteoblasts, osteocytes and osteoclasts.
• Osteoblasts are usually cuboidal and slightly elongated in shape.
They synthesise both collagenous ad non-collagenous bone
proteins. These cells have a high level of alkaline phosphatase on
the outer surface of their plasma membrane. The functions of
osteoblasts are bone formation by synthesising the organic matrix
of bone, cell to cell communication and maintenance of bone
matrix.
• Osteocytes are modified osteoblasts which become entrapped in
lacunae during the secretion of bone matrix. The osteocytes have
processes called canaliculi that radiate from the lacunae. These
canaliculi bring oxygen and nutrients to the osteocytes through
blood and remove metabolic waste products.
• Osteoclasts are multinucleated giant cells. They are found in
Howship’s lacunae.
Alveolar Bone Loss
Bone is lost through the process of resorption which involves
osteoclasts breaking down the hard tissue of bone. A key
indication of resorption is when scalloped erosion occurs. This is
also known as Howship’s lacuna. The resorption phase lasts as
long as the lifespan of the osteoclast which is around 8 to 10
days. After this resorption phase, the osteoclast can continue
resorbing surfaces in another cycle or carry out apoptosis. A
repair phase follows the resorption phase which lasts over 3
months. In patients with periodontal disease, inflammation lasts
longer and during the repair phase, resorption may override any
bone formation. This results in a net loss of alveolar bone.
Alveolar bone loss is closely associated with periodontal disease.
Periodontal disease is the inflammation of the gums. Studies in
osteoimmunology have proposed 2 models for alveolar bone
loss. One model states that inflammation is triggered by a
periodontal pathogen which activates the acquired immune
system to inhibit bone coupling by limiting new bone formation
after resorption. Another model states that cytokinesis may
inhibit the differentiation of osteoblasts from their precursors,
therefore limiting bone formation. This results in a net loss of
alveolar bone.
Alveolar Bone Loss In Osteoporosis
Mechanisms of Bone Resorption in
Periodontitis
Alveolar bone loss is a hallmark of periodontitis progression and
its prevention is a key clinical challenge in periodontal disease
treatment. Bone destruction is mediated by the host immune and
inflammatory response to the microbial challenge. However, the
mechanisms by which the local immune response against
periodontopathic bacteria disturbs the homeostatic balance of
bone formation and resorption in favour of bone loss remain to
be established. The osteoclast, the principal bone resorptive cell,
differentiates from monocyte/macrophage precursors under the
regulation of the critical cytokines macrophage colony-
stimulating factor, RANK ligand, and osteoprotegerin. TNF-α, IL-
1, and PGE2 also promote osteoclast activity, particularly in states
of inflammatory osteolysis such as those found in periodontitis.
The pathogenic processes of destructive inflammatory
periodontal diseases are instigated by subgingival plaque
microflora and factors such as lipopolysaccharides derived from
specific pathogens. These are propagated by host inflammatory
and immune cell influences, and the activation of T and B cells
initiates the adaptive immune response via regulation of the Th1-
Th2-Th17 regulatory axis. In summary, Th1-type T lymphocytes, B
cell macrophages, and neutrophils promote bone loss through
upregulated production of proinflammatory mediators and
activation of the RANK-L expression pathways.
Bone Remodeling
The maintenance of bone is achieved by a fine balance between
bone formation and bone resorption. The differentiation and
activation of osteoclasts are tightly regulated by osteoblasts.
Osteoblasts express at least two cytokines essential for
osteoclast differentiation; they are receptor activator of NF-
kappaB ligand (RANKL) and macrophage colony stimulating
factor (M-CSF). On the other hand, differentiation of osteoblasts
is regulated by the transcription factors Runx2 and Osterix. The
recent progress of genetic experiments has revealed that
osteoclasts also regulate the differentiation of osteblasts in vivo.
This review describes the recent studies on the communication
between osteoblasts and osteoclasts in the process of bone
remodeling.
Thank You
